Health
Researchers find sources of four brain disorders, which could lead to new treatments
Researchers may have found a new way to target the sources of certain brain disorders.
In a study led by scientists at Mass General Brigham, deep brain stimulation (DBS) was able to pinpoint dysfunctions in the brain that are responsible for four cognitive disorders: Parkinson’s disease, dystonia (a muscle disorder condition that causes repetitive or twisting movements), obsessive compulsive disorder (OCD) and Tourette’s syndrome.
The discovery, published in Nature Neuroscience on Feb. 22, could potentially help doctors determine new treatments for these disorders.
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The study included 261 patients worldwide — 70 had dystonia, 127 were Parkinson’s disease patients, 50 had been diagnosed with OCD and 14 had Tourette’s syndrome.
The researchers implanted electrodes into the brains of each participant and used special software to determine which brain circuits were dysfunctional in each of the four disorders.
Deep brain stimulation has been used to pinpoint dysfunctions in the brain that are responsible for four cognitive disorders. (iStock)
“In simplified terms, when brain circuits become dysfunctional, they may act as brakes for the specific brain functions that the circuit usually carries out,” Andreas Horn, M.D., PhD, associate professor of neurology at Brigham and Women’s Hospital, said in a press release.
“Applying DBS may release the brake and may in part restore functionality.”
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Horn, one of the 39 researchers from 16 institutions who co-authored the study, went into more detail in a conversation with Fox News Digital.
“Based on the present findings, we can better understand why deep stimulation to a small subcortical structure in the brain has been helping patients with various disorders,” he said.
The researchers implanted electrodes into the brains of each participant (not pictured) and used special software to determine which brain circuits were dysfunctional in each of the four disorders. (iStock)
For each of the disorders, a different brain network was identified as “dysfunctional,” leading to the condition, the doctor said.
“Identifying these ‘malfunctioning networks’ may help us better understand the four disorders and better target neuromodulation to help patients by alleviating symptoms,” he noted.
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In three cases, the researchers found that applying DBS led to “preliminary improved results.”
At Massachusetts General Hospital, one female patient in her early 20s was diagnosed with severe, treatment-resistant OCD.
After receiving electrode implantation and targeted stimulation, the researchers measured a “significant improvement” in her symptoms one month after treatment, according to the release.
Obsessive-compulsive disorder was one of the cognitive conditions targeted in the new study. (iStock)
Dr. Shannon Dean, a pediatric neurologist with the Kennedy Krieger Institute in Maryland, was not involved in the study but shared her reaction to the findings.
“This study is an elegant demonstration of how treatment-focused and basic mechanism-based research can help guide each other,” she told Fox News Digital.
“The authors used deep brain stimulation electrodes, which is an invasive surgical treatment for a variety of neurological disorders when medications alone are not enough,” Dean went on.
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“I was interested to see the researchers then used their findings to refine exactly how they were treating several patients — and saw their patients’ symptoms improve as a result,” she said.
Given the small number of participants, Dean stressed the need for caution in interpreting the results.
“What the authors found for those disorders will need to be replicated for us to be sure the conclusions are right,” she said.
“However, what they have found is exciting and makes sense based on what we already know about these disorders. This points us to where future studies should be looking.”
For each of the disorders, a different brain network was identified as “dysfunctional,” leading to the condition, a researcher said. (iStock)
“This research provides hope for people living with these diseases who are resistant to standard medical therapy,” she added.
Dr. Arif Dalvi, a neurologist on staff at St. Mary’s Medical Center in Florida, also commented on the study as an outside expert.
“Even though deep brain stimulation has been part of the standard of care for neurological conditions such as Parkinson’s disease and tremors for decades, the technology continues to evolve,” he told Fox News Digital.
“This research provides hope for people living with these diseases who are resistant to standard medical therapy.”
“This analysis identified ‘sweet spots’ within these circuits that could significantly alleviate symptoms, demonstrating the efficacy of DBS in modulating neural activity.”
The findings highlight the need for personalized therapies, Dalvi noted.
“This emphasizes a need for neurologists to carefully evaluate each patient as a unique individual and tailor a specific treatment plan, rather than working off generic best practices or therapeutic guidelines,” he said.
Study was limited, researchers say
This research is seen as the first step in what will be a long process, Horn said.
“The study is based on retrospective data — main results should be confirmed by prospective trials, which represent the gold standard to accumulate evidence in science and medicine,” he told Fox News Digital.
Developing more sophisticated mapping techniques and understanding the long-term effects of deep brain stimulation will be crucial, a neurologist said. (iStock)
The study’s sample size was also relatively small, he said, especially for Tourette’s.
“Even globally, not many patients have undergone deep brain stimulation surgery for this disorder,” Horn said.
This study is the first step in defining what the researchers call the “human dysfunctome,” the set of connections that may become dysfunctional in specific neurological or psychiatric disorders of the human brain.
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“We first paint a picture of the dysfunctome, but need additional data to complete the picture and map other symptoms onto the circuits of the human brain,” Horn said.
While the study findings might not lead to drastic changes just yet, Horn said they may help experienced clinicians fine-tune their approaches to neurology treatments.
The findings from this study point in the direction of more personalized cognitive therapies, experts said. (iStock)
“It could give additional clarity or small refinements here and there to make interventions more successful,” Horn said. “However, the information should not be followed blindly, but instead should be validated in prospective studies.”
The researchers are already starting to plan for clinical trials to validate the results.
As Dalvi pointed out, developing more sophisticated mapping techniques and understanding the long-term effects of deep brain stimulation will be crucial.
“Additionally, expanding this approach to other brain regions and disorders could uncover new therapeutic avenues, marking a new era in the treatment of neurological conditions,” he added.
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A new study suggests that middle-aged men may be more vulnerable to faster biological aging, potentially linked to exposure to “forever chemicals.”
The research, published in the journal Frontiers in Aging, examined how perfluoroalkyl and polyfluoroalkyl substances, more commonly known as PFAS, could impact aging at the cellular level.
PFAS are synthetic chemicals commonly used in nonstick cookware, food packaging, water-resistant fabrics and other consumer products, the study noted.
Their chemical structure makes them highly resistant to breaking down, allowing them to accumulate in water, soil and the human body.
Chinese researchers analyzed blood samples from 326 adults enrolled in the U.S. National Health and Nutrition Examination Survey between 1999 and 2000.
A new study suggests that middle-aged men could face accelerated biological aging at the cellular level due to exposure to PFAS. (iStock)
The researchers measured levels of 11 PFAS compounds in participants’ blood and used DNA-based “epigenetic clocks” — tools that analyze chemical changes to DNA to estimate biological age — to determine how quickly their bodies were aging at the cellular level, the study stated.
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Two compounds, perfluorononanoic acid (PFNA) and perfluorooctanesulfonamide (PFOSA), were detected in 95% of participants.
Higher concentrations of those chemicals were associated with faster biological aging in men of certain age groups, but not in women.
“People should not panic.”
The compounds most strongly linked to accelerated aging were not the PFAS chemicals that typically receive the most public attention, the researchers noted.
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“The associations were strongest in adults aged 50 to 64, particularly in men,” Dr. Xiangwei Li, professor at Shanghai Jiao Tong University School of Medicine and the study’s corresponding author, told Fox News Digital.
“While this does not establish that PFAS cause aging, it suggests that these widely present ‘forever chemicals’ may be linked to molecular changes related to long-term health and aging.”
The study found that two of the compounds were detected in 95% of participants, and higher levels were linked to faster biological aging in men ages 50–64. (iStock)
Midlife may represent a more sensitive biological period, when the body becomes more vulnerable to age-related stressors, according to the researchers.
Lifestyle factors, such as smoking, may influence biological aging markers, potentially increasing vulnerability to environmental pollutants.
While Li said “people should not panic,” she does recommend looking for reasonable ways to reduce exposure.
That might mean checking local drinking water reports, using certified water filters designed to reduce PFAS, and limiting the use of stain- or grease-resistant products when alternatives are available.
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Meaningful reductions in PFAS exposure will likely depend on broader regulatory action and environmental cleanup efforts, Li added.
The researchers noted that midlife could be a particularly sensitive stage, when the body is more susceptible to stressors associated with aging. (iStock)
Study limitations
The researchers outlined several important limitations of the research, including that the findings show an association, but do not prove that PFAS directly causes accelerated aging.
“The study is cross-sectional, meaning exposure and aging markers were measured at the same time, so we cannot determine causality,” Li told Fox News Digital.
The study was also relatively small, limited to 326 adults age 50 or older, which means the findings may not apply to younger people or broader populations.
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Researchers measured PFAS levels using data collected between 1999 and 2000, and today’s exposure patterns may differ.
Li added that while PFAS is known to persist in the environment and the body, these results should be validated through larger, more recent studies that follow participants over time.
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A drug that has long been used to treat seizures has shown promise as a potential means of Alzheimer’s prevention, a new study suggests.
The anti-seizure medication, levetiracetam, was first approved by the FDA in November 1999 under the brand name Keppra as a therapy for partial-onset seizures in adults. The approval has since expanded to include children and other types of seizures.
Northwestern University researchers recently found that levetiracetam prevented the formation of toxic amyloid beta peptides, which are small protein fragments in the brain that are commonly seen in Alzheimer’s patients.
The medication was found to prevent the formation of amyloid-beta 42 in both animal models and cultured human neurons, according to the study findings, which were published in Science Translational Medicine.
The effect was also seen in post-mortem human brain tissue obtained from individuals with Down syndrome, who are at high risk for Alzheimer’s disease.
The medication was found to prevent the formation of amyloid-beta 42 in both animal models and cultured human neurons. (iStock)
“While many of the Alzheimer’s drugs currently on the market, such as lecanemab and donanemab, are approved to clear existing amyloid plaques, we’ve identified this mechanism that prevents the production of the amyloid‑beta 42 peptides and amyloid plaques,” said corresponding author Jeffrey Savas, associate professor of behavioral neurology at Northwestern University Feinberg School of Medicine, in a press release.
“Our new results uncovered new biology while also opening doors for new drug targets.”
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The brain is better able to avoid the pathway that produces toxic amyloid‑beta 42 proteins in younger years, but the aging process gradually weakens that ability, Savas noted.
“This is not a statement of disease; this is just a part of aging. But in brains developing Alzheimer’s, too many neurons go astray, and that’s when you get amyloid-beta 42 production,” he said.
The effect was also seen in post-mortem human brain tissue obtained from individuals with Down syndrome, who are at high risk for Alzheimer’s disease. (iStock)
That then leads to tau (“tangles”) — abnormal clumps of protein inside brain neurons — which can kill brain cells, trigger neuroinflammation and lead to dementia.
In order for levetiracetam to function as an Alzheimer’s blocker, high-risk patients would have to start taking it “very, very early,” Savas said — up to 20 years before elevated amyloid-beta 42 levels would be detected.
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“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death,” the researcher noted.
The researchers also did a deep dive into previous human clinical data to determine whether Alzheimer’s patients who were taking the anti-seizure drug had slower cognitive decline. They reported that the patients in that category had a “significant delay” in the span from cognitive decline to death compared to those not taking the drug.
“This analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” the researcher said. (iStock)
“Although the magnitude of change was small (on the scale of a few years), this analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” Savas said.
Looking ahead, the research team aims to find people who have genetic forms of Alzheimer’s to participate in testing, Savas said.
Limitations and caveats
The study had several limitations, including that it relied on animal models and cultured cells, with no human trials conducted.
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Because the study was observational in nature, it can’t prove that the medication caused the prevention of the toxic brain proteins, the researchers acknowledged.
Savas noted that levetiracetam “is not perfect,” cautioning that it breaks down in the body very quickly.
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The team is currently working to create a “better version” that would last longer in the body and “better target the mechanism that prevents the production of the plaques.”
“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death.”
The medication’s common documented side effects include drowsiness, weakness, dizziness, irritability, headache, loss of appetite and nasal congestion.
It has also been linked to potential mood and behavior changes, including anxiety, depression, agitation and aggression, according to the prescribing information. In rare cases, it could lead to severe allergic reactions, skin reactions, blood disorders and suicidal ideation.
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Funding for the study was provided by the National Institutes of Health and the Cure Alzheimer’s Fund.
Fox News Digital reached out to the drug manufacturer and the researchers for comment.
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