Abstract
The functions of platelets are broad. Platelets function in hemostasis and thrombosis,
inflammation and immune responses, vascular regulation, and host defense against invading
pathogens, among others. These actions are achieved through the release of a wide
set of coagulative, vascular, inflammatory, and other factors as well as diverse cell
surface receptors involved in the same activities. As active participants in these
physiological processes, platelets become involved in signaling pathways and pathological
reactions that contribute to diseases that are defined by inflammation (including
by pathogen-derived stimuli), vascular dysfunction, and coagulation. These diseases
include Alzheimer's and Parkinson's disease, the two most common neurodegenerative
diseases. Despite their unique pathological and clinical features, significant shared
pathological processes exist between these two conditions, particularly relating to
a central inflammatory mechanism involving both neuroinflammation and inflammation
in the systemic environment, but also neurovascular dysfunction and coagulopathy,
processes which also share initiation factors and receptors. This triad of dysfunction—(neuro)inflammation,
neurovascular dysfunction, and hypercoagulation—illustrates the important roles platelets
play in neuropathology. Although some mechanisms are understudied in Alzheimer's and
Parkinson's disease, a strong case can be made for the relevance of platelets in neurodegeneration-related
processes.
Keywords
systemic inflammation - neuroinflammation - infection - neuropathology - platelets
