Inquiring about the health advantages of living near a golf course might come off as someone attempting to leverage scientific studies to persuade their partner that residing adjacent to Gleneagles is a wise choice.
Fair play. I genuinely respect this transparent application of science. So, here’s some evidence from the archives.
When you tee off, appreciate all that lush greenery. Research consistently indicates that residing near green spaces correlates with a diminished risk of conditions such as cardiovascular disease and obesity.
While quantifying these effects is challenging, the study suggests it might lower stress hormones, enhance exercise, and benefit cognitive functions like memory and attention.
In one investigation, researchers concluded that a 10 percent increase in access to green and blue spaces resulted in a 7 percent decrease in anxiety and depression risk.
It’s well recognized that playing golf offers health benefits. In 2023, a Finnish study compared the cardiovascular impacts of playing an 18-hole round of golf (walking – no cart) to one hour of brisk walking and one hour of Nordic walking.
All three activities were beneficial, but golf proved to be the most effective, reducing blood pressure, cholesterol, and blood sugar levels.
Additional research has shown that golf training can provide cognitive benefits, particularly for older adults. It’s also advantageous for mental health due to its focus on fostering social connections.
In summary, regular golfing contributes to a longer and healthier life. Researchers found that individuals who played golf consistently experienced a 40 percent reduction in mortality.
That’s not a bad score, but there are some hazards to be aware of. At the start of 2025, a study explored the possible link between Parkinson’s disease and proximity to golf courses, highlighting potential exposure to pesticides.
Some chemicals used to maintain greens and fairways are neurotoxic, and numerous studies have associated them with Parkinson’s disease (although the risks are influenced by factors such as the type of pesticide and level of exposure).
Chemicals used on golf courses to maintain grass health may contribute to Parkinson’s risk – Credit: David Madison via Getty
In recent studies, researchers surveyed residents living near 139 golf courses in the United States. They discovered that individuals living within one mile of a golf course faced a 126 percent higher likelihood of developing Parkinson’s disease compared to those more than 6 miles away.
The risk nearly doubled for those sharing the same water supply zone as a golf course, suggesting that groundwater contaminated with pesticides, along with airborne transmission, may also play a role.
It’s crucial to note that the risk of Parkinson’s disease arises from a complex interplay of genetic and environmental factors. Risks associated with these chemicals are predominantly linked to occupational exposure rather than recreational exposure.
If you happen to reside in the UK, your risk might be lower, as paraquat, a chemical linked to Parkinson’s disease, is prohibited.
Thus, living next to a golf course presents a multifaceted situation, much like residing anywhere else. Why not head to the 19th hole and ponder this?
This article (by Carlisle native Paul Leach) addresses the question: “Will I be healthier if I move next to a golf course?”
If you have any inquiries, feel free to email us at:questions@sciencefocus.com or send us a messagefacebook,×orInstagramPage (please include your name and location).
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Parkinson’s disease is currently the fastest-growing neurological disorder in the United States; currently, 90,000 individuals have been diagnosed—a staggering 50% increase since the mid-1980s. The situation mirrors global trends, with an expected 25 million diagnoses by 2050, effectively doubled compared to today’s figures.
In summary, this is a significant issue. However, these numbers aren’t entirely surprising, considering longer life spans and growing populations. What is truly alarming, and frankly, unsettling, is how unprepared we are for this impending wave.
The available treatments are limited. Diagnostic tools are inadequate. Honestly, we still don’t really understand what causes Parkinson’s disease.
Yet, before you plunge into the depths of neurodegenerative despair, there is hope. Scientists worldwide are actively working to change the narrative surrounding Parkinson’s.
In particular, researchers are revolutionizing how we can detect Parkinson’s disease. Armed with cutting-edge technologies, AI, and a fundamentally evolving understanding of disease manifestation throughout the body, they’re aiming to detect it decades before any symptoms present themselves, rather than years.
Presently, there is no single definitive test for Parkinson’s disease. Instead, doctors diagnose it based on physical symptoms like tremors, slow movement, and muscle stiffness, often requiring assessments of tasks such as writing and speaking.
“Today’s neurodegenerative disease is what cancer used to be 50 years ago,” states Professor Hermona Solek, a leading researcher in next-generation diagnostic tools. “We often finalize a diagnosis only when all involved nerve cells are already dead, leaving us unable to properly treat the patient.”
But what if there were a way to diagnose Parkinson’s disease before it could do any significant harm? What if it could be caught on its way, before brain cells face irreversible damage?
This is no longer just a theory. In fact, there are multiple methods emerging.
AI Desk Accessories
Not all breakthroughs in diagnostics require a blood sample; some new innovations could be found right on your desk.
At the University of California, Los Angeles, Professor Junchen‘s lab claims to have developed a diagnostic pen that detects Parkinson’s disease by analyzing your writing.
This unique pen’s soft tip is crafted from an innovative magnetoelastic material that alters the magnetic field in response to pressure or bending—a phenomenon previously known in rigid metals but now applied to soft polymers, creating a new type of highly sensitive and user-friendly sensor.
“Utilizing magnetoelastic effects with soft materials represents a new operational mechanism,” Chen explains. “It can translate small biomechanical pressures, like arterial vibrations, into high-fidelity electrical signals.”
The pen, filled with magnetized ink, captures movements occurring both on paper and in the air, subsequently sending this data to a computer. Here, AI models analyze specific patterns linked to Parkinson’s motor symptoms.
Smart pens can be especially beneficial in countries where affordable diagnostic tools are needed—UCLA Jun Chen Lab
In a pilot study, the system successfully distinguished individuals with Parkinson’s disease from healthy controls with over 96% accuracy. Even better, Chen believes this pen can be mass-produced for merely $5 (£3.70).
“We have already filed for a patent and aim to commercialize this pen,” Chen states. “Simultaneously, we are working on optimizing it to improve our diagnostics’ accuracy.”
If handwriting isn’t your preferred method, Chen’s team has you covered. They’ve also created a Smart Keyboard utilizing the same principles.
This keyboard tracks subtle changes in pressure and rhythm as users type—often imperceptible to the naked eye—and relays that information to machine learning algorithms.
Initial tests indicate that it can identify characteristic motor abnormalities in Parkinson’s disease, and the team is combining this technology with a mobile app for continuous remote monitoring.
Together, these intelligent desk tools offer a glimpse into what Chen describes as the “personalized, predictive, preventive, participatory” future of Parkinson’s healthcare; a future where diagnosis is as simple as taking notes or sending emails.
This portable, soft keyboard employs magnetic elasticity to detect Parkinson’s disease and sends results to your smartphone—UCLA Jun Chen Lab
Parkinson’s Eye Test Detects Changes Two Decades in Advance
Picture diagnosing Parkinson’s disease during a routine eye exam, potentially decades before symptoms manifest. This is the promise of new non-invasive techniques developed by Victoria Soto Linan and her colleague at Laval University in Canada, using an established eye test known as electroretinography (ERG).
According to Soto Linan, this eye test serves as a “window to the brain,” as it’s part of the central nervous system. Issues like blurred vision and diminished contrast sensitivity manifest long before the well-known symptoms of tremors and stiffness.
The Soto Linan team collected data on how the retina responds to light flashes from both mice engineered to develop Parkinson-like symptoms and newly diagnosed human patients.
They identified unique retinal signals demonstrating “sick signatures,” particularly in women. Crucially, this weakened signal appeared in the mice prior to any behavioral disease signs.
This leads Soto Linan to believe that this eye test could detect Parkinson’s as much as 20 years before symptoms arise.
Read more:
And unlike other early diagnostic methods, this one is already well ahead of the game.
“ERGs are now employed in clinics to diagnose eye diseases,” she explains. “They also have the major advantage of being non-invasive.”
The patient sits before a dome that flashes lights, capturing how the retina responds. This could easily be integrated into a few minutes of your annual vision test.
The team is currently focusing on enhancing the testing process, with hopes of linking it to machine learning algorithms that will accelerate results, perhaps even making them portable to smartphones.
While the research is still in its early stages, its potential ramifications are enormous. As Soto Linan states, “This tool could identify at-risk individuals up to 20 years before symptoms emerge. Imagine how much less damage could be done by then.”
“Even if there is no treatment available, early intervention can often improve the quality of life in the long run.”
Detecting Parkinson’s Through Vocal Patterns
Can your voice indicate Parkinson’s disease before your physical body does? Recently, preprint research has explored whether AI can identify Parkinson’s simply by analyzing a person’s speech.
Around 90% of individuals with Parkinson’s develop motor speech disorders known as dysarthria, which can lead to issues like irregular pitch and breath control.
Globally, over 8.5 million individuals live with Parkinson’s disease—Getty
These vocal changes often arise earlier than more noticeable motor symptoms like tremors, thus serving as promising early indicators.
The research team collected brief audio recordings from 31 to 195 individuals, which included 33 individuals with the disease. Their data served to train four different AI models to recognize disease-related vocal patterns. When tested on new recordings from the same participants, the models identified Parkinson’s with an accuracy exceeding 90%.
These changes are subtle and occur early, and researchers suggest that speech-based assessments could provide low-cost, non-invasive diagnostic options.
Blood Tests for Diagnosing Parkinson’s
In April 2025, SOREQ and her colleagues—including her son—announced a groundbreaking new study.
The findings were surprising; they revealed a simple and inexpensive blood test utilizing PCR technology (remember this from COVID-19?) that can accurately detect Parkinson’s disease a few years prior to symptom onset.
This test functions by measuring the ratio between two markers that SOREQ and her team discovered in human blood.
Specifically, individuals with Parkinson’s exhibit abnormally high levels of certain molecules known as transfer RNA (tRNA) fragments, identifiable by a specific repeating pattern called conserved sequence motifs.
A new blood test can detect early Parkinson’s by analyzing the unique imbalance of small RNA molecules in your blood—Credit: Getty
Simultaneously, the team uncovered reduced levels of tRNA associated with mitochondria (the “powerhouses” of cells, responsible for producing most of your body’s energy) in the blood of Parkinson’s patients.
“We proposed that if there’s an increase in one sequence and a decrease in another, we could calculate the ratio and identify a probable diagnosis,” says Soreq.
If this ratio exceeds a specific threshold, it strongly indicates a diagnosis.
According to SOREQ, a traditional diagnosis of Parkinson’s can cost up to $6,000 (£4,400). The two PCR tests required for their method? Only $80 (£60).
“This is monumental. It makes a substantial difference,” she states. With some luck, the team anticipates this will become widely available within the next decade, potentially providing a crucial lifeline for patients globally.
For the first time, researchers have successfully visualized and quantified small protein clusters in the human brain that may signal the onset of Parkinson’s disease.
These clusters, known as alpha-synuclein oligomers, have long been implicated in some of the fastest-expanding neurological disorders worldwide but had never been observed in brain tissue until now.
To identify these elusive proteins, the research team utilized a novel imaging method called Advanced Sensing of Parkinson’s Disease (ASA-PD) aggregates, which renders these nanometer-scale (one billionth of a meter) oligomers visible.
For decades, clinicians could confirm a diagnosis of Parkinson’s disease only by detecting larger deposits of proteins that build up in neurons. However, many researchers believe the disease actually initiates with these smaller oligomers.
“You can think of Lewy bodies as a sort of morbid gravestone,” stated Professor Stephen Lee from Cambridge’s Yusuf Hameed Department of Chemistry, who co-led the study. BBC Science Focus. “They indicate where the disease resides and its progression.”
To investigate the earlier phases of the disease, the team compared post-mortem brain samples from individuals with Parkinson’s disease to those from healthy individuals. Oligomers were present in both cohorts, surprising scientists, but were more abundant and vibrant in the brains of Parkinson’s patients.
“This marks the first occasion we’ve directly observed oligomers in human brain tissue at this scale, akin to spotting stars in daylight,” commented Dr. Rebecca Andrews, Co-First Author and former postdoctoral researcher in Lee’s lab.
The researchers also discovered subtle variations in the distribution of oligomers, which could signify the earliest stages of the disease prior to the onset of symptoms.
Scientists were able to visualize and count α-synuclein oligomers (shown in red) in brain tissue samples. Interestingly, these puncta were present in both Parkinson’s patients and healthy individuals, as depicted in the images of two Parkinson’s patients (top) and two healthy controls (bottom) – credits: Andrews et al. (2025)
Lee emphasized that while this study is a significant advancement, it should not be misconstrued as a means to directly find treatments. “We’re not at that stage,” he noted. “This research actually allows us to engage with the very early stages of the disease. From a therapeutic standpoint, it lays the groundwork for future developments.”
Currently, over 10 million people globally suffer from Parkinson’s disease, which lacks a treatment that addresses the underlying condition. Existing medications can manage symptoms like tremors, but none target the disease’s root cause or halt its progression.
A collaborative team from the University of Cambridge, the University of London, the Francis Crick Institute, and Polytechnique Montreal aims to utilize these findings to enhance methods for monitoring the efficacy of diagnostic tests and experimental treatments.
This imaging technique is also applicable beyond just Parkinson’s disease. “This approach provides more than just a snapshot,” said Professor Lucian Weiss from Polytechnique Montréal, who co-led the study. “It maps protein changes throughout the brain and similar techniques can be applied to other neurodegenerative disorders such as Alzheimer’s and Huntington’s diseases.”
“Oligomers were once like needles in a haystack, and now that we know their precise locations, it enables us to target specific cell types in designated areas of the brain.”
According to Borghammer’s “Aha” moment, it came almost 20 years ago. Neuroscientists were reading papers from researchers investigating REM sleep behavior disorders (RBD). This is a condition in which people develop dreams, often discovered in people who develop Parkinson’s disease, and may be a form of early neurological symptoms.
However, rather than starting from the brain, the team looked for the loss of nerve cells in the heart instead. Parkinson’s disease has historically been linked to depletion of neurons in the brain, but it also affects cardiac neurons that manage autonomic nervous functions such as heart rate and blood pressure. And say Borgamer“In all these patients, the heart is invisible. It’s gone.”
Of course, it’s not literal. However, in these people, neurons that produce the neurotransmitter norepinephrine, which helps control heart rate, were depleted to the point that the heart did not appear on scans using radioactive tracers. This type of neuronal loss is linked to Parkinson’s disease, but no one was diagnosed with the disease at the time, and brain scans appeared to be normal.
What struck Borghammer was that Parkinson’s disease appears to have not followed the same trajectory in all affected people. Although RBD strongly predicts Parkinsonson’s predictions No one has Parkinson’s experience. RBD.
Parkinson’s disease is rapidly becoming one of the most prevalent neurodegenerative conditions globally, impacting over 10 million individuals worldwide. It ranks as the second most common neurodegenerative ailment following Alzheimer’s disease. As of now, there is no known cure. However, recent advancements have raised hopes for the development of new treatments in the near future.
The disease is closely associated with a protein known as Pink1, which carries a mutation in the Park6 gene responsible for encoding this protein.
Malfunctions in Pink1’s functioning are directly linked to Parkinson’s disease, especially in individuals with early onset, affecting 1.2% of Parkinson’s patients in the UK.
Recent scientific progress has shed light on the interaction between Pink1 and mitochondria. Mitochondria, known as the powerhouse of cells, produce energy within the cells of all organisms.
From left, Professor David Commander, Dr. Nicholas Kirk, Dr. Sylvie Karegari and Dr. Alisa Grukova stand before the discovery of Pink 1. – Wehe
The link between Pink1 and Parkinson’s disease has long been recognized, but its potential as a cure for Parkinson’s disease has only recently been explored.
When mitochondria are damaged, Pink1 signals the need for their removal. However, in Parkinson’s patients, mitochondrial defects accumulate unnoticed, releasing toxins that eventually lead to cell death.
Currently, researchers at the Parkinson’s Center for Research in Walter and Eliza Hall (WEHI) in Australia have elucidated the structure and activation process of Pink1. Their findings on how Pink1 interacts with dysfunctional mitochondria are published in Science today.
“This is a significant milestone in Parkinson’s disease research,” stated corresponding author Professor David Commander, head of WEHI’s ubiquitin signaling division. “Understanding Pink1’s binding to mitochondria is truly groundbreaking.”
Lead author and Senior Researcher at WEHI, Sylvie Callegari, explained that Pink1 functions in four distinct steps, with the first two being newly discovered in this study.
Furthermore, Pink1’s role in detecting mitochondrial damage and initiating the process of mitophagy, the recycling of damaged mitochondria, is crucial for addressing Parkinson’s disease.
Parkinson’s disease is associated with physical tremors, as well as other symptoms like language and vision impairments – Credit: Witthaya Prasongsin
In conclusion, understanding the Pink1-mitochondrial relationship is crucial for developing therapies for Parkinson’s disease, a condition characterized by the decline of brain cells.
Given the increasing prevalence of Parkinson’s disease over the past 25 years, the need for effective treatments is more urgent than ever. The researchers behind this study aim to accelerate drug development and halt the progression of Parkinson’s disease.
Parkinson's disease is a neurodegenerative disease that makes it difficult for people to regulate their voluntary movements. Parkinson's disease affects about 500,000 Americans and causes symptoms such as stiffness, slowness of movement, and a hunched back. For this reason, the way the patient walks; How to walkis one of the main ways doctors determine the quality of life of Parkinson's disease patients. Doctors have developed a variety of treatments for Parkinson's disease, but few have been able to help patients walk.
Scientists have discovered that walking problems in Parkinson's disease patients are related to brain overactivity. This hyperactivity is caused by brain wave patterns. beta bandIt is located in a specific area of the brain that regulates movement, known as the . subthalamic nucleusor STN. Researchers have developed treatments that modulate STN activity, but it is not known whether changing the associated brain wave patterns can help patients walk more easily.
Previous researchers have shown that electrical stimulation of a patient's skin in different areas can stimulate nerves that regulate muscle tone and other bodily functions. vagus nerve. Scientists in Italy and the United Kingdom recently discovered that a form of electrical stimulation Transauricular vagus nerve stimulation taVNS may help people with Parkinson's disease walk.
To perform taVNS, researchers placed electrodes in the outer ears of Parkinson's disease patients to stimulate the vagus nerve. Scientists had two main questions. Does taVNS reduce STN beta-band wave activity, and does this reduction in activity allow Parkinson's disease patients to walk more easily?
Researchers enrolled 10 people with Parkinson's disease in the study. Each patient was treated with a different type of electrical stimulation to the STN. They asked participants to stop taking traditional Parkinson's medications the night before the taVNS test and turned off electrical stimulation an hour before the test.
During the taVNS test, scientists applied two types of stimulation to each patient. One stimulated the vagus nerve through the ear, and the other stimulated another area that did not affect the brain. imitative stimulus. They ran each type of simulation on the patient four times for two minutes, with one minute in between.
The researchers also measured the patients' involuntary side-to-side movements while walking. swaythe time it took to change direction mid-test, or Rotation timemeasure the total number of steps, step length variability, total walking time, and walking speed, and compare the effects of real and imitation treatments on patients. Finally, each patient's quality of life was physically assessed using the Unified Parkinson's Disease Rating Scale Part III.
The scientists found that during taVNS, patients' STN beta-band waves were 7% weaker on the right side than during mimic stimulation. They also found that taVNS improved patients' step length variability, total walking time, and walking speed. The researchers also used statistical tests to show that participants with less active STN beta-band brainwave patterns walked faster. However, there was no significant improvement in patients' quality of life based on rating scale scores.
The researchers concluded that taVNS could help Parkinson's patients walk faster, perhaps by altering brain waves in the STN beta band. They also pointed out that taVNS is a non-invasive treatment, meaning it does not require surgery or implantation into the body, and is much more affordable than invasive treatments. The scientists acknowledged that their study was small, and future researchers will look to do more research to further understand how STN beta-band waves are related to gait in Parkinson's disease. He emphasized the need to conduct trials in large patient groups.
Aggregates of protein α-synuclein (brown) and antibody (green)
Biolution GMBH/Science Photo Library
Drugs that target protein accumulations associated with Parkinson's disease may slow the progression of motor symptoms in patients with advanced Parkinson's disease. This shows potential as a disease-modifying treatment for Parkinson's disease, but it is unclear whether the drug actually removes the protein from the brain.
Accumulation of a misfolded protein called alpha-synuclein in the brain has long been thought to be the underlying cause of Parkinson's disease. This results in the loss of neurons that produce the neurotransmitter dopamine, which is involved in motor control.
Some existing treatments aim to alleviate these symptoms by improving dopamine levels in the brain, but their long-term effects are limited. To date, there are no approved disease-modifying treatments to stop or slow the progression of Parkinson's disease.
In an effort to counter this, Gennaro Pagano Swiss pharmaceutical company Roche and colleagues recruited 316 people who appeared to have early stages of Parkinson's disease. Of these people, 105 received an intravenous infusion of a placebo, and 211 received a low or high dose of Roche's drug plasinezumab every four weeks for a year.
Placinezumab is an antibody designed to bind to aggregates of misfolded alpha-synuclein within dopaminergic neurons. “It is hypothesized that placinezumab may reduce neurotoxicity, prevent cell-to-cell movement of pathological alpha-synuclein aggregates, and slow disease progression,” Pagano says.
Trial results initially suggested the antibody had no significant effect, but the team later realized it may have an effect in trial participants with more severe forms of Parkinson's disease. I did.
These people suffered from rapid eye movement sleep behavior disorder, which causes intense, often violent dreams that are common in Parkinson's disease. He was taking a drug called an MAO-B inhibitor to manage his symptoms. Or, he has been rated by an expert at 2 out of 5 on a symptom scale, with higher numbers indicating greater severity.
Additional analyzes showed that both low and high doses of the drug had greater effects than seen in the first study, especially among critically ill participants. The rate at which participants' motor symptoms worsened over a one-year period was significantly reduced compared to those taking a placebo.
For example, based on the Parkinson's Disease Rating Scale for Motor Symptoms, patients who took an MAO-B inhibitor and then received a placebo infusion had a score of 6.82 at the end of the year, compared to Patients who took the drug had a score of 4.15.
“These results suggest that potential treatment benefits may be more likely to be achieved in populations that experience greater deterioration over time and more rapid progression,” Pagano says. This is because patients with Parkinson's disease, which progresses more rapidly, have higher amounts of misfolded alpha-synuclein in their brains, so they may benefit more from drugs that can remove this protein. There is a possibility.
However, Professor Pagano said researchers lacked a biomarker that could monitor how participants' levels of misfolded alpha-synuclein changed, so it was unclear what was happening in the participants' brains. He said it was not possible to make an accurate assessment.
Vinata Vedam Mai Researchers at the University of Florida Health say a limitation of the study is that it did not assess whether alpha-synuclein was cleared from the brain. Without this, she says, the results cannot conclusively show that plasinezumab is disease-modifying. Vedam-Mai said he would also like to see long-term data to better assess the drug's safety and effectiveness. No serious adverse events occurred in the latest trial.
Researchers could also investigate whether plasinezumab, when taken over a long period of time, is effective for patients with mild Parkinson's disease, Pagano said.
Researchers have discovered a way to detect Parkinson’s disease up to 30 years before symptoms appear using biomarkers and PET scans. This breakthrough includes tracking neurodegeneration more sensitively than current methods and shows that rapid eye movement sleep behavior disorder (RBD) is an important early indicator of Parkinson’s disease. is identified. This discovery could lead to earlier diagnosis and treatment, potentially up to 10 years earlier than currently.
Researchers at The Florey and Austin Health in Melbourne, Australia, have demonstrated the potential to identify early indicators of Parkinson’s disease 20 to 30 years before the onset of symptoms. This breakthrough paves the way for early screening programs and intervention, potentially allowing treatment before significant damage occurs.
Researchers at the Florey Institute and Austin Health have demonstrated the possibility of identifying early indicators of Parkinson’s disease 20 to 30 years before the onset of symptoms. This breakthrough paves the way for early screening efforts and preventive treatment, long before permanent damage occurs.
Florey Professor Kevin Burnham said that although Parkinson’s disease, a debilitating neurodegenerative disease, is often thought of as a disease of the elderly, it actually begins in midlife and can last for decades. He said it may not be detected.
“Parkinson’s disease is very difficult to diagnose until symptoms become apparent, by which time up to 85 percent of the neurons in the brain that control motor coordination have been destroyed. At that point, many treatments are likely to be ineffective,” Professor Burnham said. “Our long-term goal is to find ways to detect diseases earlier and treat people before they cause harm.”
Advanced diagnostic technology
In a recently published study, neurologylead researcher Professor Burnham and colleagues explore how a known biomarker called F-AV-133 can be used in positron emission tomography (PET) scans to diagnose Parkinson’s disease and accurately track neurodegeneration. I’m explaining how it can be done.
In the Melbourne study, Austin Health’s Frawley Professor Chris Rowe and his team studied 26 patients with Parkinson’s disease, 12 controls, and 11 patients with rapid eye movement sleep behavior disorder (RBD), a strong indicator of Parkinson’s disease. I checked the name. .
Each person underwent two PET scans two years apart. Key findings include:
Currently available assessments of Parkinson’s disease showed no significant changes in clinical symptoms in any of the participants.
In contrast, PET scans showed “significant neuronal loss” in three key areas of the brains of people with the disease, making F-AV-133 more effective than what is currently available. also suggests that it is a sensitive means of monitoring neurodegeneration.
Further mathematical modeling yields the following calculation:
Slow nerve cell loss over a total of approximately 33 years in Parkinson’s disease
This loss takes about 10.5 years before the disease is detected on a PET scan.
Even if a PET scan detects the disease, it will take another six and a half years for motor symptoms to appear.
It takes about 3 years after physical symptoms appear until a clinical diagnosis is confirmed.
This corresponds to approximately 22.5 years of neuronal loss before clinical symptoms are sufficient for diagnosis.
Professor Burnham said the findings pave the way for the development of screening protocols to diagnose and treat Parkinson’s disease up to 10 years earlier than is currently possible. It may also help identify patients for clinical trials.
What is RBD?
RBD stands for Rapid Eye Movement Behavior Disorder.
Patients with RBD scream, thrash, and sometimes move violently during sleep, enacting vivid and disturbing dreams.
RBD is caused by a lack of muscle relaxation (sleep paralysis).
90% of RBD patients develop Parkinson’s disease.
Half of all Parkinson’s patients have RBD.
RBD is an important warning sign for early Parkinson’s disease.
If you have RBD, see a sleep specialist or neurologist.
Reference: “Use of 18F-AV-133 VMAT2 PET Imaging to Monitor Progressive Nigrostriatal Degeneration in Parkinson’s Disease”, Leah C. Beauchamp, Vincent Dore, Victor L. Villemagne, SanSan Xu, David Finkelstein, Kevin J. Barnham, Christopher Rowe, 28 November 2023 neurology. DOI: 10.1212/WNL.0000000000207748
Stanford Medicine and international collaborators have discovered that around 20% of individuals carry genetic mutations that reduce their risk of Alzheimer’s disease or Parkinson’s disease by 10% or more. This particular variant, known as DR4, has the potential to enhance future vaccines for these neurodegenerative diseases. In addition, the study found a potential link between the tau protein and both diseases, providing new possibilities for targeted therapies and vaccines.
The large-scale analysis included medical and genetic information from a wide range of individuals across different continents. This data analysis revealed that certain gene variants related to immune function are associated with a lower risk of developing Alzheimer’s and Parkinson’s diseases. Approximately one in five people possess a specific genetic mutation that provides resistance to both diseases.
The research, led by Stanford Medicine, indicates that individuals with this protective genetic mutation may be less likely to benefit from future vaccines aimed at slowing or stopping the progression of these common neurodegenerative diseases. Results from the analysis of medical and genetic data from hundreds of thousands of people from diverse backgrounds confirmed that carrying the DR4 allele increased the average chance of developing Parkinson’s or Alzheimer’s disease by more than 10%. New evidence has also surfaced suggesting that the tau protein, which is known for aggregating in the brains of Alzheimer’s patients, may also play a role in the development of Parkinson’s disease.
The study, published in the Proceedings of the National Academy of Sciences, was a collaboration between researchers at Stanford Medicine and international partners. The researchers involved in this study were Emmanuel Mignot, MD, Michael Gracius, MD, Iqbal Farooq, and Asad Jamal from Stanford Medicine, as well as Dr. Jean-Charles Lambert from Inserm, University of Lille, France. The lead author was Yan Le Nguyen, Ph.D., and other contributors included Dr. Guo Luo, Dr. Aditya Ambati, and Dr. Vincent Damot.
Further findings from the study showed that individuals with the DR4 allele were more likely to develop neurofibrillary tangles, characteristic of Alzheimer’s disease, in their brains. The study also suggests that tau, a protein central to Alzheimer’s disease, may have an unknown role in Parkinson’s disease.
DR4 is a particular allele of the DRB1 gene, which is a part of the human lymphocyte antigen complex. This complex is crucial in allowing the immune system to recognize the internal contents of cells. One of the significant findings of this study was that the specific peptide fragment that DR4 recognizes and presents is a chemically modified segment of the tau protein, which plays a role in both diseases. The study suggests that the DR4 allele could be used to create a vaccine targeting this modified peptide as a potential way to interfere with tau aggregation and the development of these neurodegenerative diseases. There may be potential to delay or slow the progression of the diseases in individuals who carry the protective variants of DR4.
The study also noted that the effectiveness of the vaccine may depend on the subtype of DR4 a person carries, which varies among different ethnic groups. For example, one subtype of DR4 that is more common among East Asians may be less protective against neurodegenerative diseases.
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