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Platelets: Their Potential Contribution to the Generation of Beta-amyloid Plaques in Alzheimer’s Disease.
Humpel C
Abstract:
BACKGROUND:
Alzheimer's disease is a severe neurodegenerative brain disorder, showing severe beta-amyloid depositions in the brain (plaques) and in vessels (cerebral amyloid angiopathy, CAA), tau pathology, neurodegeneration (and loss of acetylcholine), inflammation with reactive astrocytes and microglia and cerebrovascular damage, all resulting in memory loss.
METHODS AND RESULTS:
In this review, I present a hypothesis that chronic vascular lesions and bleedings cause platelet overactivation and repair. Platelets express large amounts of amyloid precursor protein (APP) and release beta-amyloid, possibly playing a role as a clotting substance. As the number of bleedings increases over lifetime, the function of platelets diminishes until they are dysfunctional. Dysfunctional processing of APP in platelets and subsequent inflammatory processes may play a role in the formation of CAA. Local lesions and acidosis may transfer a pathological cascade including silent strokes into the brain, causing irreversible APP dysfunction, tau dysregulation and beta-amyloid deposition.
CONCLUSION:
Platelets may play a central role in the processing of plaque deposition in the Alzheimer brain and may be of interest for diagnostic as well as therapeutic strategies.
Alzheimer's disease is a severe neurodegenerative brain disorder, showing severe beta-amyloid depositions in the brain (plaques) and in vessels (cerebral amyloid angiopathy, CAA), tau pathology, neurodegeneration (and loss of acetylcholine), inflammation with reactive astrocytes and microglia and cerebrovascular damage, all resulting in memory loss.
METHODS AND RESULTS:
In this review, I present a hypothesis that chronic vascular lesions and bleedings cause platelet overactivation and repair. Platelets express large amounts of amyloid precursor protein (APP) and release beta-amyloid, possibly playing a role as a clotting substance. As the number of bleedings increases over lifetime, the function of platelets diminishes until they are dysfunctional. Dysfunctional processing of APP in platelets and subsequent inflammatory processes may play a role in the formation of CAA. Local lesions and acidosis may transfer a pathological cascade including silent strokes into the brain, causing irreversible APP dysfunction, tau dysregulation and beta-amyloid deposition.
CONCLUSION:
Platelets may play a central role in the processing of plaque deposition in the Alzheimer brain and may be of interest for diagnostic as well as therapeutic strategies.
