According to a study presented by the European Society of Neurology, routine blood tests measure insulin resistance can identify cognitive declines in patients with Alzheimer’s disease.
Triglyceride-Glucose Index has been obtained in hospital laboratories worldwide, providing families and doctors with a simple tool to predict the rate of mild cognitive impairment that can lead to severe dementia.
Italian researchers tracked 315 cognitive deficits for three years, including 200 with biologically confirmed Alzheimer’s disease. People with the highest insulin resistance scores lost more than 2.5 points per year on standard cognitive tests, worsening faster than those with lower scores.
Metabolic markers reveal disease trajectories
“Once a mild cognitive impairment is diagnosed, families always ask how fast it is progressing,” explains Dr. Bianca Gumina, principal investigator at the University of Brescia. “Our data suggest that simple metabolic markers available in each hospital lab can help identify more vulnerable subjects who may be candidates for targeted treatments or specific intervention strategies.”
Triglyceride-Glucose (TYG) index calculates insulin resistance using two conventional blood measurements. When the researchers divided patients into three groups based on their TYG score, the highest third of patients had a risk ratio of 4.08, with a decrease in rapid cognitive abilities, which means they were four times more likely to deteriorate rapidly.
Alzheimer’s specific vulnerability was discovered
Surprisingly, this predictive ability appears only in patients with Alzheimer’s disease, not in patients with other forms of cognitive decline. This specificity suggests a unique biological pathway that links metabolism to neurodegeneration in Alzheimer’s disease.
In Alzheimer’s, insulin resistance appears to be:
- Impairs the ability of brain cells to absorb glucose
- Promote the accumulation of toxic amyloid
- Protective function that destroys the blood-brain barrier
- Fuel-harm brain inflammation
“We were surprised to see the effects only in the spectrum of Alzheimer’s and not in other neurodegenerative diseases,” Dr. Gumina noted. “This suggests disease-specific vulnerability in the prodromal window when interventions may still change the trajectory.”
Clinical applications are coming soon
Researchers led by Professors Padovani and Professor Pilotto also found that high tyg scores were associated with disruption of the blood-brain barrier and cardiovascular risk factors. Importantly, metabolic risk is independent of APOEε4 gene variants, suggesting that different biological pathways contribute to the development of Alzheimer’s disease.
The independence between genetic and metabolic risk factors was not emphasized in the original press release, but it seems crucial in the detailed study results. This means that patients can face complex risks through a variety of biological mechanisms.
Clinical care can be changed by identifying high-risk patients as early as possible. Doctors may include these people in clinical trials of experimental treatments or implement active lifestyle interventions for insulin sensitivity. Researchers are now investigating whether TYG levels are associated with brain imaging markers, or even with earlier detections.
“If targeted metabolism can delay progression, we will have an easily modified target that works with emerging disease-improving drugs,” concluded Dr. Gumina. Unlike genetic factors, insulin resistance responds to diet, exercise and drugs, which brings hope for a slowdown in progress in Alzheimer’s.
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