Unforeseen vaccine side effects: Staying sharp is a bonus!
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Recent studies indicate that chronic inflammation in various body areas could contribute to Alzheimer’s disease. While it may take time to fully understand these connections, it’s evident that persistent inflammation has adverse effects and that reducing it can provide numerous health benefits.
Inflammation is the body’s response when immune activity exceeds normal levels, such as when a wound becomes infected. While short-term inflammation is beneficial, prolonged inflammation can lead to serious health issues, including cancer, heart disease, stroke, rheumatoid arthritis, and mental health disorders like depression and anxiety.
To combat long-term inflammation and enhance both physical and mental health, consider the following tips:
1. Get Vaccinated
Vaccines, including those for shingles, tuberculosis, and influenza, have demonstrated a reduced risk of dementia. For instance, individuals who received the Shingrix vaccine experienced a 17% lower chance of developing dementia compared to those who had the older Zostavax vaccine, which also lowers dementia risk. Though the exact mechanism remains unclear, vaccines likely reduce inflammation.
2. Maintain Good Oral Hygiene
Gum disease is another inflammatory condition linked to an increased risk of Alzheimer’s and heart disease. Bleeding gums can allow harmful bacteria to enter the bloodstream, which is why good dental hygiene is essential for preventing periodontal disease and maintaining overall health.
3. Embrace a Mediterranean Diet
A Mediterranean diet is rich in anti-inflammatory foods such as fruits, beans, nuts, whole grains, fish, and olive oil, while minimizing inflammatory foods like red and processed meats. This dietary approach not only helps in reducing inflammation but is also associated with longevity and overall wellness.
4. Exercise Regularly
Sedentary lifestyles contribute to increased inflammation. Numerous studies suggest that regular exercise diminishes inflammation. Whether it’s vigorous workouts or gentler activities like yoga, incorporating movement into your routine can provide significant health benefits.
5. Achieve a Healthy Weight
Although the connection is still being explored, obesity is often linked to ongoing inflammation. It raises an interesting question: Could medications like GLP-1, often used for weight loss, reduce Alzheimer’s risk? Current evidence shows that those using GLP-1 medications may experience lower dementia risk, but results for those without diabetes are still unclear.
6. Cultivate Happiness
While occasional stress is normal, chronic stress can lead to inflammation. Striving for happiness and emotional balance can help mitigate inflammation and improve overall mental well-being.
Amyloid plaques in the brain are a defining feature of Alzheimer’s disease, but what if the roots of the condition start elsewhere in the body?
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Alzheimer’s disease has traditionally been believed to originate in the brain. However, comprehensive genomic analysis indicates that inflammation in distant organs such as the skin, lungs, or intestines may initiate the condition, potentially decades before noticeable memory decline occurs. This shift in understanding could shed light on why Alzheimer’s treatments have been largely ineffective. Current drugs intervene too late; a focus on early-stage inflammation in peripheral organs may be crucial.
“As neuroscientists, we tend to focus on the brain, but this study highlights that the brain is interconnected with the body, and changes elsewhere can impact brain function,” states Donna Wilcock from Indiana University, not involved in the study. “Although Alzheimer’s is a brain disorder, we must consider the entire body when discussing its genesis.”
To explore the genetic underpinnings of Alzheimer’s disease, researchers including Cesar Cunha from Denmark’s Novo Nordisk Foundation Basic Metabolic Research Center analyzed genetic data from the European Alzheimer’s and Dementia Biobank, encompassing over 85,000 individuals with the disease and approximately 485,000 without it. They also evaluated gene activity in 5 million single cells across 40 body regions and 100 brain regions.
The study scrutinized 1,000 genes linked to an increased Alzheimer’s disease risk, surprisingly finding these genes were more abundant in organs like the skin, lungs, and digestive system than in the brain. “It was counterintuitive at first because the expression of these risk genes in brain cells seemed low,” notes Cunha. “Our continued analysis revealed their primary presence in other body parts.”
Many of these Alzheimer’s risk genes are tied to immune regulation and are particularly abundant in barrier tissues like the skin and lungs, which defend against bacteria and toxins through inflammatory responses. “This suggests that Alzheimer’s might initiate due to inflammation in these peripheral organs,” Cunha explains. Genetic variations may even dictate the extent of inflammation and its impact on brain health. Hence, individuals with a family history of Alzheimer’s could be more vulnerable to the disease amidst infections or inflammatory episodes.
Interestingly, the highest expression of these gene variants occurs when individuals reach ages 55 to 60. Inflammation during this period seems likely to trigger Alzheimer’s, corroborated by long-term studies from Hawaii. Inflammatory markers rise in individuals in their late 50s, with those in their 70s and 80s exhibiting increased Alzheimer’s likelihood. “A person could suffer from lung inflammation due to a viral infection at age 55, which might initiate Alzheimer’s 30 years later, but the exact mechanisms remain elusive,” Cunha remarks.
Rezanur Rahman, a researcher at QIMR Berghofer Medical Research Institute, has identified a genetic mutation associated with Alzheimer’s that appears concentrated in the skin and lungs. More research is essential to understand their functional role in symptom progression, Rahman states. “Association does not imply causation.”
Previously, the brain was deemed immune-privileged and largely unaffected by inflammatory processes elsewhere in the body. Bryce Vissel from St. Vincent’s Hospital in Sydney, Australia, among those who first proposed inflammation as a trigger for Alzheimer’s, acknowledges that while initially contentious, new evidence supports that peripheral inflammation from infections or injuries may indeed instigate the disease.Infection or injury can affect brain function.
When inflammation occurs, immune cells are activated, releasing signaling proteins like cytokines that can cross into the brain via the bloodstream. An unpublished study by Vissel and his team indicates that cytokines may disrupt neuronal connections, potentially leading to memory impairment.
Concurrently, research has shown that the blood-brain barrier becomes more permeable with age, allowing inflammatory cytokines and immune cells easier access, which might elucidate why inflammation poses more of a risk during mid-life compared to youth, Cunha notes.
Current theories posit that Alzheimer’s disease stems from the accumulation of misfolded beta-amyloid and tau proteins within the brain. Yet, treatments aimed at eliminating these proteins have yielded minimal success, indicating that such accumulation might be a symptom rather than the core issue. “We’ve been trying to treat the result of the disease, not its cause,” Cunha argues.
Cunha likens this to past mistakes in obesity treatments, which initially targeted excess fat directly, failing until genetic research revealed that mutations connected with obesity are often highly expressed in the brain, disrupting appetite and energy balance. This led to the development of the weight-loss medication semaglutide (marketed as Ozempic and Wegovy), which modulates brain pathways to curb appetite.
If Alzheimer’s originates from peripheral inflammation, its treatment would necessitate a paradigm shift, Cunha asserts. Data indicate that midlife vaccinations may offer protective benefits against Alzheimer’s disease. A recent Californian study revealed that adults receiving both doses of the shingles vaccine recommended for individuals aged 50 and older were 50% less likely to develop Alzheimer’s by age 65. Another investigation found that those aged 50 and older treated with the Bacillus Calmette-Guérin (BCG) vaccine for bladder cancer had a 20% reduced risk of onset.
This phenomenon might arise as vaccines bolster the aging immune system and mitigate inflammation, suggests Wilcock. “At age 55, we should invigorate our immune systems and remind them to stay active, as most vaccinations occur in childhood.”
Beyond vaccinations, several lifestyle interventions have been shown to diminish inflammation and avert Alzheimer’s disease. These include adopting a Mediterranean diet, limiting alcohol consumption, exercising, quitting smoking, and managing blood pressure and cholesterol levels.
Professor Cunha emphasizes that the challenge lies in convincing fellow neuroscientists to recognize peripheral inflammation as a potential contributor to Alzheimer’s disease. “I’ve encountered skepticism at academic conferences, being told, ‘If you aren’t focusing on amyloid, you’re not studying Alzheimer’s disease,'” he shares. “After decades entrenched in amyloid research, adapting one’s perspective can be daunting.”
Airway inflammation can arise from smoking or air pollution exposure
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Severe airway inflammation hampers the ability of mice to discern when dangerous situations are no longer a threat, indicating that lung conditions may influence emotions and behaviors. This connection between lung health and brain function could clarify why a small number of individuals who undergo trauma develop post-traumatic stress disorder (PTSD).
Sah and her team delved deeper into the correlation by observing eight mice exhibiting severe asthma-like symptoms. Their lungs were exposed to mites, inducing an allergic response and subsequent inflammation. Three days afterward, the mice were placed in cages and subjected to three mild electric shocks.
Over the subsequent six days, researchers returned the mice to the cage for five minutes daily, monitoring the duration they stood frozen in fear. On average, these mice were immobilized for about 40% of the final session, which was twice as long compared to another group of 11 mice without lung inflammation who faced the same electrocution.
The two groups did not exhibit differences in fear response the day after the shocks. However, the first group’s prolonged fear response after several days suggests that significant airway inflammation hampers the brain’s ability to recognize when a threat has subsided. “In PTSD patients, this process is dysfunctional, leading to persistent fear memories,” Sah elucidates.
The experiment was replicated with another set of mice experiencing severe lung inflammation, but this time, a medication inhibiting an inflammatory molecule called interleukin-17a was administered. During their final session in the previously shocked cage, these mice displayed about half the freezing response of those that did not receive the medication.
Further analysis revealed that immune cells in brain regions known as subcutaneous organs have receptors for this inflammatory molecule. Unlike most brain areas, subcutaneous organs lack a blood-brain barrier, a protective layer that limits substance exchange between blood and neurons. Consequently, it serves as a “window to the brain,” allowing it to monitor bodily changes and respond accordingly, according to Sah.
The team discovered that immune cells in this region sense inflammatory signals from the lungs, activating adjacent neurons that relay information to the cerebral cortex, a brain region associated with threat recognition.
Using a specialized compound known as chemogenetics, researchers inhibited this signaling pathway in mice with severe lung inflammation, resulting in a notable decrease in their freezing behavior post-shock.
“In essence, severe lung inflammation can impact higher cognitive functions and the ability to navigate traumatic experiences,” asserts Sah. She posits that similar pathways likely exist in humans, as the brain circuits regulating fear are comparable across species.
Other studies suggest that chronic psychological stress diminishes immune responses. Sah speculates that a heightened immune response, in turn, impairs cognitive functions such as the recognition of a threat’s resolution, possibly due to the body reallocating resources from the brain to combat lung issues.
“This research is crucial for understanding the connection between the body and mind,” states Douglas Vanderbilt from Los Angeles Children’s Hospital. He further discusses how his research indicated that children with severe asthma exhibit more pronounced PTSD symptoms. “What we’re uncovering suggests that these brain-body interactions are intricate, so this is likely not the only pathway,” he notes, pointing out that psychological stress from asthma attacks could also influence PTSD risk.
Sah emphasizes that this pathway might vary in women, as only male mice were utilized in her study, suggesting potential differences across genders that warrant additional investigation.
Ultimately, these discoveries may enhance our ability to identify individuals more susceptible to PTSD. For instance, medical professionals might consider screening children with severe asthma for mental health issues, as proposed by Vanderbilt. He further suggests that this line of research could lead to innovative PTSD treatments, such as immunotherapy aimed at reducing inflammation.
The immune system may be even more intricate than we previously realized
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Having an adequately functioning immune system for extended lifespans might come with the trade-off of chronic inflammation. Some immune cells are programmed to undergo inflammatory deaths to protect against infections, but this can also happen randomly when no pathogens are present.
Our innate immune system comprises cell groups that react swiftly to invasive pathogens such as viruses and bacteria. These cells typically detect microorganisms when they invade or infect them.
“With minimal information such as molecules of viral DNA, immune cells can swiftly decide on a course of action, often opting for self-destruction,” says Randal Halfman from the University of Kansas Cancer Center.
This type of cell death, known as pyroptosis, is triggered by a double death domain protein. These proteins usually float within innate immune cells, but upon encountering pathogens, they assemble into crystal-like structures. This action activates another protein that kills the cells by creating holes, leading to ruptures and releasing inflammatory signals that assist the immune system in pathogen clearance.
To delve deeper into this process, Halfman and his team carried out various laboratory experiments investigating human death-fold domain proteins in yeast cells. This process allowed them to identify five types of these proteins with chemical characteristics that predispose them to naturally form crystal-like structures in the absence of pathogens. They then analyzed existing data to assess the levels of these proteins in uninfected human immune cells.
From this analysis, we determined that certain innate immune cells, such as macrophages that engulf and eliminate pathogens, possess five times more death-fold domain proteins at concentrations sufficient to spontaneously assemble and trigger cell death. “At high enough concentrates, these particles are more likely to randomly conform into crystal structures during the cell’s lifespan,” Halfman explains.
Such phenomena can accumulate with age, contributing to chronic inflammation associated with various conditions, including cancer and Alzheimer’s disease, according to Halfman. “It seems we’ve evolved this way to fend off infections, but it may also lead to chronic inflammation,” he asserts.
This pathway provides protection against infections from birth and enhances our likelihood of aging, though it might also predispose us to inflammation-related diseases later in life, Halfman notes. “If these persistent irritations continue over time, the resulting inflammatory damage can accumulate,” he elaborates. Andy Clark from the University of Birmingham, UK, agrees.
The development of medications that prevent spontaneous cell death could potentially alleviate chronic inflammation related to aging, Halfman suggests. However, Clark cautions that this might render individuals more vulnerable to infections.
In an extensive community-based investigation, researchers from the Fatty Acid Institute identified a weak yet statistically significant inverse relationship between various inflammatory biomarkers and omega-6 fatty acids.
This image features Oenothera biennis, plants that produce oils with a high linolenic acid content. Image credit: Georg Slickers/CC by-sa 4.0.
“Chronic inflammation is acknowledged as a significant risk factor for various health disorders,” stated President William Harris of the Fatty Acid Institute and his colleagues.
“Omega-6 fatty acids, especially linoleic acid (LA) and arachidonic acid (AA), have been identified as either anti-inflammatory or pro-inflammatory agents. Researchers have considered both positions regarding dietary intake.”
The researchers utilized data from the Framingham Offspring study, a prominent cohort study in the Boston region.
This groundbreaking longitudinal research initiative began in 1971 and follows children from the original Framingham Heart Study, examining genetic and lifestyle factors influencing cardiovascular and metabolic health.
It has yielded valuable insights into chronic disease risks and prevention for decades, establishing itself as one of the most dependable sources for understanding long-term health trends.
This investigation is cross-sectional, meaning LA and AA levels were evaluated alongside 2,700 inflammation-related biomarkers in the same blood samples.
We statistically analyzed the association between the levels of these two omega-6 fatty acids and the levels of 10 blood and urine biomarkers related to inflammation and oxidative stress.
After statistically controlling for several potential confounding variables (such as age, race, gender, smoking status, blood pressure, and weight), researchers discovered that elevated LA levels were significantly linked to lower levels of five out of the 10 biomarkers.
For AA, higher levels were associated with reduced concentrations of four markers; however, there was no statistically significant relationship with higher inflammation/oxidation levels, unlike LA.
“These new findings clearly indicate that individuals with the highest LA (and AA) levels in their blood exhibit less inflammation than those with lower levels,” Dr. Harris remarked.
“This result contradicts the expectation if omega-6 fatty acids were deemed ‘pro-inflammatory.’ In fact, they seem to exhibit anti-inflammatory properties.”
“Amidst discussions in the media about the dangers of seed oils—the primary source of LA in diets—numerous voices advocate for reducing LA consumption.”
“This recommendation lacks a scientific basis, and this study, along with others, suggests the opposite: rather than decreasing LA intake, increasing it may be the healthier choice.”
“These findings diverge from the prevailing narrative but are consistent with earlier studies.”
“Numerous studies within medical literature support the findings presented here.”
The study was published in the journal Nutrients on June 22nd.
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Heidi T.M. Lai et al. 2025. Erythrocyte omega-6 fatty acids and biomarkers of inflammation in the Framingham offspring study. Nutrients 17 (13): 2076; doi: 10.3390/nu17132076
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Taking refuge in the shade is a simple way to steer clear of harmful UV rays from the sun.
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Since ancient Egyptian times, individuals have sought ways to shield their skin from the sun, as over a century ago, we recognized the link between ultraviolet (UV) light and skin injuries, including burns and cancers. Yet, there remains some uncertainty regarding the most effective methods to evade sunburn, how to remedy it, and whether each occurrence escalates the chances of developing cancer. It’s beneficial to grasp the cellular dynamics of tanning.
“Sunburn is an inflammatory response,” explains Leslie Rhodes from the University of Manchester, UK. UV rays inflict damage to proteins, fats, and DNA in skin cells located in the epidermis, triggering a cascade of inflammatory reactions resulting in redness, swelling, pain, and peeling.
Though UVB radiation is chiefly responsible for this damage, UVA rays, which have longer wavelengths, penetrate the skin more deeply. “Typically, UVB is approximately 1,000 times more effective than UVA for sunburning,” states Antony Young from King’s College London.
In reaction to UV injury, skin cells emit inflammatory molecules that enlarge blood vessels in the dermis, the layer of skin beneath the epidermis. Within hours, this increased blood circulation facilitates the influx of immune cells from the bloodstream into the skin, heightening inflammation.
For individuals with lighter skin tones, this augmented blood flow may cause sun-damaged skin to appear pink or red, while those with darker skin might notice skin changes in various shades including red, gray, brown, and black. The enhanced blood supply also results in greater fluid leakage from blood vessels to the skin, leading to swelling. Both swelling and inflammatory molecules activate the nerves, rendering the tanned skin hot and painful.
In extreme cases, blisters may form if patches of epidermal cells become severely damaged and begin self-destructing. As these dead patches detach from the underlying layer, the resulting spaces fill with liquid, creating a foamy structure within the skin.
How does tanned skin heal?
According to Rhodes, “A mild tan will diminish more rapidly than a severe burn if the effects persist beyond 72 hours.”
Healing initiates when skin immune cells start generating anti-inflammatory molecules a few days post UV exposure. “It’s a self-resolving inflammation,” Rhodes notes. “The various molecules and cells transition over time from pro-inflammatory to anti-inflammatory states.” Consequently, blood vessels cease to dilate, and the redness, swelling, and pain gradually subside.
Stem cells situated at the base of the epidermis accelerate healing by producing new skin cells at an increased rate. These cells replace the damaged ones, often shedding or peeling off in large sheets to facilitate growth. “You always shed skin, but UV damage accelerates the conversion of those cells,” says Young.
Regrettably, there is insufficient evidence to suggest that applying after-sun or aloe vera gels can hasten healing of tanned skin, according to Rhodes. Most of these lotions aim to alleviate pain by providing a cooling sensation. Cold showers, cool compresses, and over-the-counter pain relievers like paracetamol (acetaminophen) and ibuprofen may also be beneficial.
What are the long-term effects?
The sunburn subsides as inflammation lessens and damaged surface cells slough off. However, DNA damage to deeper stem cells in the epidermis may leave a lasting legacy.
“DNA damage occurs, and while cells attempt to repair it, their efforts are not flawless,” notes Young. This leads to genetic mutations that accumulate over time in genes governing cell growth and division, resulting in uncontrolled skin cell proliferation, heightening cancer risks.
Numerous studies indicate that experiencing five sunburns within a decade more than doubles the risk of melanoma, a type of skin cancer. However, these findings often rely on individuals’ recollections of their sunburn occurrences, which may not be precise, complicating the accurate assessment of how a single sunburn contributes to skin cancer risk.
What is the best method to prevent sunburn?
The skin pigment melanin encircles skin cell DNA, offering some level of protection from UV damage. Consequently, individuals with darker skin tones face a significantly lower risk of skin cancer compared to those with lighter complexions, though they are not immune to sunburn or DNA damage.
To assess the risk of burning on any given day, monitor the UV index, which measures ultraviolet radiation levels. Rachel Abbott from the University Hospital of Wales, Cardiff, advises applying sunscreen if the index reaches 3 or higher. Typically, UV indexes seldom exceed 3 early in the morning, evening, or between October and March in the UK. Nonetheless, UV rays are more intense near the equator and may necessitate sunscreen application at any time. Fortunately, free apps provide local UV index information. “I use one daily,” Abbott shares.
Most individuals don’t apply sunscreen with the thickness utilized in testing—2 milligrams per square centimeter—making an SPF 50 sunscreen a wise default choice, according to Young.
Nevertheless, one of the most effective strategies to prevent sunburn is to avoid direct sunlight when it is highest in the sky. In the UK, this window is between 11 a.m. and 3 p.m., while in the US, it generally extends from 10 a.m. to 4 p.m. During this time, sunlight takes a shorter route through the atmosphere, allowing more UVB radiation to reach the skin. When outdoors, donning a hat and long-sleeved clothing can further diminish the risk.
Itching is a dominant symptom of dermatitis (eczema), and scratch promotes skin inflammation, which deteriorates the disease. However, it is almost unknown whether scratching can make the spots and the lord benefit the mechanism that worsens inflammation. New research conducted in the mouse reveals the double nature of scratching. It can worsen skin inflammation, but can also increase immunity against bacterial infections at the site of injury.
Scratch is synergistic with the activation of FCεRI mast cells and promotes inflammation of allergic skin. Image credit: LIU et al。 , Doi: 10.1126/Science.adn9390.
Scratch is an attractive, typical, evolved behavioral reaction to the sensation of itching of the skin.
In many common skin diseases such as dermatitis, prolonged itching is a dominant symptom, indicating a substantial source of affection.
In response to itching, scratch is well -clinically recognized to worsen dermatitis, and some diseases are pathogenic.
However, itching is often a fun feeling and does not cause evasion behavior. This suggests that it can have some benefits to the host.
“Scratch is often fun. This suggests that this behavior must be a profit to evolve,” said Professor Daniel Kaplan of Pittsburgh University.
“Our research helps solve this paradox by providing evidence that scratches also provide bacterial defense against skin infections.”
How to use a new genetic modification mouse model to eliminate the function of neurons that senses itching, called non -peptide giku 2 (NP2), is in the relationship between scratches, injuries, and inflammation. We investigated whether it will affect.
They discovered that they revitalized neurons that sensed the pain that releasing a substance P (SP) when scratched.
However, scratch can worsen problems such as dermatitis, but reducing bacteria can help you to use immune protection. Staphylococcus aureusInfection.
Furthermore, the wound affects the microorganisms in the skin at the damaged site, and can prevent the imbalance of microorganisms, but chronic conditions such as atopic dermatitis complicate this.
The survey suggests that scratching functions as a pathological factor in inflammation and as an evolved mechanism to strengthen protection against infections.
“Discover that scratch improves defense Staphylococcus aureus It suggests that some context may be useful, “said Professor Kaplan.
“But if the itch is chronic, the damage caused by the skin will probably exceed this advantage.”
Survey results It will be displayed in the journal Science。
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Andrew W. Rue et al。 2025. Scratch promotes allergic inflammation and host defense through the activation of nerve gesturing mast cells. Science 387 (6733); DOI: 10.1126/Science.adn9390
Stroke can cause irreversible, life-altering, and long-term brain damage. A stroke can be caused by a blood clot called a thrombus. ischemic strokeor a ruptured blood vessel. hemorrhagic stroke. Our brains require large amounts of oxygen, so when blood flow is interrupted, oxygen-dependent brain substances are damaged in the short term.
Think of the blood vessels in your brain as a perfectly designed highway. When an ischemic stroke occurs, blood clots block these blood vessels, preventing oxygen from reaching the brain. When an ischemic stroke occurs, microglia It acts as our body's “ambulance” and focuses on the site of the blood clot. Scientists classify microglia into two types: anti-inflammatory and pro-inflammatory. Anti-inflammatory microglia help fight inflammation in the brain. Pro-inflammatory microglia cause further brain inflammation by damaging nerve cells. neuronremove the protective sheath known as . myelin.
Chinese researchers recently developed a hypothesis that inhibits an enzyme associated with inflammation called histone deacetylase 3 or HDAC3 may reduce proinflammatory microglial production in mice. They reasoned that because HDAC3 enzymes activate proinflammatory immune cells, inhibiting these enzymes may reduce inflammation.
To study how stroke affects the production of inflammatory cells, the researchers first determined which cell types in mice were most likely to be affected by HDAC3. They induced strokes in mice and found that HDAC3 was more active in the mice's microglia than in other cells. High levels of HDAC3 were present in the mice's neurons, but they were not active. The researchers interpreted this data to suggest that HDAC3 plays a more important role in microglia than in other types of brain cells.
Next, the researchers genetically engineered mice that lack microglial HDAC3. knockout mouse. They compared the knockout mice to a control group of mice that retained microglial HDAC3. They induced strokes in both groups of mice for 60 minutes. They then examined the mice's brains using MRI after three, 14, and 35 days to see how the brain damage caused by the stroke progressed in the two different groups. They found that the knockout mice had less brain damage than control mice on all three days.
The researchers also found that the knockout mice had better scores on motor, learning, memory, and behavioral tests than control mice. For example, when scientists applied sticky tape to the soles of mice's feet, the knockout mice removed the tape about 50 seconds faster than control mice. The knockout mice had less myelin loss and less degeneration of electrical pathways in the brain. The researchers interpreted these results to suggest that inhibiting microglial HDAC3 in mice prevented brain damage and improved mental performance after stroke.
The researchers also investigated which gene There were active and inactive forms in two sets of mice. They found that all pro-inflammatory genes tested were inactive in knockout mice, but highly active in mice with microglial HDAC3. They also found that the knockout mice had less activity in genes that produce inflammatory cells.
The researchers concluded that deleting microglial HDAC3 can prevent brain inflammation, myelin removal, and brain tissue damage during stroke. However, before HDAC3 deletion becomes a treatment, they recommended that future researchers determine whether there are any serious side effects. The reduction in inflammation in mice means the same technology could one day be used to reduce the inflammatory effects of stroke in humans.
Ozempic is a diabetes drug, but it is also often used for weight loss.
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Weight loss and diabetes injections such as Wigovy and Ozempic (both semaglutide) are more widely used than initially thought after studies in mice suggest they act on the brain and reduce inflammation throughout the body. Possible medical benefits.
This finding may explain why this class of drugs appears to reduce heart attacks more than would be expected from weight loss effects alone.
It also supports their use in combating a wide range of health conditions that involve inflammation, including Alzheimer’s disease and Parkinson’s disease, which is being studied in clinical trials.
Semaglutide works by mimicking a gut hormone called GLP-1. Normally released after a meal, GLP-1 reduces appetite, makes you feel full, and triggers the release of insulin, a hormone involved in blood sugar regulation.
Some studies suggest that semaglutide not only reduces weight, but also reduces inflammation, and is a mild increase in certain types of immune system activity.Lowers levels of a compound in the blood called C-reactive protein (CRP) is a well-established sign of inflammation. Daniel Drucker At the University of Toronto, Canada.
A growing body of research suggests that inflammation is involved in many conditions not previously associated with the immune system, such as heart disease and Alzheimer’s disease, but this does not yet lead to new treatments available in the clinic. has not been applied.
Because obesity is also associated with inflammation, semaglutide’s effect on CRP may simply be a side effect of weight loss, rather than the drug itself reducing inflammation.
To find out, Drucker and his colleagues investigated how several GLP-1 mimics affect inflammation in mice. First, they injected bacteria from the mice’s intestines into other parts of their abdomens, causing bacterial infections in their blood. This triggers a strong immune response and causes inflammation.
Some mice were also injected with GLP-1 mimics, either semaglutide or another member of this drug class called exenatide.
GLP-1 mimics reduced the animals’ inflammatory response to infection, but this did not occur when the researchers used mice genetically modified so that their brain cells lacked receptors for GLP-1. Ta.
The researchers also found no reduction in inflammation when they tested genetically normal mice whose brains were injected with compounds that block GLP-1 receptors.
Taken together, these results show that GLP-1 mimetics such as Ozempic act on brain cells to reduce inflammation, and that this is not just a side effect of weight loss.
“Losing weight is good, but you don’t need to lose weight to be effective,” Drucker says. For example, in Wegovy’s recent randomized trial, he says, the drug started preventing heart attacks within the first few months, before people lost significant weight.
“It was known that these drugs acted on inflammation,” he says. Ivan Koichev at Oxford University. “This paper is helpful because it reveals the underlying mechanism.”
In theory, anti-inflammatory drugs could cause people to develop additional infections, but this has so far not been observed in people who received the shots for weight loss or diabetes, Koychev says. .
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