Researchers from the Örebro University found evidence that clopidogrel, a well-known blood-thinner drug, may slow down Alzheimer’s Disease (AD) progression. The study published in the journal Science Signaling was led by Professor Margitta Elvers and included researchers from Sweden, Italy, and Germany.
Alzheimer’s Disease is characterized by a progressive build-up of pathological β-amyloid plaques that slowly accrue within the brain and central nervous system (CNS). Those plaques are abnormal clusters of proteinic material that clump inside neurons, blocking synapses signaling. They also trigger inflammation signals that attract immune system cells that will target damaged nerve cells and destroy them. As soon as neurons start dying, the patient progressively loses his mental faculties, slowly losing his ability to communicate, think and even walk and eat.
These dangerous plaques can “travel” through the bloodstream by sticking to the surface of blood platelets (thrombocytes). The β-amyloid aggregation with platelets may also initiate a chain reaction that contributes to a quick growth of the plaque itself. Scientists theorized that a drug that may interfere with the normal platelet aggregation mechanisms could stop, or at least reduce the speed at wich plaques grow. Clopidogrel is a heart medication used to prevent the formation of blood clots by inhibiting platelet activation. Researchers found that mice treated with this drug showed a reduction in β-amyloid plaques formation, showing that the theory holds true. Although further studies are required to understand whether clopidogrel may have the same effects on humans, an interestingly new mechanism of plaque formation has been successfully identified.
Article by Claudio Butticè, PharmD.
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