Alzheimer disease and platelets: how's that relevant

Area of Science:

• Neuroscience
• Biochemistry
• Gerontology

Background:

• Alzheimer Disease (AD) is a leading cause of neurodegeneration, characterized by neuronal loss, synaptic degeneration, senile plaques, and neurofibrillary tangles.
• AD pathogenesis begins decades before clinical symptoms, involving amyloid precursor protein (APP) and amyloid-beta (Aβ) peptide.
• Human platelets express APP and possess enzymatic machinery for its processing, mirroring brain pathways.

Purpose of the Study:

• To review current knowledge on the involvement of platelets in Alzheimer Disease.
• To explore the utility of platelets as a peripheral model for AD research.
• To highlight ongoing debates and challenges in understanding the role of platelets in AD pathophysiology.

Main Methods:

• Literature review of studies investigating APP processing in platelets.
• Analysis of evidence supporting platelets as a peripheral model for AD.
• Discussion of current controversies and unresolved questions regarding platelets in AD.

Main Results:

• Accumulated evidence suggests platelets are a viable peripheral model for studying APP metabolism and AD onset.
• Platelets share key molecular pathways with brain cells involved in AD.
• Significant scientific interest exists, yet many concepts remain debated and controversial.

Conclusions:

• Platelets represent a promising peripheral model for Alzheimer Disease research, particularly for studying APP metabolism.
• Despite acceptance as a suitable model, inconsistencies and debates persist, hindering the establishment of definitive parameters for their role in AD.
• Further research is needed to resolve current divergences and solidify the understanding of platelets in AD pathophysiology.