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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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.

Breaking New Ground: Immune System Discovery Offers Potential Solution to Alzheimer’s

A groundbreaking study has shed new light on the relationship between the immune system and Alzheimer’s disease. Researchers at the University of Virginia School of Medicine have discovered that an immune molecule called STING plays a crucial role in driving the formation of amyloid plaques and tau tangles, hallmarks of Alzheimer’s.

The study found that blocking STING activity in lab mice protected them from mental decline, suggesting a promising new target for developing treatments. This breakthrough has far-reaching implications for understanding and treating not only Alzheimer’s but also other neurodegenerative diseases like Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and dementia.

“The findings demonstrate that the DNA damage that naturally accumulates during aging triggers STING-mediated brain inflammation and neuronal damage in Alzheimer’s disease,” said researcher John Lukens, PhD. “These results help to explain why aging is associated with increased Alzheimer’s risk and uncover a novel pathway to target in the treatment of neurodegenerative diseases.”

The study, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, involved a team of researchers from UVA’s Department of Neuroscience and Center for Brain Immunology and Glia (BIG Center). They found that removing STING dampened microglial activation around amyloid plaques, protected nearby neurons from damage, and improved memory function in Alzheimer’s model mice.

The discovery of STING as a key player in the development of neurodegenerative diseases opens new doors for research into potential treatments. While much more work is needed to translate these findings into effective therapies, this breakthrough has sparked hope among researchers and patients alike.

“Our hope is that this work moves us close to finding safer and more effective ways to protect the aging brain,” said Lukens. “Shedding light on how STING contributes to that damage may help us target similar molecules and ultimately develop effective disease-modifying treatments.”