Does increased platelet release of Abeta peptide contribute to brain abnormalities in individuals with depression?

Increased platelet activation with release of procoagulant factors from their alpha granules has been demonstrated in individuals with major depression. Platelet activation has also been shown to be associated with release of beta-amyloid peptides, which have been implicated in Alzheimer's disease. Thus, we are hypothesizing that sustained elevations of Abeta peptides might occur in individuals with recurrent depression. We further hypothesize that such elevations contribute to brain abnormalities in depressed individuals through the formation of neurotoxic oligomeric forms of Abeta peptides and amyloid deposition. We also propose that increased amyloid Abeta peptides from platelet activation may be a mechanism underlying the increased risk for cognitive impairment in nondepressed patients who have other reasons for such activation. If true, our hypothesis would imply that platelet inhibitors may have a role in preventing or delaying the neuronal consequences of disorders characterized by activated platelets.