Simple Blood Test Identifies Alzheimer’s Patients at Risk of Faster Decline: Study Shows

Published On 2025-06-25 02:45 GMT   |   Update On 2025-06-25 02:45 GMT

Insulin resistance, as measured by a routine triglyceride-glucose index, may help identify early Alzheimer’s patients at risk of rapid cognitive decline, according to new research presented at the European Academy of Neurology Congress 2025 and soon to be published in Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring. The study suggests that a low-cost, widely available blood test could play a vital role in predicting disease progression and guiding early interventions.

In this study, neurologists at the University of Brescia reviewed clinical records of 315 non-diabetic patients with cognitive deficits, including 200 with biologically confirmed Alzheimer’s disease (AD). Each participant underwent triglyceride-glucose index testing to assess insulin resistance and was followed for three years to monitor cognitive changes using the Mini-Mental State Examination.

The researchers divided participants into thirds based on their triglyceride-glucose index. Among patients with mild cognitive impairment due to Alzheimer’s, those in the highest triglyceride-glucose group experienced significantly faster cognitive decline—losing over 2.5 Mini Mental State Examination points per year—compared to those in the lower two-thirds. The hazard ratio for rapid decline in this group was 4.08. No similar trend was found in patients with non-Alzheimer’s forms of cognitive impairment.

"Once mild cognitive impairment is diagnosed, families always ask how fast it will progress," said lead investigator Dr. Bianca Gumina. "Our data show that a simple metabolic marker available in every hospital laboratory can help identify more vulnerable subjects who may be suitable candidates for targeted therapy or specific intervention strategies."

High triglyceride-glucose levels were also linked to cardiovascular risks and blood-brain barrier disruption, but showed no interaction with the APOE ε4 gene, suggesting metabolic and genetic risks operate through different pathways.

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

Reference: https://www.ean.org/congress2025

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