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Study finds blood test can predict cognitive decline in dementia patients

“We were surprised to see the effect only in the Alzheimer’s spectrum and not in other neurodegenerative diseases."

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By Stephen Beech

A simple blood test can predict cognitive decline in dementia patients, shows new research.

Insulin resistance detected by the test can flag people with early Alzheimer’s disease who are four times more likely to suffer rapid cognitive decline, according to the findings.

Neurologists at the University of Brescia in Italy reviewed records for 315 non-diabetic patients with cognitive issues, including 200 with biologically confirmed Alzheimer’s disease.

All the participants subjects underwent an assessment of insulin resistance using the routine triglyceride-glucose (TyG) index and a clinical follow-up three years later.

When patients were divided according to TyG index, those in the highest third of the Mild Cognitive Impairment Alzheimer's subgroup deteriorated far more quickly than their lower-TyG peers.

But no link appeared in the non-Alzheimer's group.

Lead investigator Dr. Bianca Gumina said: “Once mild cognitive impairment is diagnosed, families always ask how fast it will progress.

“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.”

While insulin resistance has been linked to the onset of Alzheimer’s disease, Dr. Gumina says its role in how quickly the condition progresses has received less attention.

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The new study aimed to fill that gap by focusing on its impact during the early mild cognitive impairment (MCI) stage.

The Italian researchers used the TyG index, which offers a low-cost, routinely available surrogate for insulin resistance, to analyse whether metabolic dysfunction could help predict the pace of cognitive decline after diagnosis.

In Alzheimer’s disease specifically, Dr. Gumina says insulin resistance is believed to impair neuronal glucose uptake, promote amyloid accumulation, disrupt the blood–brain barrier, and fuel inflammation – pathways that are less relevant or differently regulated in other neurodegenerative diseases.

She said: “We were surprised to see the effect only in the Alzheimer’s spectrum and not in other neurodegenerative diseases.

“It suggests a disease-specific vulnerability to metabolic stress during the prodromal window, when interventions may still change the trajectory.”

The research team found that high TyG was also associated with blood–brain barrier disruption and cardiovascular risk factors.

They believe that identifying high-TyG patients could refine enrollment for anti-amyloid or anti-tau trials and prompt earlier lifestyle or pharmacological measures to improve insulin sensitivity.

The team is now investigating whether TyG levels also track with neuroimaging biomarkers to aid earlier detection and stratification.

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

The findings were presented at the European Academy of Neurology (EAN) Congress in Helsinki, Finland.

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