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Alzheimer's

ATP’s Surprising Role in Preventing Harmful Protein Aggregation in Parkinson’s and ALS

While a comprehensive cure-all to these neurological conditions is unlikely, scientists are making headway into understanding their fundamental characteristics with the hope of preventing or alleviating cognitive and motor impairments. Researchers have now discovered that ATP, which is most commonly thought of as the ‘fuel’ of our cells, plays a surprising role in relation to neurodegenerative diseases.

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ATP, commonly known as the “fuel” of our cells, has long been thought to be solely responsible for powering cellular processes. However, recent research has revealed that ATP plays a surprising role in preventing harmful protein aggregation associated with neurodegenerative diseases like Parkinson’s and ALS.

In a groundbreaking study published in Science Advances, researchers from the Okinawa Institute of Science and Technology (OIST) have discovered that ATP regulates protein condensation and the overall viscosity of cytoplasm in neurons. When the cytoplasm becomes more viscous, proteins are more prone to aggregate, leading to harmful tangles that damage cells.

Through both in vitro and in vivo trials, the researchers found that boosting ATP production decreases cytosolic viscosity in affected cells, dispersing existing protein aggregates and preventing future pathological aggregations. This finding has significant implications for our understanding of neurodegenerative diseases and may lead to new therapeutic approaches.

In many neurodegenerative diseases, the formation and accumulation of insoluble, membrane-less protein condensates via liquid-liquid phase separation is a common symptom. These protein aggregates can accumulate both inside and outside cells, as seen in late-stage Alzheimer’s disease where they appear as neurofibrillary tangles.

The researchers observed a direct relationship between the intracellular concentration of ATP and the solubility of proteins associated with neurodegenerative disorders like SNCA in Parkinson’s, Tau in Alzheimer’s, and TDP-43 in ALS. They found that boosting ATP production using NMN rescued cytosolic fluidity by breaking up and solubilizing existing protein aggregates in axons from ALS neurons.

This study highlights the complex interplay between cellular energy metabolism and neurodegenerative diseases. While a comprehensive cure for these debilitating conditions is unlikely, this discovery brings us closer to understanding the underlying mechanisms and developing effective treatments.

The researchers’ findings suggest that targeting ATP production may be a viable therapeutic strategy for preventing or alleviating cognitive and motor impairments associated with neurodegenerative diseases. As we continue to unravel the mysteries of cellular metabolism and its connection to disease, we may uncover new avenues for prevention and treatment, ultimately improving the lives of those affected by these debilitating conditions.

Alzheimer's

Groundbreaking Study Suggests Link Between Semaglutide and Lower Dementia Risk in Type 2 Diabetes Patients

A blockbuster diabetes and weight-loss drug might be doing more than controlling blood sugar—it could also be protecting the brain. Researchers at Case Western Reserve University found that people with type 2 diabetes who took semaglutide (the active ingredient in Ozempic and Wegovy) had a significantly lower risk of developing dementia. The benefit was especially strong in women and older adults.

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A recent study by researchers at the Case Western Reserve School of Medicine has made an astonishing discovery that may revolutionize the way we approach dementia prevention. The research team found that semaglutide, a popular medication used to treat diabetes and aid in weight loss, could significantly lower the risk of dementia in people with type 2 diabetes (T2D).

Dementia is a devastating condition that affects millions worldwide, causing memory loss and cognitive decline. It occurs when brain cells are damaged, disrupting their connections and ultimately leading to this debilitating state. Encouragingly, studies indicate that approximately 45% of dementia cases could be prevented by addressing modifiable risk factors.

The study, published in the Journal of Alzheimer’s Disease, analyzed three years’ worth of electronic records from nearly 1.7 million T2D patients nationally. The researchers used a statistical approach that mimicked a randomized clinical trial to determine the effectiveness of semaglutide in preventing dementia.

Their findings suggest that patients prescribed semaglutide had a significantly lower risk of developing Alzheimer’s disease-related dementia compared to those taking other anti-diabetic medications, including GLP-1R-targeting medications. These results were even more pronounced in women and older adults.

Semaglutide, a glucagon-like peptide receptor (GLP-1R) molecule that decreases hunger and regulates blood sugar levels in T2D patients, has shown remarkable benefits beyond its primary use as a diabetes treatment. It also reduces the risk of cardiovascular diseases, further solidifying its potential in preventing dementia.

The study’s lead researcher, biomedical informatics professor Rong Xu, stated, “There is no cure or effective treatment for dementia, so this new study provides real-world evidence for its potential impact on preventing or slowing dementia development among at-high risk populations.”

While the findings are promising, it’s essential to note that further research through randomized clinical trials will be necessary to confirm the causal relationship between semaglutide and dementia prevention. Nevertheless, this groundbreaking study offers a glimmer of hope in the quest to combat dementia and improve the lives of millions worldwide.

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Alzheimer's

The Common Blood Test That Could Predict Alzheimer’s Progression

A simple blood test could reveal which early Alzheimer’s patients are most at risk for rapid decline. Researchers found that people with high insulin resistance—measured by the TyG index—were four times more likely to experience faster cognitive deterioration. The study highlights a major opportunity: a common lab value already available in hospitals could help guide personalized treatment strategies. This discovery also uncovers a unique vulnerability in Alzheimer’s disease to metabolic stress, offering new possibilities for intervention while the disease is still in its early stages.

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The common blood test known as the triglyceride-glucose (TyG) index has long been used to detect insulin resistance. New research presented at the European Academy of Neurology Congress 2025 suggests that this simple test could also be used to predict how fast Alzheimer’s disease progresses in individuals with mild cognitive impairment.

A team of neurologists from the University of Brescia reviewed records for 315 non-diabetic patients with cognitive deficits, including 200 with biologically confirmed Alzheimer’s disease. All subjects underwent an assessment of insulin resistance using the TyG index and a clinical follow-up of 3 years. The results showed that when patients were divided according to their TyG index levels, those in the highest third of the Mild Cognitive Impairment subgroup deteriorated far more quickly than their lower-TyG peers.

The researchers found that high TyG was associated with blood-brain barrier disruption and cardiovascular risk factors, yet it showed no interaction with the APOE ε4 genotype. This suggests that metabolic and genetic risks may act through distinct pathways.

Identifying high-TyG patients could refine enrolment for anti-amyloid or anti-tau trials and prompt earlier lifestyle or pharmacological measures to improve insulin sensitivity.

“If targeting metabolism can delay progression, we will have a readily modifiable target that works alongside emerging disease-modifying drugs,” concluded Dr. Bianca Gumina.

The study aimed to fill the gap in understanding how quickly Alzheimer’s progresses by focusing on its impact during the prodromal mild cognitive impairment (MCI) stage.

This research has significant implications for individuals with mild cognitive impairment and their families, as it could provide a simple and cost-effective way to predict the pace of cognitive decline.

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Alzheimer's

Epilepsy Strikes with Surprising Frequency in Frontotemporal Dementia Patients

According to a recent study, in patients with frontotemporal dementia (FTD), epileptic seizures are significantly more common than previously known. The discovery deepens understanding of the symptoms of this memory disorder and emphasises the importance of taking epileptic seizures into account in the treatment and monitoring of patients.

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Epileptic seizures are more common in patients with frontotemporal dementia (FTD) than previously known, according to a recent study. This discovery sheds new light on the symptoms of this memory disorder and emphasizes the importance of considering epileptic seizures in treatment and monitoring patients.

The research project, led by Neurocenter Finland, analyzed data from 12,490 medical records at the University Hospitals of Kuopio and Oulu between 2010-2021. The study identified 245 patients with FTD and found that epilepsy was significantly more common among them than those with Alzheimer’s disease or healthy controls.

“Our results show that epilepsy is considerably more common among those with FTD than those with Alzheimer’s disease or in healthy controls,” says Doctoral Researcher Annemari Kilpeläinen, the first author of the research article and a medical specialist in neurology. “It is noteworthy that epilepsy occurred in some patients with FTD already ten years before their dementia diagnosis, and it was more common in all the examined stages of the disease than previous international studies have reported.”

The prevalence of epilepsy increased over time in patients with FTD, reaching approximately 11% five years after the diagnosis. In addition to diagnosing epilepsy, medications used for epilepsy were more common among patients with FTD, further strengthening the reliability of the results.

Diagnosing epilepsy in patients with FTD can be challenging due to the resemblance between the symptoms of the disease and epileptic seizures. However, untreated epilepsy can significantly worsen patients’ condition. Identifying epilepsy is essential because its treatment can improve patients’ functional capacity and quality of life.

“Knowledge about the association between epilepsy and FTD raises new research questions: do these diseases share some pathophysiological mechanisms and could some FTD symptoms be caused by alterations in the specific electrical systems of the brain?” asks Associate Professor Eino Solje, the principal investigator of the project.

The recently published study is part of an extensive project that combines real-life patient data with different kinds of unique registers. The project involves a strong cooperation between the University of Oulu and the University of Eastern Finland as well as different fields of science, including between researchers in medicine and law.

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