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Alzheimer's

Immune cells drive congenital paralysis disease

Patients with spastic paraplegia type 15 develop movement disorders during adolescence that may ultimately require the use of a wheelchair. In the early stages of this rare hereditary disease the brain appears to play a major role by over-activating the immune system, as shown by a recent study.

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In a groundbreaking study published in the Journal of Experimental Medicine, researchers from the University of Bonn and the German Center for Neurodegenerative Diseases (DZNE) have made a significant discovery about the underlying causes of spastic paraplegia type 15. This rare hereditary disease affects patients during adolescence, ultimately leading to paralysis and the need for a wheelchair.

Spastic paraplegia type 15 is characterized by the progressive loss of motor neurons in the central nervous system, which are responsible for controlling movement. Initial symptoms typically appear in late childhood, manifesting first in the legs as uncontrollable twitching and paralysis. The researchers, led by Professor Elvira Mass from the LIMES Institute at the University of Bonn, set out to investigate the potential role of the immune system in this process.

Their experiments used mice that shared the same genetic defect responsible for spastic paraplegia type 15. The researchers found that microglia cells, which are the immune cells of the brain, undergo dramatic changes in the early stages of the disease. These altered microglia cells, known as “disease-associated microglia,” release signaling molecules that call for the help of cytotoxic T-cells from the bone marrow. This interplay between microglia and T-cells drives the inflammatory process, which ultimately contributes to the loss of motor neurons.

The researchers’ findings open up new therapeutic possibilities for spastic paraplegia type 15. Immune suppression drugs could potentially help slow the progression of the disease. Moreover, their discovery has implications for other neurodegenerative diseases, such as Alzheimer’s, where inflammatory processes in the brain play a crucial role.

This interdisciplinary research was made possible by the close collaboration within the ImmunoSensation2 Cluster of Excellence, where Professor Mass and Dr. Marc Beyer from the DZNE are members. Their work highlights the importance of combining immunology and neurobiology with cutting-edge single-cell technology to shed light on complex diseases.

The study’s findings were published in the Journal of Experimental Medicine and were funded by grants from the German Research Foundation (DFG), the Federal Ministry of Education and Research (BMBF), and the European Research Council (ERC). The research involved a collaborative effort with the universities of Bonn, Jena, and Melbourne.

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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