A man who underwent brain stimulation had previously tried 20 treatments for his depression
Damien Fair et al./cc-by 4.0
Men suffering from severe depression for over 30 years have seemingly found relief through a personalized brain “pacemaker” designed to selectively stimulate various brain regions.
“He’s felt joy for the first time in years,” states Damien Fair from the University of Minnesota.
Treatment-resistant depression is often characterized by minimal improvement after trying at least two antidepressants. While procedures like electroconvulsive therapy (ECT) may provide some benefits, they don’t always yield relief. “They’re effective for all sizes. You’ll target the same brain area,” Fair explains. Yet, as every brain is unique, he often doesn’t hit the exact target needed for individual relief.
Fair and his team have now created a tailored method for a 44-year-old man, who was first hospitalized for depression at 1 PM. He had attempted 20 different treatments, including antidepressants, therapy, ECT, and more, all without lasting success. “It’s one of the most severe depression cases I’ve seen; he has attempted suicide three times,” Fair notes.
Initially, the researchers conducted a 40-minute MRI scan to delineate the boundaries of four brain activity networks linked to depression. This particular network in the man was found to be four times more active than that of individuals without depression, potentially exacerbating his symptoms, according to Fair.
The team then surgically implanted clusters of four electrodes at these defined boundaries, entering through two small openings in the skull. Just three days later, they began sending weak electrical pulses through wires attached to the electrodes, stimulating each brain network separately.
Upon stimulating the first network—default mode, related to introspection and memory—the man cried tears of joy. “I felt so much better,” Fair recalls.
Stimulation of the Action Mode and Salience Networks also led to reduced feelings of anxiety, while the team noticed enhanced focus when targeting the parietal networks involved in decision-making.
Using the man’s feedback, the team connected the electrode wires to tiny batteries placed just beneath the skin near the collarbone, allowing him to maintain these benefits outside the hospital. This setup acts like a “brain pacemaker,” as Fair describes it, stimulating various networks for a minute each day.
For six months, the man utilized an app linked to the pacemaker to alternate between different stimulation patterns crafted by the team every few days. He also documented his depression symptoms daily. The team optimized the stimulation based on this data during the first six months post-surgery.
Even seven weeks post-surgery, the man reported no suicidal thoughts. By the nine-month mark, he was in remission as per the Hamilton Depression Rating Scale. This improvement persisted for over two and a half years, apart from a brief period when his symptoms slightly recurred after contracting Covid-19.
“This is an incredible outcome,” states Mario Juruna from King’s College London. “It serves as a crucial proof of concept for patients unable to tolerate traditional depression treatments.”
It’s plausible that the expanded salience network of the man played a role in the treatment’s success. This is often present in depression; however, it’s premature to conclude if individuals with a lower level of salience network expansion would respond similarly, Juruena states.
To confirm the safety and effectiveness of this approach, randomized controlled trials assigning various individuals with depression to either stimulation or placebo will be necessary, according to Juruena. The team aims to conduct these trials within two years after testing the method on additional individuals, according to Fair.
If you need someone to listen, reach out: Samaritans in the UK at 116123 (Samaritans.org); US 988 Suicide & Crisis Lifeline: 988 (988lifeline.org). Visit bit.ly/suicidehelplines for resources in other countries
If you think we’ve already asked, do you know precisely what Déjà Vu is? If you’re among the wise, you’ll say it’s a peculiar sensation that you’ve experienced something before.
However, many neuroscientists argue that this definition lacks a touch of the enigmatic. Experts like Dr. Akira O’Connor, a Senior Psychology Lecturer at St Andrews University, indicates that Déjà Vu (French for ‘already seen’) is not just a friendly notion but also a metacognitive perception where these feelings can be misleading.
“Déjà Vu essentially represents a conflict between the perception of familiarity and the realization that something feels incorrectly familiar. This deception makes Déjà Vu unique compared to other memory occurrences,” he explains.
“Most healthy individuals recognize a sense of familiarity but do not tend to alter their behavior, even when they know something feels logically off.”
So, what occurs in the brain during Déjà Vu? And why do some individuals experience this phenomenon more frequently than others? Dive into the complete guide below for more insight.
However, neuroscientists have determined that this memory illusion does not signify an unhealthy brain. Far from a memory error, it is more about the brain’s functions. According to O’Connor, Déjà Vu surfaces when the frontal lobe attempts to rectify inaccurate memories.
“For most individuals, experiencing Déjà Vu is likely a positive sign that the brain regions responsible for factual checks are functioning effectively and preventing misremembering events.
“In healthy individuals, such false memories can emerge daily due to the complexity of memory involving millions and billions of neurons. It’s quite intricate,” he states.
Regrettably, there isn’t a universally accepted model that clarifies what transpires in the brain during Déjà Vu. Nevertheless, most leading theories converge on the idea that Déjà Vu arises when a brain area (like the temporal lobe) provides the frontal region with signals that past experiences are being replayed.
“Afterward, the decision-making region at the front checks if this signal aligns with reality. It’s essentially asking, ‘Have I been here before?'”
“If you have actually been in that location before, you might strive to recall more memories. Otherwise, the realization of Déjà Vu kicks in.”
Why Do Some Individuals Experience Déjà Vu More Frequently?
O’Connor estimates that the average healthy person feels Déjà Vu around once a month, but certain factors can heighten the chances of feeling this sensation.
First, your level of fatigue and stress plays a significant role. “When your brain is exhausted, it hasn’t had the chance to recover and regulate itself. Consequently, your neurons may be slightly misaligned, making you more prone to experiencing Déjà Vu,” he explains.
“Dopamine is what we label as an excitatory neurotransmitter. When discussing brain areas that signal familiarity, there’s a dopaminergic influence on those neurons, indicating dopamine’s involvement,” O’Connor adds.
“This might explain why recreational drugs, which affect dopaminergic activity, frequently lead to experiences of Déjà Vu.”
There are additional factors as well. Have you ever wondered why your Déjà Vu experiences have diminished? According to rigorous scientific studies, it could be because you’re inadvertently a step ahead.
“Unfortunately, like many memory phenomena, it is a natural consequence of aging, and you might not be capable of noticing the discrepancies,” O’Connor clarifies.
“It’s intriguing to observe that younger individuals frequently experience more Déjà Vu. Older adults are generally expected to have more memory issues; however, this generally results from them having heightened excitatory activity in their brains.
“When I embarked on my research into Déjà Vu nearly 20 years ago, I experienced it regularly, but now it’s much less frequent!”
Is Déjà Vu Ever Unhealthy?
Now that we know Déjà Vu is a healthy cognitive mechanism—far from dangerous—what if you find yourself experiencing it constantly? What could it mean if all new encounters feel familiar?
Interestingly, this can happen to some individuals. “In Finland, there are intriguing cases of individuals who have taken a combination of flu medications known to overly stimulate certain dopamine neurons.
“They found it particularly fascinating and continued taking those medications for a while.
However, not everyone can afford to step back from this existential déjà vu. Those who suffer from ‘Déjà vécu’ (French for ‘already experienced’) have an ongoing sensation of having already undergone their current situation. Essentially, nothing feels novel to them.
“What’s particularly captivating about individuals with Déjà vécu is that they often lose their ability to fact-check these feelings. Many cease watching television because they feel they’ve already seen every episode,” O’Connor observes.
“It sounds fascinating and innovative, but it’s genuinely distressing because it can often occur in individuals with dementia and may signal worsening degeneration.”
Explore More About Memory Science:
Déjà Vu: Jamais Vu is another curious phenomenon of similarity. It refers to the inability to recognize familiar scenarios logically. Though often linked with amnesia, it goes beyond mere memory lapses.
“This isn’t a typical form of forgetfulness,” O’Connor elaborates. “When you recognize a task at hand but are puzzled because you can’t identify something familiar. The crucial aspect is the perception element. You recognize that feeling as being fundamentally incorrect.”
“It occurs more frequently than Déjà Vu, yet likewise tends to happen when individuals are fatigued and is more common among younger people than older adults.”
Some laboratory experiments appear to induce Jamais Vu in participants. For instance, one study from the University of Leeds instructed 93 participants to write down the word ‘door’ as many times as possible within two minutes.
What’s particularly intriguing about this study is that it can be replicated anywhere. So, if you have two minutes and a pen handy, we encourage you to repeat after us: door, door, door, door, door…
About Our Expert – Dr. Akira O’Connor
Akira O’Connor is a senior lecturer at the School of Psychology and Neuroscience at St. Andrews University. His primary focus is on how memories influence decision-making and how we perceive them.
Research indicates that individuals are more inclined to forge friendships if their brains react similarly to movie clips, implying that neural responses can forecast relationships.
Humans typically gravitate toward others with similar mindsets, a phenomenon that helps to explain why prior studies have identified neural parallels among friends. However, the question remained whether these similarities emerged because friends experienced similar upbringings or were attracted to those with comparable thought processes.
Carolyn Parkinson and her team at UCLA gathered brain scans from 41 students before they entered a graduate program. During the scan, participants viewed 14 diverse film clips, ranging from documentaries to comedies, covering topics like food, sports, and science. The researchers then assessed neural activity across 214 regions of each participant’s brain.
Two months later, participants completed a survey along with an additional 246 students in the program. The findings showed that those who were closer to Mark in terms of friendship tended to display more similar neural responses than those further removed in the social network, particularly in areas of the left preorbital cortex associated with subjective value processing. This correlation held true even after accounting for personal tastes based on individual enjoyment and interest in the clips.
After two months, the neural similarity between friends remained consistent, suggesting that initial friendships may form based on proximity before evolving into closer relationships over time. This was further supported when the researchers analyzed changes in friendships over the interim. Participants approaching this phase exhibited notable neural similarities compared to those whose activity drifted among 42 brain regions. These connections remained significant even after considering variables such as age, gender, and hometown. “The sociodemographic factors seem to account for some variations observed, at least in terms of measurable factors,” stated Parkinson.
Many of these brain regions are part of networks that facilitate understanding narratives, which may explain the similarity in how individuals perceive the world around them. “Individuals with like-minded thought processes find it easier to connect,” noted Robin Dunbar from Oxford University. “When they communicate, they intuitively grasp what others are thinking because it’s aligned with their own thought patterns.”
Dunbar, who did not participate in the study, expressed that these results resonate with long-held assumptions. “It’s akin to random groups of people unintentionally forming bonds based on compatibility; they are inherently attracted to one another,” he explained. “In essence, close friendships are not merely coincidental; they are composed and cultivated.”
Ibogain, a psychedelic substance, is derived from the roots of the Iboga plant
Farmer Dods / Alamy
The psychedelic substance ibogaine has been shown to slow brain wave activity in individuals with traumatic brain injuries, potentially accounting for its effectiveness in treating symptoms of post-traumatic stress disorder (PTSD).
A study conducted last year revealed that ibogaine, sourced from the African Iboga plant, significantly enhanced the overall mental and physical well-being of military veterans suffering from traumatic brain injuries. Yet, the precise mechanisms behind these effects were previously unknown.
To investigate further, Jennifer Lismore from Stanford University and her team examined brain imaging of 30 individuals involved in the initial study. During a 5-day treatment session at a facility in Mexico, participants received a dosage of 12 milligrams of ibogaine per kilogram of body weight and participated in supportive activities like yoga, meditation, and therapy.
As part of the study, the researchers collected EEG data that recorded participants’ brain electrical activity. These scans were taken 2-3 days prior to and 3.5 days following the ibogaine treatment.
By comparing the EEG findings, Lismore and her team observed an overall deceleration in brain wave activity post-treatment, particularly in the gamma waves—the fastest brain waves—which exhibited nearly a 16% reduction in strength in the occipital region after ibogaine therapy. While gamma wave intensity saw a slight rebound after one month, levels remained significantly below those recorded prior to treatment.
Additionally, the intensity of slow theta waves rose by approximately 17% in the back of the brain and 13% at the front 3.5 days post-treatment. However, this increase lost its significance after one month.
Lismore suggests that the observed reduction in brain wave activity may clarify why ibogaine is effective for alleviating PTSD symptoms in many patients. “The deceleration of brain function has allowed patients, particularly those experiencing hyperawareness and sensitivity associated with PTSD, to find relief,” she noted. “One way to understand this slowing process is as a mitigation of the heightened distress often seen in PTSD cases.”
The temporary spike in slow theta waves could also indicate that ibogaine promotes neuroplasticity—the brain’s ability to adapt and rewire itself. Previous studies in animals have associated theta wave activity with brain adaptability, Lismore explains. By inducing a short-term increase in theta wave presence, ibogaine may create conditions conducive to improving mental health.
“Ibogaine essentially addresses the chaotic, restless nature of the brain, facilitating a sort of normalization,” remarked Conor Murray from the University of California, Los Angeles. “Ultimately, it instills a sense of security for participants, reassuring the brain.”
However, he cautions that these findings don’t fully reveal the mechanisms through which ibogaine effects these brain changes.
Another challenge is the absence of control measures, complicating the assessment of the influence from other treatment components, points out Lismore. Nonetheless, she asserts that these insights represent “a significant first step toward understanding why this treatment is so impactful.”
Our brains are glowing. While this phenomenon isn’t visible to the naked eye, scientists have the ability to detect faint light that permeates the skull. Recent studies indicate that this light varies based on our activities.
All living tissues generate a subtle light known as Ultraweak Photon Emissions (UPE). This emission ceases once the organism dies. The human brain, however, emits a considerable amount of this light due to its high energy consumption, accounting for around 20% of the body’s total energy.
“Ultraweak photon emissions, or UPE, are extremely faint light signals produced by all types of cells throughout the body—trillions of times weaker than the light from bulbs,” stated Dr. Nirosha Murugan, an Assistant Professor of Health Sciences at Wilfrid Laurier University in Ontario, Canada. BBC Science Focus.
“Although UPE is a weak signal, the energy expenditure of the brain generates more light than other organs,” she explained. “Consider the hundreds of billions of brain cells; each one emits a weak light signal, but together they create a measurable collective glow outside the head.”
Murugan’s research team aimed to explore whether this glow fluctuated with brain activity and if it could be utilized to assess brain functions.
To investigate, scientists equipped participants with caps containing electrical sensors to track both electrical impulses and light emitted from the brain. Twenty adults were invited to sit in a darkened room.
Participants were directed to open and close their eyes and follow simple audio instructions.
Comparisons were made between the captured electrical signals and UPEs, revealing notable correlations.
“We discovered that the optical signals detected around the head correlate with electrical activity in the brain during cognitive tasks,” Murugan noted. “These patterns of light emission from the brain are dynamic, intricate, and informative.”
The brain emitted this light in a slow, rhythmic pattern, occurring less than once per second, creating the illusion of stability throughout the two-minute tasks.
All living cells emit ultrawave light as a byproduct of chemical reactions such as energy metabolism – Credit: Sean Gladwell via Getty
Murugan indicated that measuring this brain light could offer scientists and medical professionals a novel method for brain imaging, potentially identifying conditions like epilepsy, dementia, and depression.
This light is not merely a by-product; it might also play a functional role in the brain. Murugan emphasized that examining it could “uncover hidden dimensions” of our cognitive processes.
“I hope that the possibility of detecting and interpreting light signals from the brain will inspire new questions previously deemed unfathomable,” she stated. “For instance, can UPEs permeate the skull and influence other brains within the vicinity?”
This study serves as a preliminary exploration, suggesting that plenty remains to be uncovered about our illuminating brains.
Nonetheless, Murugan expressed hope that the team’s discoveries will “ignite a new discussion regarding the significance of light in brain functionality.”
read more:
About our experts
Dr. Nirosha Murugan is an assistant professor in the Department of Health Sciences at Wilfrid Laurier University, Ontario, Canada. She was recently appointed as Tier 2 Canada Research Chair of Biophysics at the University of Algoma in Ontario.
Ribosome (center) responsible for synthesizing protein (red) from mRNA. Dark purple strands illustrate transfer RNAs involved in protein production.
The underlying factors contributing to cellular senescence may have been uncovered, revealing insights into various aging processes at the cellular level.
Studies on the brains of a type of freshwater fish known as Killifish reveal that as these fish age, their internal protein factories begin to malfunction, leading to critical protein classes being synthesized abnormally and creating a damaging feedback loop.
This revelation could pave the path for innovative approaches to addressing cognitive decline in aging; Alessandro Cellerino from the Leibniz Institute on Aging in Germany states, “Our focus is more on enhancing cognitive function and preventing cognitive impairment, rather than merely extending life span.”
Within cells, the templates for protein synthesis are encoded in DNA. When proteins are required, these instructions are transcribed into mRNA molecules.
This mRNA is then processed and transported to ribosomes, the cellular factories responsible for protein assembly. Ribosomes attach to and traverse mRNA strands, interpreting the three-letter codons and translating them into amino acid sequences, ultimately forming proteins.
Typically, a greater quantity of mRNA leads to increased protein synthesis. However, numerous studies indicate that this relationship falters in aging human cells, suggesting that protein output may diminish even if mRNA levels remain unchanged.
Through their investigation of aging ribosomes in the brains of Killifish, Cellerino and his team may have identified the cause of this phenomenon. Employing advanced imaging techniques, the researchers captured dynamic movements of ribosomes on constrained mRNA.
The findings revealed that, as the Killifish brain aged, an unexpected buildup of ribosomes occurred, particularly at codons for the amino acids arginine and lysine, leading to stalled ribosome activity and incomplete protein synthesis.
Arginine and lysine are crucial for numerous biomolecules associated with DNA and RNA, and their charged nature suggests that these stallings could significantly disrupt RNA and DNA-binding proteins.
These protein malfunctions pose a serious issue, as they are integral to crucial cellular processes such as RNA synthesis, splicing, and DNA repair.
“Aging is associated with increased DNA damage, reduced RNA production, decreased splicing efficiency, and diminished protein synthesis,” explains Cellerino. “We propose that this ribosome stalling binds these diverse senescence phenomena together.”
Moreover, Cellerino notes that ribosomes themselves harbor RNA-binding proteins, creating a detrimental cycle of stalling that further reduces ribosome availability and, accordingly, protein production.
The pressing question remains whether ribosomal stalling is also present in the human brain. Recent work by Jean Yeo at UC San Diego indicates that RNA-binding proteins diminish in aging human neurons, echoing Cellerino’s findings, although the underlying causes are still uncertain. “This change in RNA-binding proteins could explain their declining levels,” Yeo states.
If these observations hold true for humans, it could herald new strategies for treating age-associated cognitive disorders. Additionally, in Killifish, ribosomal stalling triggers stress signals that instigate inflammatory responses. “The persistent activation of this pathway leads to chronic inflammation,” warns Cellerino. “Chronic inflammation is a significant factor in brain aging.”
Experimental drugs that may mitigate this condition by blocking the associated signaling pathways are on the horizon, according to Cellerino.
“However, it is premature to draw definitive conclusions regarding their potential impact on longevity,” he cautions. This uncertainty arises from the lack of understanding regarding the initiation of ribosomal stalling at specific amino acids, as well as whether the same stalling mechanism exists across all organs.
Mitochondria may have more functions than just energy production
CNRI/Science Photo Library
The energy-producing organelles in cells, known as mitochondria, may also influence sleep patterns. Research on fruit flies indicates that these organelles in the brain can promote sleep after prolonged wakefulness.
“Sleep presents one of biology’s significant mysteries,” notes Gero Miesenböck of Oxford University. To delve deeper, he and his research team employed gene sequencing and fluorescent markers to observe gene activity in sleep-related neurons from around 1,000 female fruit flies (Drosophila melanogaster), which typically sleep for 13-16 hours, mainly during daylight hours.
The group allowed half the flies to rest overnight while keeping the others awake by gently agitating their containers or through genetic modifications that activated wake-promoting neurons with temperature increases.
Among the sleep-deprived flies, the researchers noted a surge in activity from sleep-inducing neurons that regulate genes tied to mitochondrial function and upkeep. The mitochondria displayed signs of stress as well, like fragmentation, damage repair efforts, and increased connections to nearby cellular structures.
This stress is likely due to the mitochondria continuing to generate energy even when neurons are inactive. The research indicates this can cause electron accumulation, leading to the formation of free radicals (unstable molecules capable of damaging DNA), thereby contributing to sleep pressure, according to Miesenböck. Once the flies were permitted to sleep, they repaired the mitochondrial damage.
Further findings showed that fragmented mitochondria in sleep-inducing neurons resulted in flies feeling less sleepy than usual and unable to recover after prolonged wakefulness. Conversely, flies engineered to facilitate mitochondrial fusion demonstrated superior repair capabilities, sleeping more than normal and bouncing back more effectively from sleep deprivation. This reinforces the hypothesis that mitochondria play a role in sleep regulation.
In another phase of the study, flies were genetically altered to enhance mitochondrial activity in response to light. This led to a 20-25% increase in sleep duration after just one hour of artificial light compared to the control group.
While this research focused on fruit fly neurons rather than human cells, mitochondria among different species share notable similarities. According to Ryan Mailloux at McGill University in Quebec, Canada, this adds credence to the idea that the energy production processes in mitochondria across various animals can underscore sleep pressure in humans.
This newfound insight could pave the way for novel treatments for sleep disorders. “This presents exciting possibilities for targeting these pathways to develop effective therapies for individuals struggling with sleep issues,” states Mailloux.
Michele Bereshi of Camerino University in Italy remarked, “This paper is certainly impactful and thought-provoking,” though he expresses concerns regarding the experimental design. “Sleep deprivation does not merely prolong wakefulness; it may introduce additional stressors that elicit cellular responses unrelated to the accumulation of sleep pressure.”
In response, Miesenböck explained that his team utilized diverse methods to keep the flies awake, including non-stressing temperature adjustments through gene editing, all achieving similar effects on mitochondrial activity. “What this study illustrates is that sleep homeostasis actively employs its own mitochondria to assess the need for sleep,” he asserts.
The Covid-19 pandemic may have hastened brain aging, even prior to infection. Studies indicate that early in the outbreak, the brain may have undergone changes equivalent to 5.5 months of aging, potentially attributed to stress and shifts in lifestyle.
Many individuals suffering from long Covid report experiencing brain fog. However, the wider neurological implications of the pandemic are not completely understood a few years post-Covid-19’s emergence.
To investigate this, Ali-Reza Mohammadi-Nejad at the University of Nottingham, along with his team, trained machine learning models using 15,000 brain scans to analyze structural changes related to aging.
A model was then applied to brain scans from 996 volunteers participating in the UK Biobank Study. This comprised 564 individuals who underwent both scans prior to March 2020, which acted as the control group. The remaining 432 volunteers had one scan before March 2020 and another later, with scans averaging three years apart and a minimum gap of two years.
The research revealed that the pandemic may have induced an acceleration of brain aging by 5.5 months, as evidenced by structural changes in both white and gray matter. This effect was also observed in individuals who had recorded Covid-19 infections as part of the Biobank project.
This accelerated aging effect was notably more significant among men and those from lower socioeconomic backgrounds. However, the results may not be generalizable, as biobank participants typically exhibit better health, higher income, and less ethnic diversity than other demographics within the UK.
Researchers propose that these alterations might have been driven by the isolation and stress of lockdowns, alongside changes in lifestyle factors like physical activity and alcohol use during that period.
In their study, the authors indicate that these structural brain changes could be “at least partially reversible,” while also acknowledging limitations stemming from the study’s UK-based participant pool, suggesting that the findings may not accurately represent lockdowns’ impact elsewhere. “Our conclusions may actually underestimate the pandemic’s effects on more vulnerable populations,” Mohammadi-Nejad asserts.
A recent study from the University of Colorado Boulder indicates that erythritol, a widely used non-nutritive sweetener, may be linked to a higher risk of cardiovascular and cerebrovascular events.
Berry et al. Our study demonstrates that erythritol, at concentrations commonly found in standard size sugar-free beverages, negatively impacts cerebral microvascular endothelial cell oxidative stress, ENOS activation, NO production, ET-1 expression, and T-PA release in vitro. Image credit: Tafilah Yusof.
Erythritol is a popular alternative to non-nutritive sugars due to its minimal effects on blood glucose and insulin levels.
This four-carbon sugar has a low-calorie content of 60-80%, being as sweet as sucrose, and commonly replaces sugar in baked goods, confections, and beverages.
Authorized by the FDA in 2001, erythritol is recommended for individuals with obesity, metabolic syndrome, and diabetes, as it aids in regulating calorie consumption, sugar intake, and minimizing hyperglycemia.
Found naturally in small amounts in certain fruits, vegetables, and fermented foods, erythritol is quickly absorbed in the small intestine through passive diffusion.
In humans, erythritol is produced endogenously from glucose and fructose by erythrocytes, liver, and kidneys via the pentose phosphate pathway, making its levels dependent on both endogenous production and external intake.
“Our findings contribute to the growing evidence that non-nutritive sweeteners, often considered safe, could pose health risks,” stated Professor Christopher Desouza from the University of Colorado.
A recent study involving 4,000 participants from the US and Europe revealed that individuals with elevated erythritol levels are at a significantly increased risk of experiencing a heart attack or stroke within three years.
Professor Desouza and his team sought to determine what factors were contributing to this heightened risk.
They exposed human cells lining blood vessels in the brain to erythritol for three hours, using concentrations similar to those found in standard sugar-free beverages.
The treated cells exhibited several alterations.
Notably, they produced significantly less nitric oxide, a molecule critical for dilating blood vessels, while increasing the expression of endothelin-1, which constricts blood vessels.
Furthermore, the challenge of a thrombogenic compound called thrombin significantly slowed the cell’s production of T-PA, a naturally occurring compound that promotes coagulation.
Cells treated with erythritol also generated more reactive oxygen species, or free radicals, which can lead to cellular damage and inflammation.
“We’ve been diligently working to share our findings with the broader community,” noted Auburn Berry, a graduate student at the University of Colorado in Boulder.
“Our research indicates that erythritol may indeed heighten the risk of stroke.”
“Our study solely focused on sugar substitutes,” emphasized Professor Desouza.
“For individuals consuming multiple servings daily, the potential impact could be even more pronounced.”
The researchers caution that their findings are based on lab research conducted on cells, necessitating larger-scale studies involving human subjects.
Nonetheless, they advise consumers to check product labels for erythritol or “sugar alcohol.”
“Considering the epidemiological evidence informing our research, along with our cellular discoveries, monitoring the intake of such non-nutritive sweeteners seems wise,” Professor Desouza remarked.
The study was published today in the Journal of Applied Physiology.
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Auburn R. Berry et al. 2025. The non-nutritive sweetener erythritol negatively affects brain microvascular endothelial cell function. Journal of Applied Physiology 138(6):1571-1577; doi:10.1152/japplphysiol.00276.2025
Recent research indicates that older adults who play musical instruments tend to have healthier brains.
One investigation examined the impacts of decades of music practice, while another focused on learning new instruments later in life.
In both studies, engaging in music was linked to better brain health and a decrease in age-related cognitive decline.
The first study was published in PLOS Biology and involved collaboration between Canadian and Chinese researchers. They recruited 50 adults with an average age of 65, half of whom had been playing instruments for at least 32 years, while the others had no musical experience.
Additionally, they included 24 young adults with an average age of 23 who had no musical training.
The researchers utilized magnetic resonance imaging (MRI) to assess blood flow in the brains of the participants.
During the scans, participants listened to a recording of speakers amid background noise, where 50 other voices were present, and were tasked with identifying what the main speaker was saying.
The scans revealed that older musicians’ brains responded to challenges similarly to those of the younger participants.
Nonetheless, older adults showed signs of cognitive decline. Specifically, musicians exhibited strong neural connections on the right side of the brain that non-musicians lacked, which could place additional strain on their brain.
“The brains of older musicians remain finely tuned due to years of training, so they don’t need to play well-tuned instruments at high volumes,” stated co-author Dr. Yi from the Chinese Academy of Sciences.
“Our findings suggest that musical experience helps mitigate the additional cognitive strain typically associated with age-related challenges, particularly in noisy environments.”
A 2025 YouGov poll revealed that 25% of UK adults can play at least one instrument, with the guitar being the second most favored instrument after the piano.
As individuals age, cognitive functions such as memory, learning, and perception often deteriorate, eventually contributing to dementia.
However, researchers posit that cognitive reserve—the brain’s capability to manage damage and decline—can enhance resilience against this deterioration.
The precise mechanisms remain unclear, as noted by Morten Scheibye-Knudsen, Associate Professor of Aging at the University of Copenhagen, Denmark, in an interview with BBC Science Focus.
Some studies suggest that “exercising” the brain through activities like playing instruments, learning new languages, and solving puzzles can improve brain health, but results from other research have been inconsistent.
“Overall, we advocate for brain training, but the evidence is not conclusive,” Scheibye-Knudsen remarked.
Conversely, another recent study, published in Imaging Neuroscience, indicated that musical practice can enhance brain health, even when individuals start playing in later life.
According to a 2024 poll from the University of Michigan, 17% of US adults aged 50-80 engage in playing instruments at least several times a year – Credit: DMP via Getty
Researchers at Kyoto University in Japan continued previous studies that included 53 elderly individuals (average age 73) who took music lessons for four months. Initial findings indicated no significant differences in brain health among participants.
Four years later, the same participants underwent MRI scans (13 of whom had maintained their music practice).
Those who ceased playing their newly learned instruments showed declines in memory performance, with a noticeable reduction in the volume of the putamen—a brain region associated with motor function, learning, and memory.
However, those who continued playing music over the four years exhibited no cognitive decline.
Scheibye-Knudsen noted that the study demonstrates that “playing an instrument not only helps preserve cognitive function as we age, but it may also directly contribute to maintaining the structural integrity of the brain.”
He added, “Engaging in music beyond what this study covered offers additional advantages, such as enhanced social interaction.”
“I encourage people to start making music; it’s never too late to learn.”
Read more:
About Our Experts
Morten Scheibye-Knudsen is an associate professor of aging at the University of Copenhagen, Denmark, and leads the Scheibye-Knudsen Research Group. He also serves as the president of the Nordic Aging Association.
False-colored nuclear magnetic resonance images of children’s brains
CNRI/Science Photo Library
New research indicates that children with anorexia nervosa are undergoing significant brain changes that go beyond what starvation can explain. This insight helps clarify the neurological mechanisms behind the disorder, potentially paving the way for improved treatment strategies.
Anorexia nervosa is noted for severe dietary restrictions and a distorted body image, making it a less understood condition. While previous studies have highlighted that the brain’s outer layer, or cortex, is notably thinner in these individuals, it remains uncertain whether such changes stem from malnutrition or are intrinsic to anorexia.
Clara Morrow from The University of Montreal, Canada, examined brain scans of children with anorexia alongside those with Avoidant/Restrictive Food Intake Disorder (ARFID). Although both conditions encompass significant food restrictions and weight loss, ARFID lacks the body image concerns that characterize anorexia. Instead, individuals with ARFID may avoid food due to sensory sensitivities, disinterest in eating, or fear of adverse consequences like choking, vomiting, or gastrointestinal distress. The comparison could shed light on the unique brain changes associated with each condition and malnutrition, according to Moreau.
The study analyzed brain scans from 124 children diagnosed with anorexia, 50 with ARFID, and 116 without eating disorders. All participants were under 13 years old and resided in France. Researchers examined the extent of brain differences between those with and without eating disorders.
On average, children diagnosed with anorexia exhibited a significantly thinner cortex compared to those without eating disorders. Once body mass index (BMI) was taken into account, anorexia correlated with cortical thinning across 32 brain regions, particularly in the superior head lobule, an area involved in sensory information processing. “This aligns with our understanding, as we know anorexic patients often struggle with their perception of weight and size,” stated team member Anael Ayrolles from the University of Paris.
These alterations are akin to those observed in older adolescents and adults suffering from anorexia, notes Moreau. “The effect size is among the most significant in psychiatry,” she comments. “It appears as if they’ve experienced accelerated brain aging or early Alzheimer’s disease, though they show no symptoms of Alzheimer’s. However, if their BMI is normalized, brain recovery is often observed, though not in every case.”
In contrast, no significant differences in cortical thickness were observed between children with ARFID and those without any eating disorders. “We anticipated some overlap with anorexia potentially reflective of BMI,” explains Moreau. “However, our findings did not reveal many similarities between the two conditions.” The reason for this remains unclear, especially since this is the inaugural brain imaging study focused on ARFID. Given that ARFID typically manifests before the age of five, the brain may have adapted to limited food intake, suggests Moreau.
The researchers subsequently contrasted these brain differences with findings from previous studies on other disorders, including obsessive-compulsive disorder (OCD), ADHD, and autism. They found a notable correlation between anorexia and OCD, whereas ARFID displayed brain changes similar to those associated with autism. This aligns with Moreau’s assertion that sensory sensitivity is prevalent in both autism and ARFID. Conversely, OCD and anorexia exhibit obsessions, rituals, and preconceived notions.
Nevertheless, individuals with OCD and anorexia frequently present other mental health challenges, notes Joanna Steinglass from Columbia University in New York. Approximately 14% of those diagnosed with anorexia also meet the criteria for OCD. This complicates the understanding of whether a genuine neurological resemblance exists between the two conditions or if other mental health challenges underpin this correlation.
“We were cautious not to over-interpret our results,” said Ayrolles. However, these discoveries imply that malnutrition alone may not account for all the brain changes observed in anorexia. “Mental illness is fundamentally a brain-based illness, and understanding this helps us address patient experiences more effectively, often leading to less blame,” remarks Steinglass. “This insight could drive the development of more effective treatments.”
Microglia are specialized immune cells in the brain
Science Photo Library/Alamy
The process of replacing immune cells in the brain halts the advancement of a rare and terminal brain disorder known as ALSP. This also paves the way for future clinical trials targeting other neurological ailments.
Extensive research indicates that impaired microglia—specialized immune cells within the brain—play a role in various neurological disorders, including Alzheimer’s disease and schizophrenia. The term ALSP stands for adult-onset leukoencephalopathy with axonal spheroids and pigmented glia, characterized by mutations in genes responsible for the survival of these cells, resulting in a reduced number of microglia and leading to progressive cognitive decline. Currently, no effective treatment exists for this fatal illness.
To address this, Bo Peng from Fudan University in China and his team employed a novel treatment called microglia replacement therapy. Prior experiments in rodents have shown that implanted stem cells—capable of developing into different cell types—can effectively replace microglia. However, it is necessary to first eliminate existing microglia in the brain to facilitate this. This can be achieved using drugs that target protein microglia.
Pursuing this avenue, Peng and his colleagues conducted initial tests on five mice with genetic mutations analogous to those associated with ALSP. As the mutations already impacted protein microglia, the researchers did not need to deplete these proteins with medication. Subsequently, they transplanted stem cells from healthy mice into the affected mice. Fourteen months later, treated mice exhibited approximately 85% more microglia in their brains compared to six untreated mice harboring the same mutation. Notably, these treated mice also demonstrated improvements in motor function and memory.
Encouraged by these promising findings, the researchers extended the treatment to eight individuals diagnosed with ALSP, using donor stem cells without preconditions. One year post-treatment, brain scans revealed minimal changes in participants compared to scans taken before the procedure. In contrast, four untreated individuals displayed significant brain deterioration and lesions over the same period. This implies that microglial replacement therapy effectively halted the progression of the disease.
At the study’s outset, all participants underwent cognitive assessments using a 30-point scale, where a decrease in score indicated cognitive decline. Reassessments a year later showed that, on average, scores remained stable for those who received the microglia replacements.
These results point to microglial replacement therapy being a potentially effective solution for ALSP. However, since this represents the inaugural human trial, “we remain unaware of any potential side effects,” comments Peng. “Given the rapidly progressive and lethal nature of this disease, prioritizing benefits over possible side effects might be crucial.”
Chris Bennett from the University of Pennsylvania cites the historical use of stem cell transplants for treating neurological disorders. “It has demonstrated effectiveness, particularly through microglia replacement,” he states. Recent FDA approvals for two similar therapies addressing other rare brain conditions further support this. “While prior studies may not have used this exact terminology, they effectively addressed similar conditions,” Bennett elaborates. “I’d describe this as a smart and innovative application of stem cell transplants. Nonetheless, microglia replacement therapy has been evolving for decades.”
Despite this, the results underscore the broader implications of microglial replacement therapy. Experts believe this strategy could one day address more prevalent brain disorders. For example, certain genetic mutations significantly heighten Alzheimer’s disease risk and affect microglial function. Replacing these malfunctioning cells with healthy human equivalents could offer a promising avenue for treatment.
All organs seem to be equally unimportant for longevity
westend61 gmbh / alamy
In the quest for a long life, it appears that not all organs hold equal significance. Research indicates that maintaining a youthful brain and immune system is crucial, overshadowing even the aging of the heart or lungs.
We already know that different organs age at varying rates, but the factors that most significantly affect lifespan remain elusive. Hamilton Sehawee from the Icahn School of Medicine at Mount Sinai, New York, leads this inquiry.
To explore this, his team assessed the levels of around 3,000 proteins in blood samples from over 44,000 participants aged between 40 and 70 years, all part of the UK Biobank Study.
Leveraging genetic data from earlier studies, the researchers mapped the locations of these proteins in the body, identifying several that were notably concentrated in 11 regions, including the immune system, brain, heart, liver, lungs, muscles, pancreas, kidneys, intestines, and adipose tissue. Elevated levels of these proteins suggest vital roles in the proper functioning of these organs and systems.
The team then employed machine learning models to estimate the ages of participants based on half of the data, developing distinct models for each of the 11 body areas. Generally, these predictions were consistent with the actual ages of the participants, although some models did occasionally overestimate or underestimate, supporting the notion that organs indeed age differently, according to Oh.
Using their trained model, the researchers predicted the organ and immune system ages of the other half of participants who were monitored for an average of 11 years after blood samples were taken.
They discovered that having even one organ showing signs of premature aging or an aging immune system correlated with a 1.5 to 3 times higher risk of death during follow-up, with the stakes increasing alongside the number of aging organs.
Interestingly, exceptions arose in cases where the heart and lungs appeared considerably younger than anticipated, which did not correlate with a lower mortality risk during the study period. However, possessing a youthful brain or immune system was associated with a roughly 40% reduction in death risk. These areas also intensified the overall risk reduction to 56%, particularly when both were young.
“The brain and immune system influence numerous other bodily functions, so it’s expected that their deterioration could significantly impact life expectancy,” remarked Alan Cohen from Columbia University in New York.
Nonetheless, Cohen cautions that protein markers may not entirely encapsulate the aging process. “There may be gaps in our understanding of the exact origins of these proteins. Certain organs may release their proteins into the bloodstream more readily than others, skewing perceptions of their importance,” he notes.
Moreover, further research involving a broader demographic that includes more ethnic and economically varied populations is necessary, as the current study participants were predominantly affluent individuals with European ancestry, according to Richard Shiou of King’s College London. Oh and his team are planning additional studies to explore this further.
Even if these findings hold true, concrete methods for curbing the aging processes in the brain and immune system remain elusive. Oh mentions that pinpointing aging markers in these areas could pave the way for medication targeting.
Numerous intriguing claims about gardening have circulated, especially one that insists, “The soil acts as an antidepressant.”
According to this notion, it’s been promoted through countless social media posts. Mycobacterium vaccae, microorganisms commonly found in soil, are said to improve your mood. Simply engaging with the earth can yield these benefits. It’s believed that these bacteria can be absorbed through your skin or inhaled, subsequently enhancing your brain chemistry. But is this as credible as it seems?
While these claims may appear peculiar at first glance, studies have indeed explored the effects of this microorganism on various health conditions, such as eczema and cancer. Interestingly, M. vaccae was first identified in Ugandan soil samples while scientists sought a non-lethal relative of Mycobacterium tuberculosis, and it has potential as a form of immunotherapy.
Researchers became intrigued by its possible benefits for depression when lung cancer patients treated with this bacteria reported improvements in their quality of life, which was an unexpected yet welcomed side effect. Current research, likely indicating an uplift in mood, has been replicated across numerous well-designed studies. Thus, the internet is rife with memes about this finding.
However, there is a caveat. All studies specifically examining this hypothesis have been conducted on mice rather than humans, which is significant because the outcomes of animal studies are often difficult to extrapolate to humans. For instance, one review of 76 animal studies found that only 37% were replicated in human trials.
Moreover, the mice used in the M. vaccae studies were male and from specific inbred strains. Researchers varied their methods for administering the bacteria, either by saturating the air in their cages or applying it directly to their skin. Most studies I found involved injecting the bacteria into the bloodstream of the mice or incorporating it into their food.
As someone captivated by the growing evidence that suggests spending time in green spaces improves mental health, I eagerly anticipate further research on M. vaccae. Nevertheless, despite the viral nature of the claim that “soil is an antidepressant,” it’s essential to acknowledge that it primarily stems from studies on male mice injected with purified bacteria.
James Wong is a botanist and science writer with a particular focus on food crops, conservation, and the environment. He trained at the Royal Botanic Garden in Kew, London, and shares a small flat with over 500 houseplants.Follow him on X and Instagram @BotanyGeek
For more projects, please visit newscientist.com/maker
Generates brain cells from the hippocampus that proliferate in culture
Arthur Chien/Science Photo Library
The ongoing debate about whether adults can produce new brain cells takes a new turn, as evidence increasingly supports that they indeed can. This revelation addresses one of neuroscience’s most disputed questions and raises hopes that this knowledge could be used in treating conditions like depression and Alzheimer’s disease.
Neurons are produced via a process known as neurogenesis, which occurs in both children and adults, as shown in research on mice and macaques. This involves stem cells generating progenitor cells, which multiply and eventually develop into immature neurons that mature over time.
Earlier studies have indicated the presence of stem cells and immature neurons in the hippocampus of adult humans. This brain area, crucial for learning and memory, is a primary site for neurogenesis in younger humans and some adult animals. However, progenitor cells have not yet been detected in adult human brains. “This link was overlooked. It forms a central argument for the emergence of new neurons in the adult human brain,” states Evgenia Salta from the Netherlands Institute of Neuroscience, who was not involved in the latest research.
To establish this link, Jonas Frisen and his team at the Karolinska Institute in Sweden developed a machine learning model capable of accurately identifying progenitor cells. They used hippocampal samples from six young children, donated by their parents for research post-mortem.
The researchers trained an AI model to recognize progenitor cells based on the activity of about 10,000 genes. “In childhood, these cells’ behavior closely resembles that of precursor cells in mice, facilitating their identification,” explains Frisen. “[The idea is] to use molecular fingerprints of childhood progenitor cells to find equivalents in adults.”
To validate the model, the team identified progenitor cells in hippocampal samples from young mice. The model correctly identified 83% of the progenitor cells and misclassified other cell types as progenitor cells in less than 1% of cases. In a further test, the model accurately predicted that progenitor cells were nearly absent in adult human cortical samples, a brain area devoid of evidence supporting neurogenesis in humans.
“They validated their models effectively by transitioning from data on human children to mice and then to adult humans,” says Sandrine Thuret from King’s College London.
With this validation in hand, the researchers can check for neurogenesis in human adults by identifying 14 hippocampal progenitor cells from individuals aged 20 to 78 at the time of their passing.
Crucially, the researchers first introduced a method to enhance the likelihood of detecting progenitor cells. Previous studies have indicated that these cells are extremely rare in adults. The team utilized antibodies to select brain cells that were actively dividing at the time of death, including non-neuronal cells such as immune cells and progenitor cells. This helped filter out common cell types that do not divide, like mature neurons, making rare progenitor cells easier to identify.
Subsequently, they organized the genetic activity data related to these dividing cells into models. “They were enriched due to the selected cells,” remarks Kaoru Song at the University of Pennsylvania. Previous research lacked this approach, he adds.
The team successfully identified progenitor cells in nine donors. “It is well established that environmental and genetic factors in rodents affect how neurogenesis occurs, so I suspect variations in humans may also be attributed to these factors,” Frisen notes.
The findings strongly indicate the presence of adult neurogenesis, according to Thuret, Song, and Salta. “We are adding this missing piece, which significantly advances the field,” Salta states.
“Neurons originate from cell division occurring in adulthood, and that is what this study definitively establishes,” Thuret comments.
Thuret suggests the possibility of examining variations in neurogenesis among adults with brain-affecting conditions such as depression or Alzheimer’s disease. She speculates that medications promoting this process could alleviate symptoms.
However, John Arellano from Yale University cautions that even if adults produce new brain cells, they may be too few in number to be therapeutically beneficial. Thuret, however, believes this is unlikely to create issues. “In mice, a small number of new neurons can significantly impact learning and memory,” she asserts.
As articulated in Gray’s Anatomy, it’s no surprise that healthcare professionals have inspired numerous popular narratives. The journey of a patient through the healthcare system mirrors the structure of classic storytelling, featuring beginnings, conflicts, and resolutions, often accompanied by various tensions.
Although medicine is often perceived as grounded in hard science (blood tests, medical imaging, treatment protocols), it fundamentally involves storytelling, a theme that Pria Anand explores in her debut book, Electric of the Mind: A Tale of the Strangeness and Wonders of Our Brains.
During her time at medical school in California, Anand was concerned that her aversion to storytelling might hinder her. Yet, she found that how individuals narrate their experiences could convey as much insight as any clinical test.
Anand pays homage to her predecessor, neurologist Oliver Sacks, drawing from his personal anecdotes while diagnosing and empathizing with patients. In Electric of the Heart, she acknowledges the influence of Sacks’s iconic work, The Man Who Mistook His Wife for a Hat.
While it’s unrealistic to expect anyone to reach Sacks’s level of ingenuity, Anand embodies his empathy, curiosity, and intellectual breadth. Her writing is both polished and insightful as she navigates complex neurological concepts, addressing the narratives of individual patients with similar finesse.
However, Electric of the Heart transcends mere “clinical anecdotes.” Anand’s core message emphasizes the vital role of storytelling in medical practice. The human craving for narratives is ancient, universal, and remarkably resilient, often thriving even in the aftermath of severe brain injuries, as she notes.
Regardless of health status, how individuals articulate their condition may diverge significantly from a physician’s evaluation or observable metrics. Anand recounts the story of a patient who entered a coma following a cerebral hemorrhage but appeared to recover fully, often mistaking Anand and her colleagues for her former medical team as she made her rounds among fellow patients.
No one can match the brilliance of Sacks, but Anand embodies the writer’s humanity and broad intellect.
Anand delves into the way our brains can mislead us, highlighting both the hurdles and the character of medical practice. However, it’s not just the patients’ misconceptions that warrant attention; doctors can exhibit similar biases and errors.
The evolution of her own health conditions has profoundly informed Anand’s work ethic—from sleep deprivation during her training to the “phantom noises” she began experiencing that prompted her concern. It was later discovered that these sounds stemmed from a vascular malformation connecting her brain to her heart.
The inherent “imbalance of power” in medicine signifies an ongoing struggle between empirical evidence and narrative, as well as between objective truths and subjective experiences—this dynamic exists not only in the realm of physicians but also among the false dichotomies pervasive in healthcare. Historically, many confidently given diagnoses have been based solely on “scientific” definitions. One can reflect on the notion of a “wandering uterus.”
Although comparisons between Anand and early reviewers might not be misleading, Electric of the Heart invites parallels with Glass Body, a personal narrative by Caroline Crampton that also explores hypochondria. Like Crampton’s insightful account, Anand elucidates “a vast liminal spread between health and illness” from her perspective as a physician.
Both works suggest a growing openness in mainstream media to not only drama but the complexities of medical intricacies, challenging the traditional notion that the divides between “healthy brains and failing brains” or illnesses and wellness are as clear-cut as they seem.
In Electric of the Heart, Anand exhibits empathy, humility, and a profound interest in humanity—qualities that define outstanding doctors and ideally should be prevalent throughout the medical profession.
Elle Hunt is an author based in Norwich, UK
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How does the brain encourage us to make up for our sleep loss?
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Researchers have identified mouse neurons that assist the brain in managing and recovering from sleep debt. Similar pathways exist in humans and could enhance treatments for conditions associated with sleep disorders, including Alzheimer’s disease.
Everyone knows the struggle of sleep debt — the difference between the sleep one needs and what one gets. However, the mechanisms through which the brain tracks sleep loss have remained largely unclear.
Mark Woo from Johns Hopkins University and his team investigated the brain pathways of mice associated with sleep by injecting tracers into 11 brain regions known to promote sleep. The tracers revealed connections to 22 regions linked to four sleep-promoting areas.
Previous studies concentrated on a limited number of unidentified regions. A method known as chemogenetics was utilized, administering specialized drugs to the mice that activated particular areas of the brain. The mice were divided into 11 groups of 3-4 and different regions were stimulated in each group.
Interestingly, an area called the thalamic nuclear reuniens proved to be significant. Stimulation of neurons in this region resulted in a substantial increase in REM sleep for the mice — about twice as much as non-stimulated counterparts. However, it took a few hours for the stimulated mice to fall asleep, during which they exhibited signs of readiness to rest.
“When you go to sleep, you likely engage in routines like brushing your teeth, washing your face, or fluffing your pillow. Mice do something similar; they groom themselves and prepare their nests,” says Wu. This suggests that these neurons are not simple on/off switches for sleep but rather promote drowsiness.
Support for this theory came from another experiment where deactivating thalamic nuclear cells in six sleep-deprived mice resulted in decreased drowsiness. These mice were more active and nested less than the control group, averaging 10% less non-REM sleep.
Additional tests have indicated that these neurons activate during sleep deprivation and become silent when sleep begins.
Collectively, these findings indicate that this brain region not only triggers sleepiness but also facilitates recovery sleep following sleep loss, according to Wu. Targeting these neurons could lead to new therapies for sleep disorders characterized by excessive drowsiness after rest, as well as conditions like Alzheimer’s disease, where individuals struggle with sleep.
However, it’s uncertain if equivalent brain circuits exist in humans. William Gialdino from Stanford University expresses caution, stating that while the immediate effects of sleep deprivation are being studied, the long-term consequences may differ significantly from those observed in humans experiencing chronic sleep loss.
A man with paralysis is connected to a brain-computer interface system
Lisa E. Howard/Mitely Wairagkar et al. 2025
Men who have lost their ability to speak can engage in real-time conversations and even sing using brain-controlled synthetic voices.
The brain-computer interface captures neural activity through electrodes implanted in the brain, instantly creating audio sounds that match intended pitch, intonation, and emphasis.
“This represents a breakthrough in instantaneous speech synthesis, achieving this within 25 ms,” says Sergei Stavisky from the University of California, Davis.
While advancements are needed to improve speech clarity, Maitreyee Wairagkar, also at UC Davis, notes that the individual who lost his speech due to amyotrophic lateral sclerosis expresses happiness and feels that he has found his true voice.
Existing speech neurospheres that utilize brain-computer interfaces typically require a few seconds to convert brain activity into sound. Stavisky mentions that this delays natural conversation and if the connection falters, it can feel like speaking on a poor-quality phone call.
To create a more seamless speech experience, Wairagkar, Stavisky, and their team implanted 256 electrodes in the areas of the male brain responsible for facial muscle control necessary for speech. In subsequent sessions, they introduced thousands of sentences on a screen, recorded brain activity, and prompted the subject to vocalize with specific intonations.
“For instance, phrases like ‘How are you today?’ or variations such as ‘How are you? today?’ can significantly alter the meaning of sentences,” explains Stavisky. “This approach allows for a richer, more natural dialog, marking a significant advancement over previous technologies.”
The researchers utilized an AI model trained to link particular patterns of neural activity with corresponding words and tonal variations, resulting in synthetic speech that mirrors both the content and emotional delivery intended by the user.
The AI was trained with audio recordings from before the male’s condition deteriorated, employing voice-cloning technology to ensure the synthetic speech bore a resemblance to his original voice.
In another phase of the study, researchers attempted to teach him to sing a simple melody with varying pitches, with their models accurately interpreting the intended pitch in real time and adjusting the produced singing voice accordingly.
He also utilizes the system to communicate spontaneously, making sounds such as “hmmm,” “eww,” and forming words, as noted by Wairagkar.
“He’s a remarkably articulate and intelligent individual,” says David Brandman from UC Davis. “Despite his paralysis, he has continued to participate actively in work and engage in meaningful conversations.”
Do our brains really develop from practically anything, allowing us to generate complex thoughts, actions, and even reflections on ourselves? Recent experiments with tadpoles have integrated electron implants into brain precursors during early embryonic stages, potentially bringing us closer to answering this question.
Earlier efforts to investigate neurodevelopment relied on tools like functional magnetic resonance imaging and rigid electrode wires. Unfortunately, the imaging resolution was often too low to be effective, while the rigid wires caused significant damage to the brain, yielding little more than a snapshot of specific developmental moments.
Researchers, including Jia Liu from Harvard University, discovered a material (a type of perfluropolymer) closely resembling brain tissue. They employed this to create a flexible, elastic mesh encasing an ultra-thin conductor, which was placed onto the neural plate—a flat structure that serves as the precursor to the brain—in the embryos of the African clawed frog (Axenopath Ravis).
As the neural plates folded and expanded, these ribbon-like meshes were enveloped by the developing brain, maintaining functionality amidst stretching and bending in the tissue. When the researchers sought to measure signals from the brain, they connected the meshes to computers to visualize neural activity.
The implants did not harm the brain nor provoke an immune reaction, and the tadpole embryos developed as anticipated. In fact, at least one grew into a normal frog, according to Liu.
“It’s incredible to integrate all these materials and ensure everything operates seamlessly,” said Christopher Bettinger from Carnegie Mellon University, Pennsylvania. “This tool has the potential to significantly advance basic neuroscience by enabling biologists to observe neural activity throughout development.”
The team derived two key insights from their experiments. First, the patterns of neural activity shifted as tissue differentiated into specialized structures, resulting in distinct functions. Liu noted that tracking an organism’s self-organization to a computer was previously deemed impossible.
The second area of focus was how brain activity in animals changes following amputation. Traditionally, it was believed that electrical activity would revert to its original developmental state. The research team confirmed this by utilizing implants in experiments with Axolotls.
Liu’s team is now broadening their research to include rodents. Unlike amphibians, rodent development occurs within the uterus, making the implantation of meshes more challenging. It requires in vitro fertilization and more intricate signaling measurement techniques compared to simply wiring the mesh to computers. Nonetheless, Liu is optimistic that the insights gained from observing early stages of conditions like autism and schizophrenia will justify the complexities involved.
Bettinger mentioned that similar devices could also be applied to monitor neuromuscular regeneration following injuries and during rehabilitation. “Overall, this highlights the remarkable potential of highly compliant electronic applications,” he stated.
Modern machine learning technology has demonstrated the ability to visualize our dreams. But what if you wish to take it a step further and share your dreams?
At present, we are capable of interpreting brain signals to obtain a vague understanding of imaginary scenes and overarching concepts, yet there is no method for transferring these ideas from one brain to another. Perhaps this is for the best. Many might feel uneasy at the thought of a computer implanting ideas into our minds while we sleep.
Our current means of communication rely on our sensory capabilities. Words that are whispered into your ears during sleep could serve as a method to convey information between two sleeping individuals. However, how can people communicate while asleep? The answer is more complicated than it seems.
Individuals who talk in their sleep (referred to as Somniloquists) often do so as a result of stress, and their peculiar utterances are not within their conscious control. Moreover, our capacity to hear while asleep is limited; sounds during sleep can disrupt it, causing both stress and dreams to the sleeper.
Yet, there is a particular dream that may be beneficial: the Akaid Dream. This unique type of dream allows the dreamer to recognize that they are still asleep. With some practice and various techniques, this can be guided.
In this state, could two dreamers actually communicate?
They employed external stimuli to aid one sleeper in transitioning to a lucid dreaming state. The sleeper then conveyed a message through earphones, which was recorded by a computer as the lucid dreamer repeated the words in their sleep.
Eight minutes later, the message was played back to the second lucid dreamer, who confirmed hearing the words upon waking. While this may not serve a practical purpose in our current state, it did represent a form of communication within a dream.
There is, however, another type of shared thought that might prove more useful.
Researchers are currently demonstrating that individuals who work closely together begin to synchronize their brain waves. This phenomenon can occur in situations where musicians are tightly synchronized or in social groups where a strong connection is felt.
Inter-brain synchronization is observable through precise “hypersensitivity” with an electroencephalography (EEG) scanner that tracks brain waves. These can originate from theta waves (produced when we are deeply relaxed), alpha waves (when we are calm), or beta waves (when we are focused and active).
When these brain waves, particularly beta waves, synchronize among two or more individuals, they often collaborate more effectively, show enhanced empathy, and even display a reduced sensitivity to pain. Teams with synchronized neural activity typically perform better overall.
The best part is that no artificial intelligence or brain scanners are required!
To cultivate neural synchronization among those who wish to share experiences: engage in activities like listening to music together, dancing, collaborating, solving problems, or simply conversing. This sort of spiritual connection is available to us for free and brings substantial benefits.
This article responds to the question posed by Idris Wise via email: “Can you communicate in a dream?”
Feel free to email us your questionsat Question @sciencefocus.com or send a message throughFacebook,Twitter orInstagram (don’t forget to include your name and location).
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A device designed for facial and neck massage suggests it might enhance the brain’s waste removal system and alleviate symptoms associated with conditions like Alzheimer’s disease.
Cerebrospinal fluid (CSF) envelops the brain and inflates it before moving through a network of delicate tubes known as grinft blood vessels. Research on mice indicates that this fluid clears waste produced by brain cells, including proteins linked to diseases like Alzheimer’s and Parkinson’s, such as beta-amyloid.
This has prompted researchers to consider whether increasing CSF flow could promote brain health. However, they note that the grinft vessels, previously only discovered deep within the neck, are difficult to access. Gou Young Koh, from the Advanced Science and Technology Research Institute in Korea, remarks on this challenge.
Recently, Koh and his team identified a network of grinft vessels located just five millimeters beneath the skin on the faces and necks of mice and monkeys. They made this breakthrough by administering fluorescent dyes that label the CSF and imaging the subjects under anesthesia. “We utilized a different kind of anesthesia than was applied in earlier studies. The previous anesthetic blocked the visualization of vessels close to the skin,” Koh explains.
In their effort to determine if massaging these vessels could boost CSF flow, the researchers developed a device with small rods attached to a 1 cm cotton ball. They used it to gently stroke down the face and neck of a 2-year-old mouse for a few months, applying strokes for one minute on younger mice. “A gentle facial and neck massage can compress the liquid and enhance the CSF flow,” Koh states.
After 30 minutes of massage, CSF flow was observed to increase nearly threefold in the brains of the mice compared to their flow prior to the massage. Furthermore, this process seemed to reverse age-related decreases in CSF flow. “After stimulation, the CSF flow in older mice appeared comparable to that of younger mice [who hadn’t received the massage],” Koh elaborates.
In their unpublished findings, the team observed similar outcomes in monkeys. They also identified glymphetic blood vessels in human cadavers, implying that massage could stimulate CSF flow in humans, as suggested by Koh.
However, due to anatomical differences between mice, monkeys, and humans, further investigations are necessary to confirm this, remarks Vesa Kiviniemi from Uru University in Finland. “It’s a slightly different scenario.”
Moreover, it remains uncertain whether increased CSF flow can genuinely mitigate brain aging or offer protection against neurodegenerative conditions like Alzheimer’s. Stephen Prucks of the University of Bern in Switzerland stated that Koh’s team aims to investigate this with mice that exhibit Alzheimer-like traits.
Six years ago, a Canadian neurologist noticed unusual symptoms among a group of patients in New Brunswick, a province next to Maine.
Dr. Arie Marrello reported that patients experienced hallucinations, convulsions, rapid memory loss, and a sensation of insects crawling under their skin, but these symptoms and brain scans didn’t align with existing diagnoses, making the cases puzzling.
Subsequent reviews by neurologists led to clear diagnoses, including Alzheimer’s disease, Parkinson’s disease, and cancer.
A recent study published in JAMA Neurology supports these findings, indicating that the likelihood of such mysterious illnesses is about one in one million.
The physicians involved in this study assessed 25 patients from the New Brunswick cluster. With 11 patients deceased, neuropathologists relied on autopsy findings to reach diagnoses. Among the 14 living patients, neurologists used cognitive assessments, concluding that all had well-documented conditions such as Alzheimer’s, Parkinson’s, cancer, traumatic brain injury, and post-concussion syndrome.
Dr. Anthony Lang, a neurologist at the Krembil Brain Institute within the University Health Network, remarked, “I was confident that there was a clear explanation for 100% of the cases.”
Nevertheless, some medical professionals are concerned that this evidence may not quell speculation about an underlying unknown cause, which many patients and their families continue to believe in.
According to the authors of the study, 52 individuals connected to the New Brunswick cluster declined a second opinion, and another 42 individuals were unreachable. This lack of response has been attributed to the spread of misinformation through both traditional and social media, undermining trust in healthcare systems.
“These instances reflect misdiagnosis, leading to misinformation. Unfortunately, the doctors involved persist in convincing patients and their families that they have a mysterious illness,” Lang emphasized.
Marello expressed skepticism regarding the study’s methods and conclusions in a statement, saying, “I hold serious reservations about the validity of the research and have numerous questions regarding its methodology and content. We believe that our patients, families, and communities share these significant concerns.”
Dr. Valerie Sim, an associate professor of neurology at the University of Alberta and not part of the study, stated there is no evidence linking the patients’ illnesses. She noted that the description of the cases is too broad and could apply to multiple conditions.
“Sadly, the unifying factor is that all these patients saw the same neurologist,” Sim pointed out. “Patients evaluated by different specialists have been diagnosed with known conditions that aren’t mysterious.”
James Mastorianni, a professor of neurology at the University of Chicago, highlighted that while not included in the study, it underscores the importance of seeking second opinions from experts in the field.
Ongoing Investigation
The Mystery Disease Theory gained traction in 2021 when Canadian health officials launched an investigation based on Marello’s observations. However, even after the inquiry determined that most patients had identifiable conditions, skepticism remained among families. In November, Susan Holt, the Prime Minister of New Brunswick, called for a scientific review of the “mysterious brain diseases.”
“The residents of New Brunswick deserve answers,” Holt stated in a public statement last year. “We must understand the source of our illnesses.”
Some advocates for patients suspect that environmental factors may be contributing to the illnesses, noting that blood tests have detected heavy metals, pesticides, and rare antibodies, warranting further investigation.
“None of our patients received an alternative diagnosis,” said Kat Lantine, an advocate in New Brunswick. “What led to their neurodegenerative disease?”
Dr. Yves Legger, New Brunswick’s chief medical officer of health, stated in a recent statement that the new study “does not alter our commitment to thoroughly investigating cases of undiagnosed neurological diseases in New Brunswick.”
His office has received 222 case reports in connection with this cluster.
Marello mentioned, “We have evaluated over 500 patients in this cluster and provided substantial evidence regarding environmental exposures, as well as rare autoimmune markers present in several cases.”
However, Lang cautioned that detecting substances in the blood or urine does not necessarily imply they are the cause of neurological symptoms.
“You cannot take a scattershot approach, where you find something and assert that it’s relevant to the health issue,” he explained.
Challenges in Diagnosing Neurological Problems
Neurologists not involved with the New Brunswick situation highlight several challenges that continue to spur discussions among advocates, doctors, and government officials about the illness’s origins.
For starters, they note that accurate diagnoses can take time. Some conditions highlighted in the study exhibit complex symptom profiles, like Alzheimer’s.
“We need a comprehensive history from the family along with a timeline to identify if someone is developing dementia. There may be early signs of confusion evident in neurological tests,” indicated Dr. Kimberly O’Neal, a neurologist at the Health Multiple Sclerosis Comprehensive Care Center at NYU Langone.
Rapidly progressing dementia was one of the key symptoms observed in New Brunswick patients. However, families sometimes overlooked early indicators of neurodegeneration, which made it appear as though dementia appeared suddenly, according to Mastorianni.
When severe symptoms manifest, patients and their families often seek answers and can be hesitant to abandon their initial diagnoses, Sim noted.
“This phenomenon is common in medicine. Patients often become attached to a diagnosis or a group of conditions,” Sim remarked. “That is evidently the case here.”
Misdiagnosis can be “truly tragic,” as it may prevent patients from receiving effective treatment and proper care.
Vitamin K is a crucial nutrient primarily found in green vegetables and may play a vital role in safeguarding the brain from cognitive decline.
Recent research suggests that vitamins, particularly vitamin K, could help in preserving the cells of the hippocampus, which is the brain’s memory center.
In a recent study, scientists conducted an experiment where 60 middle-aged mice were fed either low or regular diets supplemented with vitamin K for six months. Subsequent behavioral tests revealed the impact of vitamin K on mouse learning and memory.
The study showed that mice lacking vitamin K struggled with memory and learning tasks. Compared to mice on a regular diet, those deficient in vitamin K had difficulty recognizing familiar objects, indicating memory loss. They also faced challenges in spatial learning tasks, as evidenced by their performance in a water maze.
Green vegetables like spinach, kale, lettuce, Brussels sprouts, broccoli, and cabbage are excellent sources of vitamin K. Avocados and kiwi fruits also contain high levels of this nutrient – Credit: Mediterranean via Getty
Further analysis of the mice’s brain tissue revealed reduced neurogenesis in the hippocampus of vitamin K-deficient mice. Neurogenesis, the process of generating new neurons, is essential for maintaining brain health and protecting against damage.
“Neurogenesis is believed to be crucial for learning and memory functions, and its impairment may contribute to cognitive decline,” stated Ton Zheng, a research scientist at Tufts’ Center for Human Nutrition (HNRCA).
In addition to reduced neurogenesis, the brains of vitamin K-deficient mice also showed signs of inflammation, further linking vitamin K deficiency to cognitive decline.
While the study highlights the importance of vitamin K, researchers emphasize the significance of obtaining nutrients from a balanced diet rather than relying on supplements.
“It’s essential for people to consume a healthy diet rich in vegetables,” advised Professor Sarah Booth, senior author of the study and director of the HNRCA.
Most individuals typically obtain sufficient vitamin K from their diet, with sources like spinach, kale, peas, Brussels sprouts, broccoli, cabbage, parsley, avocados, and kiwi. However, older adults are more prone to vitamin K deficiency.
The human brain is so complex that the scientific brain has a hard time understanding it. Nerve tissue, the size of a grain of sand, could be packed with hundreds of thousands of cells connected by miles of wiring. In 1979, Nobel Prize-winning scientist Francis Crick concluded that the anatomy and activity of only a cubic millimeter of brain material would forever surpass our understanding.
“It’s useless to seek the impossible,” says Dr. Crick. I wrote it.
46 years later, a team of over 100 scientists achieved that impossible by recording cell activity and mapping the structure of cubic millimeters of the mouse brain. In achieving this feat, they accumulated 1.6 petabytes of data. This is equivalent to 22 years of non-stop high-resolution video.
“This is a milestone,” said Davi Bock, a neuroscientist at the University of Vermont. the studywas published in the journal Nature on Wednesday. Dr. Bock said that it enabled advances that allowed it to cover the cubic bones of the cubic brain to map the entire brain wiring of a mouse.
“It’s completely doable and I think it’s worth doing,” he said.
Over 130 years It has passed since Spanish neuroscientist Santiago Ramon y Kajal first spies on individual neurons under a microscope, creating a unique branching shape. Scientists from subsequent generations have resolved many of the details about how neurons send voltage spikes into long arms called axons. Each axon makes contact with small branches or dendrites of adjacent neurons. Some neurons excite their neighbors and fire their own voltage spikes. Some quiet other neurons.
Human thinking emerges in some way from this combination of excitation and inhibition. But how this happens remains a ridiculous mystery as scientists could only study a small number of neurons at a time.
Over the past few decades, technological advances have allowed scientists to begin mapping the whole brain. 1986, British researcher Published A small worm circuit made up of 302 neurons. The researchers then charted larger brains, including 140,000 neurons in the fly’s brain.
After all, is Dr. Crick’s impossible dream possible? The US government began in 2016 100 million dollar effort Scan cubic millimeters of mouse brain. The project was called Cortical Network (or Mechanical Intelligence from Microns) and was led by scientists from the Allen Institute of Brain Science, Princeton University, and Baylor School of Medicine.
Researchers have zeroed into part of the mouse’s brain, which receives signals from the eyes and reconstructs what the animal is seeing. In the first phase of the study, the team recorded the neuronal activity in that area as they showed mouse videos of different landscapes.
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In the dimly lit room, broken symphonies of rattles, hums, and wobbles danced off the walls. However, the musicians responsible were nowhere to be seen.
Upon closer inspection, fragments of performers could be discerned, although their presence was not palpable.
In the midst of the room, spectators floated around an elevated pedestal, craning their necks to catch a glimpse of the brain behind the operation. Beneath the magnifying lens lay two white masses resembling miniature jellyfish. Together, they constituted a “mini-brain” cultivated in the laboratory of the late American composer Alvin Lucier.
“You’re peering into the Abyss”: the central pedestal of the revival, housing the “mini-brain” grown in Lucier’s lab. Photo: Rift Photography
Lucier, a trailblazer in experimental music, passed away in 2021. However, here in the art galleries of Western Australia, his legacy has been resurrected through cutting-edge neuroscience.
“Gazing down at its central pedestal, one pierces the veil,” remarks Nathan Thompson, the project’s artist and creator. “You peer deep within, observing what is alive. Unlike yourself.”
The Four Monsters who orchestrated the resurrection: Guy Benley, Matt Gingold, Nathan Thompson, and Stuart Hodgitz. Photo: Rift Photography
The revival is the handiwork of a self-proclaimed “four monsters” alongside a tight-knit team of scientists and artists who have dedicated decades to pushing the boundaries of biological arts: Thompson, along with fellow artists Ben Ally and Matt Gingold, and neuroscientist Stuart Hodgetts.
Lucier proved to be an ideal collaborator. In 1965, he became the first artist to utilize brain waves to produce live sounds in innovative solo performances. In 2018, the revival team, long-time admirers of Lucier’s work, brainstormed ideas with him. By 2020, at the age of 89 and battling Parkinson’s disease, Lucier consented to provide blood for the resurrection.
Dear reader, I have a confession: I suffer from the illness that young people call “Brain corruption” Things I can’t think deeply after scrolling too much on my phone. It’s difficult to complete a book these days.
Many people have this problem. Many have created a category of minimalist tech products that strive to eliminate us to be distracted, from AI pins, the artificially intelligent lapel pins that take notes to phones that only have basic features.
The latest example, $600 Light Phone IIIa peeled mobile phone that does little from a Brooklyn startup. The latest version, which began shipping in March and has been set to a wider release in July, can call, text, take photos, view map instructions, play music and podcasts, and many others can’t.
There is no web browser. Also, there is no app store. That means there are no Ubers who welcome rides, slacks, or social media. There’s no even an email.
“When you use it when you need it and turn it back on, it goes away in your life,” said Kaiwei Tang, chief executive of Light, a startup that has developed multiple iterations of light phones over the past nine years. “We tell many customers that they feel less stressed, they become more productive and creative.”
I used it as my main phone for a week, because I wanted to know if a light phone can cure me brain rot. There was a moment when I enjoyed it. I didn’t want to stare at the phone screen while I was waiting for the train, resting at the gym or eating alone. The phone sounded wonderful and clear. The Maps app did an amazing job navigating me around town.
It reminded me of a simple time when we mostly used our phones for Converse before we put them away to focus on other tasks.
But for a week, the flaws of the stupid phone call were lacking in my enjoyment. I suddenly realized I couldn’t enter the station. We looked up the names of our new restaurants and controlled the garage doors.
Part of it has nothing to do with the light phone itself, which is a decent product, but how society as a whole relies on advanced smartphone capabilities.
This is how my week ran errands, commute, and went out on Lower Technology phones.
Get started
When I set up a light phone review unit over the weekend, the phone, which looked like a black rectangular slab, was quite bare bones. The phone’s menu was a black screen showing a white text list for mobile phones, cameras, photo albums and alarm functions. To add more tools, I had to access the dashboard using a web browser on my computer. There, we were able to install features such as the map app, notepad, and timers.
I was ready to go, so I decided to live without my iPhone for at least a while.
I’m commuting
On Monday morning, I took the train from Oakland, California to San Francisco and started commuting. When I arrived at the station I realized that I couldn’t get in without an iPhone. This is because many years ago, I had converted my physical transit pass, Clipper cards, into virtual cards stored in my smartphone’s mobile wallet.
The light phone didn’t have a mobile wallet to load a virtual transit card, so I went back home badly to get my iPhone and eventually showed up in the office 30 minutes late.
Go to the gym
One night, I got a similar hit at a rock climbing gym. To enter, members use their mobile phones to log in to the gym website and generate a temporary barcode that is scanned at the entrance. The light phone didn’t have a web browser and could not create a barcode, so we had to wait in line at the front desk.
Text a friend and take photos
I added some of my closest friends to my address book over a light phone and texted them explaining my experiment. When I typed the device’s keyboard, some felt slow as there was no auto-correct feature to fix typos. As a result, the conversation was concise.
The cheer continued as I sent pictures of people. The unlit and grainy image appeared to have been created with telephone cameras for at least 15 years.
“Retro!” said one friend in response to a blurry photo of my daughter.
“Wow, that’s bad,” another friend said of the dimly lit photo of my corgi Max.
Photo taken on the author’s Corgi’s light phone, Max looked unlit and grainy.credit…Brian X. Chen/New York Times
The founders of Light said they are proud of the Light Phone camera, which has a nostalgic feel to it.
I’m running errands
One afternoon I had to drop off Amazon’s return at the UPS store. We have selected the most convenient shipping options, including displaying QR codes for scanning.
problem? Light phones didn’t have an email app or web browser to download codes. Instead, I loaded it onto my computer screen and snapped mediocre photos on my phone.
When I brought the package to UPS and presented the photos, I held my breath and hoping the image was clear enough. UPS employees kept the scanner and after three attempts they heard beeps and transport labels printed.
Not only is it a relief, but how troublesome.
lunch
Another afternoon my wife and I went out for an improvised lunch. I had to back out the car and ask my wife to use her iPhone to close the garage door with the app myq. (Our physical garage door opener stopped working years ago.)
After that, I was trying to remember the name of a new sushi restaurant I read recently on my food blog. It was inevitable that I would dig deeper into my blog posts on a light phone. In the end we speculated and went to the wrong restaurant. However, it was good to have lunch together without the temptation to check my email.
Conclusion
I admire the goal of light phones, but my experience shows that there is nothing realistically possible or can buy to bring us back to a simpler era. Many aspects of our lives revolve around highly capable smartphones, travelling around town, working, paying for things, dominating home appliances.
This light cell phone experiment reminded me of glamping.
I can’t think of many people who make them work to make light phones realistically use only their mobile phones. Many of us rely on tools like Slack and email to communicate.
A light phone may be a good choice for unplugging while you’re off work, as a secondary leisure phone similar to a weekend car. But even so, camera quality may be a contract breaker for some.
Light’s CEO Tang admitted that Light Shone is not for everyone, but added that parents are considering buying a mobile phone for their children not distracted at school. The company is also working on adding more tools, including the ability to request mobile payments and Lyft cars.
An investigation is underway at a Boston area hospital involving five nurses who worked in the same department and developed brain tumors.
Mass General Brigham Newton Wellesley Hospital reported a total of 11 employees in the fifth floor obstetrics department have raised health concerns, with five of them being diagnosed with benign brain tumors. Two of these tumors are meningiomas, the most common and benign types of brain tumors.
“The investigation did not find any environmental risks associated with the development of brain tumors,” said hospital administrator Jonathan Sonis, in a statement alongside Associate Nurse Sandy Muse Jonathan Sonis.
The hospital conducted the investigation in collaboration with government health and safety officials, ruling out disposable masks, water supplies, nearby X-rays, and chemotherapy treatments as possible sources of the issue.
“Based on these findings, we can assure our staff and patients that there are no environmental risks within our facilities,” the administrator assured.
Exterior of Mass General Brigham Newton Wellesley Hospital in Newton, Massachusetts. Google Maps
The Massachusetts Nurse Association, currently negotiating nurse compensation at the hospital, expressed their commitment to ongoing investigation.
The union highlighted nurses’ concerns about workplace health, leading to the discovery of individuals with tumors.
“The hospital’s environmental tests were not comprehensive, and they only spoke to a few nurses,” stated MNA spokesman Joe Markman. “The hospital cannot sweep this issue under the rug.”
The state agency and federal Occupational Safety and Health Administration are yet to provide conclusive information on the matter.
According to the American Cancer Society, a cancer cluster would involve an unusually high number of cancer cases within a specific area sharing common characteristics.
“Four out of ten people in the US develop cancer during their lifetime,” stated the association, emphasizing the frequency of cancer occurrences.
Ralph Hollogay, a pioneering anthropologist who emphasized the importance of changes in brain structure in human evolution, passed away on March 12th at his Manhattan home at the age of 90.
His death was announced by the School of Anthropology at Columbia University, where he had been a professor for nearly 50 years.
Holloway’s theory challenged the notion that brain size alone distinguished humans from apes and early ancestors, highlighting the significance of brain organization.
Although no brains from millions of years ago exist, Dr. Holloway focused on creating fossil skull endocasts from latex to overcome this limitation.
In a 2008 paper, he detailed how he obtained information from these casts, providing insight into brain structure by examining the outer edges of the brain.
Using endocasts, Dr. Holloway concluded that the fossil skulls from South Africa’s Town’s Children quarry belonged to early human ancestors, supporting Raymond Dart’s controversial discovery.
His meticulous research included studying natural endocasts found in the quarry to validate his conclusions, emphasizing the importance of independent investigation in scientific discovery.
Dr. Holloway’s focus on the Lunath groove behind the endocast provided evidence that aligned with human brain positioning, confirming the accuracy of Dr. Dart’s initial findings.
The contentious debate surrounding the Town’s Children’s findings has subsided, with Dr. Holloway’s and Dr. Dart’s conclusions about the Lunate Sulcus now widely accepted in the scientific community.
Dr. Holloway’s emphasis on brain structure over volume played a pivotal role in validating human ancestry, highlighting the significance of reorganization in evolutionary development.
Throughout his career, Dr. Holloway’s dedication to studying brain evolution through three-dimensional modeling remained unwavering, emphasizing the importance of understanding the human brain’s journey to its current complexity.
His contributions, such as his work on TaungChild, continue to shape our understanding of human origins and evolution.
Dr. Holloway’s legacy extends beyond his scientific achievements, as he leaves behind a lasting impact on the field of anthropology and evolutionary studies.
His commitment to rigorous research, innovative methods, and interdisciplinary collaboration sets a standard for future generations of scientists.
Dr. Hollogay’s contributions will continue to inspire and guide anthropologists, researchers, and educators in their quest to unravel the mysteries of human evolution.
His impact will be felt for generations to come, shaping the future of evolutionary studies and advancing our understanding of human origins.
Ralph Hollogay’s legacy lives on through his groundbreaking research and profound influence on the field of anthropology.
His work continues to shape our understanding of human evolution and the complexities of brain development.
A device has been created by scientists that can translate speech ideas into spoken words in real time.
Although still in the experimental stage, the goal is to develop a Brain Computer Interface that can give voice to individuals unable to speak.
In a recent study, the device was tested on a 47-year-old woman with quadriplegia who had been speech-impaired for 18 years since experiencing a stroke. The device was implanted in her brain during surgery as part of a clinical trial.
According to Gopala Anumanchipalli, co-author of the study published in Nature Neuroscience, the device “translates the intent to speak into fluent text.”
Most brain computer interfaces for speech experience a delay between thought and speech, which can disrupt conversations and cause misunderstandings. However, this new device is considered a significant advancement in the field.
The device works by recording brain activity using electrodes and generating speech based on this activity. An AI model is then trained to translate this neural activity into spoken words.
The UCSF Clinical Research Coordinator will connect a neural data port to the head of the ANN, a participant in El Cerrito, California, on May 22, 2023.Noah Berger/UCSF, via AP files via UC Berkeley
Anumanchipalli of the University of California, Berkeley, explains that the device operates similarly to existing systems used for transcribing meetings and phone calls in real time.
Located in the brain’s speech center, the implant translates signals into spoken sentences as they are heard. This “streaming approach” ensures a constant flow of audio to the recorder without waiting for the sentence to finish.
Rapid speech decoding enables the device to keep up with natural speech pace, enhancing language naturalness according to Brumberg.
Funded in part by the National Institutes of Health, further research is necessary before the technology can be widely available. Anumanchipalli suggests that with sustained investment, the device could potentially be accessible to patients within the next decade.
Chinese researchers have made progress in the field of inter-animal organ transplantation with a successful pig kidney transplant reported on Wednesday. They believe that pig liver may also prove to be useful in the future.
This Chinese patient is the third person worldwide known to be living with gene-edited pig kidneys. The research team has also successfully experimented with implanting pig liver into brain-dead individuals.
Scientists are genetically modifying pigs to make their organs more human-like in the hopes of addressing the shortage of organ transplants. While previous xenografts in the US were short-lived, two recipients of pig kidneys – an Alabama woman in November and a New Hampshire man in January – have shown promising results. Clinical trials in the US are now commencing.
Nearly three weeks after the kidney transplant, the Chinese patient is reported to be doing “very well” with the pig kidneys functioning effectively, according to Dr. Lin Wang of Xijing Hospital. The patient is a 69-year-old woman who has been suffering from kidney failure for eight years.
The next challenge for xenotransplantation is learning to transplant pig livers. In an experiment reported on Wednesday, pig liver was successfully transplanted into a brain-dead individual for 10 days. While the pig liver produced bile and albumin, essential for basic organ function, it did not perform as well as a human liver.
Dr. Wang believes that the pig liver could potentially support a failing human liver to some extent. In the US, a similar approach is being studied by pig developer Egenesis, where a pig’s liver is externally attached to support a brain-dead individual’s liver function.
In China, the team led by Dr. Wang did not remove the deceased person’s own liver but instead implanted the pig liver nearby.
Dr. Parsia Vagefi, a liver transplant surgeon, commented on the experiment, stating that while it shows promise, there are still many questions that need answers. Dr. Wang’s team plans to analyze the results of another brain-dead individual who received a pig liver transplant.
Last year, another Chinese hospital reportedly transplanted a pig liver into a living patient after removing part of their cancerous liver, but the outcome of the experiment is unclear.
The Budgerigars are some of the most fashionable birds, and it is reflected in their brains. The Budgie Brains contain maps of voice sounds similar to those found in the human brain, not seen in other birds.
Budgerigars (Melopstitacus undulatus), also known as a paraquiet, is a small parrot native to Australia. They are epic vocal learners and can mimic a variety of sounds, including human speech. The boudgie, known as the pack, had a vocabulary of about 1,728 words. According to the Guinness World Records. “The ability to mimic phonetically is very rare in the animal kingdom,” Long says.
and Zetian Yang, Additionally, NYU medical schools used silicon probes for a long time to record electrical activity in the Budgies' brains. They focused on a part of the forebrain, the central nucleus of the forebrain horn, which was known to be involved in motor control of vocalization. When Budgies made the call, Long and Yang tracked how their electrical activity had changed.
“Our research was the first to measure parrot brain activity during vocalization,” Long says.
The pair discovered neurons in the central nucleus of the anterior horn thyroid. “There are cells that are active because of consonants,” Long says. Others make vowels, but some are active for high-pitched sounds, others for low pitch.
This brain structure is compared to a keyboard. “There's this kind of key, or in this case, a set of brain cells, and you can represent each of these vocal outcomes and play whatever it wants,” he says. “What the parrot presented is this beautiful and elegant solution to creating vocal sounds.” The human brain has a similar vocal map.
Long and Yang repeated the experiment with a zebra finch (taeniopygia guttata), not vocal mimic. “They have one song they learn,” Long says. “It's about two seconds, sometimes less.” It takes several months to perfect.
Unlike the Budgerigars, the Zebra Finch showed no signs of a “map” of the sound of the brain's voice. Instead, “A Zebra Finch develops chords that are almost almost inexplicable for this song,” says Long. He says that Budgie's brain uses a simple, intuitive system to generate complex calls, while Zebra Finch Brain uses a complex system to make something simple.
“It shows that neural activity and associated vocal behavior are closer to parrots and humans than songbirds and parrots.” Erich Jarvis At Rockefeller University in New York.
“Almost everything we know about the detailed mechanistic basis of learned vocalization comes from several species of songbirds singing relatively simple songs.” Jesse Goldberg At Cornell University in New York. “The parrot therefore offers an incredible opportunity to study both the mechanisms and evolution of complex vocal learning and production.”
I say there are several reasons why I evolved imitation. Zhilei Zhao At Cornell University. One is courtship. “Women actually prefer men with the ability to copy,” he says, and if a man loses his ability, “they are more likely to fool him.” Also, the Budgies have a very dynamic social life. “Form small groups for several days.” Once the group is established, members begin to create unique “contact calls.” “People think it might be something like a password for this group,” says Zhao.
Other skilled mimics may have similar vocal maps in their brains. “My very strong speculation is that other parrots have the same functionality, but they are simply not explored.” He also doubts something similar, the Lyrebirds, a phenomenal mimic that can even mimic artificial sounds like camera shutters.
In the long run, I hope that studying how boudgies produce sounds for a long time will help people understand language disorders. People with strokes often experience aphasia. I can't call the correct words in my head. “You reach for those words and it’s not there,” Long says. “Now we have the opportunity to fight to understand what we think is at the root of many communication disorders that affect people in devastating ways.”
We share 98.8% of DNA with our closest living relatives, chimpanzees. However, despite this almost identical genetic blueprint, chimpanzees have not built civilizations, fought wars, or mastered the art of Tiktok dance routines.
But what exactly makes us stand out? Now, neuroscientists may finally have the answer.
New research published in the journal jneurosci looks at new data from the brains of humans, chimpanzees, and macaques.
“We were interested in finding things that ticked different brains.” Professor Logier Mars, the study co-author said to BBC Science Focus. “And the human brain is something we were particularly interested in, for obvious reasons.”
According to Mars, most studies comparing human brains with other animal brains tend to focus on factors such as overall size, the size of a particular region, or the number of neurons. “But our philosophy is that if we really want to understand what is going on, we need to look into how our brains are organized,” he said.
With that approach in mind, Mars and his team set out to investigate. Similar to the scans used in hospitals, published MRI data were used to create a “connectivity blueprint” for three different species of brains. These blueprints essentially map out whether different regions of the brain communicate with each other.
One area the team expected to find a difference was in the prefrontal cortex. This region is related to complex thinking, planning, and decision making.
This area, often referred to as the “personality center” of the brain, plays an important role in regulating emotions and teaching behaviors. At first glance, it seems to be an obvious place to search for the essence of what makes us human. In fact, this study revealed that this region exhibited more connectivity than in other species.
But was that the whole story?
This image highlights the (red) behavioral domains of the left and right hemispheres showing high divergence after comparison. -Bryant et al. , Jneurosci 2025
“The prefrontal cortex is where researchers tend to see when they look for something unique about humans,” Mars said. “But we have found a difference in many places in the cortex of time just above your ears.
Temporal cortex plays an important role in the processing of sensory information – especially visual, sound, and language. Given our highly social and cooperative nature, it is probably not surprising that these areas are connected more intricately in the human brain.
“We are a very social and cooperative species,” explained Mars. “So these properties are likely the driving force behind the changes we observe.”
All of these suggest that there is no single definition switch that makes humans human. Some believe that highly evolutionary events have led us to dominance, but reality can be more complicated.
Like relatives not too far in the trees, we are the result of the progressive, widespread evolutionary changes that have shaped us over time.
Or, as Mars said, “There’s nothing big that makes us different.”
About our experts
Rosier Mars is a professor of neuroscience at Oxford University. His work focuses on the differences between primate brains, especially humans. Mars’s research is published in the following journals: Natural Communication, Frontiers of human neuroscience, and Science.
Have you ever measured your hip to hip ratio? Chances are, you probably haven’t. However, there is an important reason why you should start.
Recent research published in Nutrition, obesity, exercise suggests that these measurements may be linked to cognitive decline. The study found that individuals with smaller hips have a significantly lower risk compared to those with larger hips.
Feeling concerned about your numbers? Don’t worry too much just yet – researchers emphasize that your risk is not set in stone. Making healthier dietary choices can actively reduce the risk of cognitive decline and support long-term brain health.
BMI and Waist-to-Hip Ratio
While most scientists use Body Mass Index (BMI) to measure body size by comparing weight to height, this system has faced criticism for its inaccuracies. For instance, muscular individuals may be categorized as overweight even if they are not at risk for diseases like type 2 diabetes or heart disease.
Therefore, researchers are increasingly turning to alternative measurements such as waist-to-hip ratios as a more accurate indicator of health risks related to size than BMI. According to the authors of the study, this measurement is more reliable.
“We found a connection between healthier waist-to-hip ratios and better cognitive function scores,” stated Dr. Dahlia Y Jensen in an interview with BBC Science Focus.
The study, which was published recently, examined the relationship between diet, body size, and brain health over several decades. 664 British civil servants had their waists and hips measured multiple times between the 1950s and 1960s over approximately 21 years.
Comparing waist and hip sizes indicates the amount of central fat accumulation, which is associated with a higher risk of diseases like type 2 diabetes and heart disease. – Credit: FluxFactory via Getty
Diet Evaluation and Brain Health Measurement
A group of 512 civil servants completed three dietary surveys between the ages of 48 and 60. Scientists assessed dietary quality based on various components including vegetables, fruits, whole grains, nuts, legumes, fats, sugary drinks, meat, salt, and alcohol.
When participants reached about 70 years of age, brain scans were conducted to measure cognitive performance. The findings revealed that middle-aged individuals with healthier diets and slimmer hips had better brain health later in life.
Brain imaging techniques such as magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) were used to analyze the brain structure of the participants, with a particular focus on the hippocampus.
“The hippocampus is crucial in dementia research, and numerous studies have highlighted its importance in memory and learning,” explained Jensen. While previous studies emphasized the significance of hippocampal volume, this study explored its associations with other brain regions.
“We observed a strong link between better diet, functional connectivity of the hippocampus with other brain regions, and waist-to-hip ratio,” Jensen added. Improved white matter connections associated with a slim waist indicated better communication between brain regions.
This suggests that individuals who follow healthier diets and maintain slimmer waists in middle age are at a reduced risk of cognitive decline and diseases like dementia later in life.
“If you’re looking to improve your brain health, it’s never too late to start, but the earlier, the better,” Jensen advised.
The study had some limitations, with only 20% of female participants as they were civil servants recruited in the 1980s. However, Jensen deemed the study “exciting” and believes it will aid in understanding the link between mid-age dietary health and future brain health.
Alzheimer’s Disease Association estimates that 982,000 people in the UK currently live with dementia. Jensen hopes the study will encourage a shift towards preventive healthcare.
About our experts:
Dr. Dahlia Y Jensen is a postdoctoral researcher at the Department of Cognitive Neuropathy Clinic, University Medical Center Leipzig, and the Department of Neurology at Max Planck Human Brain Science Institute in Germany. She also serves as a visiting researcher at the Oxford University School of Psychiatry and is a corresponding author of the study.
Have you found that the orange circle on the left is smaller than the orange circle on the right?
Radoslaw Wincza et al. (2025)
Optical fantasies may make you feel like a fool, but you may be able to train your brain to resist your brain.
“People in the general population are very likely trained to unravel illusions and have the ability to perceive the world more objectively,” he says. Radoslaw Wincza At Lancaster University, UK.
Wincza and his colleagues recruited 44 radiologists with an average age of 36. He spent over a decade finding small details such as fractures from a medical scan. They also saw 107 college students, an average of 23 years old, studying medicine and psychology.
Each participant displayed four fantasies one at a time on the screen. With each illusion, participants had to look at size or length size or length shape or line pairs and choose larger or longer ones.
In the three illusions, other objects made larger shapes or longer lines smaller and shorter lines. The team found that radiologists were less susceptible to these illusions than students.
“Radiosists have this ability to really focus on the key elements of the visual scene, where they ignore unrelated contexts and have tunnel vision,” says Wincza. “By adjusting your targets, they don’t experience that much illusion.”
In the fourth illusion, one of the shapes was vertical, and the pair was horizontal. This made the latter look even wider, even if it was actually narrower. Both groups were equally susceptible to fantasy. This is probably because this didn’t involve much of an adjustment to background distraction, as it didn’t contain any surrounding objects.
“It suggests that if everyone trains themselves, they can gain the ability to be susceptible to illusions,” he says. Carla Evans At York University, UK. Focusing on certain aspects of photography, for example, could improve this ability, but she says there is more work to see how fast this can be. “It could take years or weeks.”
Are you looking to keep your mind sharp as you age? One secret could be as simple as regularly exercising your brain with mathematics and reading comprehension, whether it’s at work, at home, or even while reading this article.
A groundbreaking new study led by Professor Eric Hanushek of Stanford University suggests that engaging in mathematics and reading can help prevent age-related cognitive decline. The research shows that individuals who regularly practice these skills do not experience significant declines in cognitive abilities over time, whether they are reading emails, doing calculations, or reading articles like this one. This challenges the notion that cognitive decline is inevitable with age.
The study reveals that cognitive skills typically peak in a person’s 40s before slowly declining. However, those who consistently engage in mathematics and reading, whether at work or in their daily activities, show no decline at all.
“Our findings indicate a significant increase in average skills in literacy and numeracy until the 40s. After this point, there is a slight decrease in literacy skills and a more noticeable decline in numeracy,” the study notes.
This study may inspire you to tackle your taxes – Credit: Skynesher
These findings challenge previous studies that suggested cognitive decline begins in early adulthood. Unlike past research that compared different age groups at one point in time, this study followed the same individuals over several years, providing a more accurate understanding of how cognitive abilities change with age.
Hanushek and his team propose that what was previously thought to be age-related cognitive decline might actually be due to differences in skill levels between generations rather than the natural effects of aging itself.
By analyzing data from language and mathematics assessments in the German population aged 16-65 and retesting the same group 3.5 years later, researchers found that women’s math skills declined significantly over time, indicating potential gender disparities. Further exploration of these differences is planned for future studies.
“Brain corruption” was named the term Oxford’s year 2024. This is defined as the “degradation of a person’s mental or intellectual state” that arises from seeing “trivial” content online, such as a Tiktok video.
It’s a term that is often joked about, but what If there is a grain of truth? This is the seemingly scary implications of a new study published by a large team of brain scientists based at Tianjin Division University in China.
What did this study find?
They scanned the brains of over 100 undergraduates and completed a survey on their habits of watching short online videos. The survey included statements such as “My life will be empty without a short video” and “Not able to watch a short video will be as painful as losing a friend,” indicating how much they agreed.
Interestingly, researchers found that those who felt most obsessed with short videos had significant differences in brain structure. These participants had more gray matter in the orbitofrontal cortex (OFC). This is an area near the front of the brain that is involved in decision-making and emotional regulation. Similarly, they had more gray matter in the cerebellum – the small cauliflower-shaped structures behind the brain play a role in movement and emotions.
The team concluded that this is bad news, as for Tiktok enthusiasts, having an oversized OFC could be a sign that it is described as “an increased sensitivity to rewards and stimuli associated with short video content.” They speculated that watching too many Tiktok videos could have led to this nerve distension.
Similarly, they suggested that enhanced cerebellum could help the brain process short video content more efficiently – perhaps the result of frequent rampages. This can create a reinforcement cycle. In this cycle, watching more videos strengthens these brain pathways and habits become even more ingrained.
Over 23 million videos are uploaded to Tiktok every day – Photo Credit: Getty
But that’s not all. The team also performed a second brain scan to track participants’ brain activity while participants were resting with their eyes closed.
They found a greater synchronization of activity within multiple regions of the brain. These include the dorsal prefrontal cortex (areas involved in self-control), the posterior cingulate cortex (areas involved in thinking about oneself), the thalamus (a type of relay station for brain signals), and the cerebellum.
The researchers suggested that these functional brain differences could reflect a variety of issues among addiction participants. The issues include the tendency to overly social comparisons while having trouble leaving the video and watching them.
They also asked participants to fill out a survey on “promising temperament.” This is a factor measured by agreeing to statements such as “I strive to reach other people’s outstanding results.”
Interestingly, scientists have found that many links between video addiction and brain differences are also linked to a higher level of envy. This suggests that feeling of envy can make someone more likely to watch a short video. And over time, this habit can lead to potentially harmful changes in the brain.
Does Tiktok cause brain decay?
If you are an avid consumer of fun online videos, or a related parent, the idea that seeing habits can reconstruct brain structures is no surprise.
However, it is important to consider this study in a broader historical context in which new technologies and media have long been causing exaggerated neurological claims. It is also important to understand the deep limitations of research.
It’s been nearly 20 years Atlantic Ocean The magazine ran a cover function that asked, “Is Google making us stupid?” And, in a nutshell, the answer that was asserted was “Yes!” Author Nicholas Kerr lamented that he was once a “scuba diver in the sea of words,” but now, thanks to Google, he zipped “along the surface like a jet ski man.”
Countless brain imaging studies of questionable quality were also published in the same era. Many aim to demonstrate the disaster effect of the World Wide Web on our vulnerable minds.
A few years later, Professor Susan Greenfield, a neuroscientist professor of Baronness, launched a media campaign claiming that “mind change” (the impact of the internet and video games on the brain) is just as serious threat to humanity as climate change.
She even wrote dystopian novels about the dehumanizing effects of the internet, but received mixed reviews (One critic (I questioned whether this was one of the worst science fiction books ever written).
Scientists still don’t know how much Tiktok affects the brains of young people, but research is still underway. – Photo credit: Getty
Almost 20 years later, we’re fine. At least I don’t think our brains have been transformed into mash. But of course, these previous horrors were before the appearance of Tiktok. Perhaps there is something uniquely damaging about the types of short, scrollable, meaningless content available today.
I asked Professor Peter Etchellsif this is plausible, expert on the psychological impact of digital technology at Bathspa University. “As far as I know, there is no good science to support the idea that short videos are either tangible or uniquely bad in terms of their impact on the brain,” he says.
read more:
Is short video brain research a good science? Not so, but the evidence suggests that it is not.
What is wrong with this research?
Let’s take a look at some of the limitations of the research. If the goal was to prove that seeing tiktok is harmful to the brain, a more effective approach would be to scan participants’ brains and then consume different amounts of harmful content.
However, this study is completely cross-sectional, meaning that only a single snapshot was captured in time. This was not a pre- and post-comparison of causes and effects.
Or, as Etchell says: “[From this study] I can’t say anything about whether watching a short video will cause brain changes, or whether certain types of brain structures precede certain types of video consumption.
“This research doesn’t really add anything that will help us understand how digital technology affects us.”
Even if we accept the speculative leap of researchers that Tiktok’s videos may have caused the brain changes they observed, there are still some issues to consider.
First, the researchers searched the entire brain for differences that correlated with the scores on the video addiction scale. This approach is a common problem in brain imaging studies as it increases the risk of finding false positives. In other words, the more comparisons you make, the more likely you will stumble over random differences that seem important but are actually just a coincidence.
Second, even if we accept that the observed brain differences are real and caused by seeing Tiktok, interpreting them involves a lot of speculation. Researchers enveloped an increase in brain synchronization (known as regional homogeneity (Reho). However, Rejo itself is not inherently a good or bad thing. In fact, other studies have associated with an increase in Reho in certain brain regions. positive Results such as results observed during meditation training.
Perhaps the biggest flaw in the study relies on questionable survey-based measures of short video addiction that lacks strong scientific validity.
As Etchells put it, “Short video addiction is essentially an invented term, not a formal diagnostic clinical disorder.”
Taken together, these issues suggest that we should not be overly concerned that Tiktok fundamentally shapes the brains of young people in harmful ways.
That said, the excessive amount of time spent watching frivolous videos can still be a problem for some. However, it is more productive to focus on developing healthy media habits rather than worrying about brain changes or addiction.
“In many cases, when research like this hits the news, it’s a good opportunity to pause and reflect on whether we’re happy with the use of the technology,” says Etchells.
“If there’s concerns there, it’s worth thinking about what you can do to eliminate your frustration, knowing that you’ll benefit a lot from these technologies.”
About our expert, Professor Pete Etchell
Pete is a professor of psychology at Bath Spa University. His research focuses on how playing video games and using social media affects our mood and behavior. He is the author of I got lost in a good game We are currently investigating whether game mechanics can promote gambling behavior in other parts of our lives.
If you’re like Khloe Kardashian, who recently turned 40, you may have considered testing your biological age to see if you feel younger than your actual age. But while these tests can tell you a lot about your body’s aging, they often overlook the aging of your brain. Researchers have now developed a new method to determine how quickly your brain is aging, which could help in predicting and preventing dementia. Learn more here.
Unlike your chronological age, which is based on the number of years since you were born, your biological age is determined by how well your body functions and how your cells age. This new method uses MRI scans and artificial intelligence to estimate the biological age of your brain, providing valuable insights for brain health tracking in research labs and clinics.
Traditional methods of measuring biological age, such as DNA methylation, do not work well for the brain due to the blood-brain barrier, which prevents blood cells from crossing into the brain. The new non-invasive method developed at the University of Southern California combines MRI scans and AI to accurately assess brain aging.
Using AI to analyze MRI brain scans, researchers can now predict how quickly the brain is aging and identify areas of the brain that are aging faster. This new model, known as a 3D Convolutional Neural Network, has shown promising results in predicting cognitive decline and Alzheimer’s disease risk based on brain aging rates.
Researchers believe that this innovative approach can revolutionize the field of brain health and provide valuable insights into the impact of genetics, environment, and lifestyle on brain aging. By accurately estimating the risk of Alzheimer’s disease, this method could potentially lead to the development of new prevention strategies and treatments.
Overall, this new method offers a powerful tool for tracking brain aging and predicting cognitive decline, bringing us closer to a future where personalized brain health assessments can help prevent and treat neurodegenerative diseases.
Could scientists use parasites in your brain to treat diseases? The concept of utilizing parasites as a medical tool may sound unconventional, but it offers hope for conditions like Parkinson’s and Alzheimer’s. Researchers believe that if parasites can transport drugs directly to the brain, it could aid in treating these ailments.
An international team of scientists is doing just that. They are utilizing single-cell parasites called Toxoplasma gondii, which causes the infection toxoplasmosis. These parasites naturally travel from the human intestine to the central nervous system and provide proteins to host cells. In their experiment, bioengineers manipulated the internal system of T. gondii cells to produce and release proteins outside the cell, creating a secretion system.
The team explained that delivering medications to the brain is challenging due to the blood-brain barriers that safeguard the brain from harmful substances. T. gondii has evolved the ability to overcome these barriers, which could be beneficial in this process. Initially, they tested whether T. gondii can cross the blood-brain barrier in mice and then in human brain cells, specifically neurons, before moving on to testing on intact mouse brains to potentially apply the findings to humans.
Their drug delivery system mediated by T. gondii consists of proteins created from at least two regions of different genes that are combined and translated into a single unit, known as a protein fusion. They incorporated a therapeutic drug with a T. gondii protein called takihorin to transport medicine to the brain.
Initially, scientists faced challenges in determining the appropriate dilution factor for the drug compound. They had to find a balance between allowing the proteins to pass through the blood-brain barrier while ensuring they were still therapeutically effective. Through trial and error, they found the correct dilution factor and successfully administered the treatment to the targeted brain area.
The next step involved delivering therapeutic proteins to brain cells through T. gondii. Researchers used lab-grown mouse brain cells and specific proteins that regulate the movement of molecules across the cell membrane, known as vesicle transport protein. They demonstrated that the engineered T. gondii successfully transported healing proteins to the brain cells of lab-grown mice.
The researchers then tested the treatment process on human brain cells cultivated outside of the body. They confirmed that the therapeutic proteins delivered by T. gondii could bind to the DNA of human brain cells. This binding altered gene expression in the laboratory-grown brain cells.
Finally, engineers demonstrated the success of this therapy on whole mouse brains. By ensuring that the therapeutic proteins could pass the blood-brain barrier in live mice, they then evaluated the brains post-euthanasia. Utilizing 3D imaging, they illuminated specific neural pathways and markers in the mouse brain, confirming that the engineered proteins effectively delivered therapeutic proteins to the brain.
The researchers concluded that their findings show progress in drug delivery via engineered parasites but emphasized the need for further research to determine the potential advantages and drawbacks of this method. With the success of this study, they proposed that utilizing engineered parasites for drug delivery could offer new treatment options for brain-related diseases.
The human brain is like an electrified sphere, considered the most complex object in the universe. Sometimes, don’t you wish it would just quiet down, especially at night?
One common symptom of insomnia is a racing mind when trying to sleep. Our brains bounce thoughts around like a pinball machine due to caffeine, anxiety, or stress.
This mental perturbation includes repetitive negative thoughts that we may not even be aware of, focusing on mistakes and worrying about the future.
While this is challenging for those with mental health conditions, it affects everyone when overwhelmed with tasks or life challenges.
Insomnia affects about 1 in 3 people – Photo Credit: Getty
Psychologist Dr. Luc Beaudoin believes that cognitive shuffle, a technique that mimics the brain’s natural processes during sleep onset, can help control runaway thoughts while trying to sleep.
The cognitive shuffle involves imagining unrelated images, like a photo show, to bring light structure to racing thoughts. By focusing on connecting images related to a chosen word, it aims to quiet the mind before falling asleep.
Counting sheep may not be as effective as cognitive shuffle – Photo credit: Getty
Cognitive shuffling strikes a balance between conscious and unconscious thoughts, keeping unwanted thoughts at bay without overwhelming executive functioning.
Dr. Beaudoin’s broader sleep initiation theory, Somnolent Information Processing, explores factors that help or hinder the process, with spiritual perturbation as a common hindrance.
Cognitive shuffling is still under research, but promising results suggest it can aid sleep initiation along with other scientifically proven techniques.
About our experts
Dr. Luc Beaudoin is an adjunct professor at Simon Fraser University and founder of Cogsest. He has published books on cognitive productivity and is recognized in various academic journals.
Manipulating neuron types can make snacks more likely to resist
5M3Photos/Getty Images
Neurons in the mouse brain tell them to stop eating when they have enough food. And since people probably have the same cells, they may one day manipulate them to help treat obesity.
“The main question we were trying to answer was how our brains sense and respond to different signals.” Alexander Nectau At Columbia University in New York.
To learn more, he and his colleagues used a kind of molecular profiling to distinguish between different cell types in the mouse brain. In the dorsal trunk nucleus, part of the brainstem associated with functions such as feeding, mood, and sleep, we encountered cells that produce a hormone called cholecystokinin, which helps regulate appetite.
To study what these cells feel to make them work, researchers measured their activity as mice spent the day. “Every time an animal eats a bite, activity has risen and then it has become corrupted,” says Nectow. “These neurons sense and use information such as food smells and sights, food tastes, food sensations in the intestines, and neurohormones released in response to intestinal foods and so on. You can actually finish your meal.
Next, researchers used a technique called optogenetics. This involves engineering neurons so that they can turn them on and off with light. The mice slowed their diet when they used light to activate them. The more intense the activation, the slower and stopped the animal.
Neurons sit in the brainstem and are similar ancestor characteristics across vertebrates, so Nectow probably thinks we have them too. “We didn’t confirm that, but my guess is that humans have these neurons.”
The team also discovered that mouse neurons can be activated by compounds called glucagon-like peptide-1 (GLP-1) agonists. Brand names such as Ozempic and Wegovy.
If these neurons have the same function in people, theoretically, they can either control the feeding habits of obese people or combine this approach with GLP-1-based drugs to increase greater weight loss. They can be adjusted to achieve, says Nectau.
“Understanding the circuits governing meal halts is particularly important in an environment of near-ubiquitous food availability,” he says. Jeff Davis At Swansea University, UK. “The authors used elegant methods to identify these important cell populations.”
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