Worldwide concern is growing due to the increasing cases of Alzheimer’s disease. But what if we knew that a simple blood test to measure platelet activity could help identify people most at risk of developing the disease decades before it appears, allowing for preventive treatment?
A joint study by researchers at the Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases at The University of Texas at San Antonio, UT Health San Antonio, and the NYU Grossman School of Medicine, showed that blood clotting in vascular dysfunction is associated with key markers of Alzheimer’s disease as early as midlife.
Vascular dysfunction refers to a condition in which blood vessels do not function properly for various reasons, ranging from abnormal blood clots to atherosclerosis, inflammation, diabetes, high blood pressure, smoking, and aging. It is generally known to contribute to the risk of Alzheimer’s disease and related dementias, but the underlying mechanisms have not been clear.
The team led by the Biggs Institute and NYU has succeeded in identifying one of these mechanisms, which is platelet aggregation, the process by which platelets, or small blood cells, form a clot.
Scientists specifically link the platelet aggregation response in the blood to brain markers revealed by positron emission tomography (PET) and magnetic resonance imaging (MRI) for the risk of Alzheimer’s disease in middle-aged people.
“We believe that since platelets are easily accessible in the blood, they may eventually become part of a midlife screening to identify people at risk and apply preventive interventions targeting platelet-related inflammation,” said Sudha Seshadri, professor of neurology and founding director of the Biggs Institute and lead author of the study, according to Medical Xpress.
The results indicated a positive correlation: people whose platelets clump together more strongly also tend to have higher levels of amyloid and tau proteins in the brain, which are the hallmarks of Alzheimer’s disease.
However, this relationship is not the same for everyone.
In this context, Alexa Beiser, professor of biostatistics at Boston University School of Public Health, who has been working on Framingham data for decades and played a key role in the statistical analysis of the study, explained:
* This relationship appears in people whose platelets are at their lowest level of activity in the experiments used.
* In this group, stronger platelet aggregation is associated with higher levels of amyloid and tau proteins in brain scans.
* As for people with higher platelet activity, this relationship is less clear.
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