Platelets move through the blood all over the body, and it´s natural to consider them as a systemic tool
, they give a response to most of the pathological pieces of evidence that running during most of the
diseases. Neurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease (the most
common degenerative diseases) are an idiopathic incurable slowly progressive degeneration of the
neurons leading to the death of neurons which are the building block in the nervous system.
In this review, it´s aimed to exhibit different researchers which handle the behavioral changes on the
structural aspects of the platelets in the pathogenesis of the neurodegenerative diseases to understand
the platelets relation with the pathogenesis of the neurodegenerative diseases.
Keywords: platelets, neurodegenerative diseases, Parkinson’s disease, Alzheimer’s disease,
amyotrophic lateral sclerosis, mitochondria, ultrastructural alterations, molecular changes, biochemical
The pathological findings of Alzheimer’s diseases, amyotrophic lateral sclerosis, and Parkinson’s
disease will be discussed, within this discussion The platelets activity and it´s components changes in
Alzheimer’s disease (AD), Parkinson´s disease (PD) and amyotrophic lateral sclerosis (ALS) will be
discussed in the same context to make it able to reveal the platelets distribution in the pathogenesis of
the Alzheimer’s disease (AD) ,Parkinson´s disease (PD) and amyotrophic lateral sclerosis (ALS).
Several original scientific studies will be reviewed to exhibiting the relationship between the platelets
and the pathogenesis of the Alzheimer’s diseases.
This review is aimed to exhibit the platelets and its components link with the pathogenesis of the
neurodegenerative diseases, and show the pathological findings which are evidence on the implication
of the platelets in the pathogenesis of the neurodegenerative diseases.
It´s hard to detect any pathological findings in the nervous tissue during the early stage of Alzheimer´s
disease But the platelet can partially reflect the changes in the nervous tissue (1). It takes 20 -30 years
after starting of the degenerative process to demonstrate in the clinical picture of the Alzheimer’s
disease (AD)case. neurotoxic amyloid-ß plaque formation in brain parenchyma and cerebral blood
vessels known as cerebral amyloid angiopathy (CAA) give the pathophysiological explanation of
Alzheimer’s disease (AD)(2). hemostasis and thrombosis are Platelets major functions, but platelets
also involved in neuroinflammatory diseases like the AD. For long years ago, platelets were
considered as the peripheral model to study the pathogenesis of AD, because they feature the
enzymatic activities to generate amyloid-ß (Aß) peptides (3)(4). platelets are supposed to be a real
element in the pathogenesis of AD. Impaction of Aß peptides effect on platelets and the role of
platelets in the development of AD are observed, but still ill-defined(5). the cellular mechanisms
stimulated through Aß in platelets was explored through treatment of platelets with Aß, but that
resulted platelet activation(30), then stimulated generation of reactive oxygen species
(ROS)(6)(chemically reactive cellular molecules in signaling and homeostasis) and membrane
scrambling, supposing started platelet apoptosis ,increase the platelets ability to platelets to up-take
Aß(7) . Aß inducing platelets apoptosis and that maybe lead to thrombocytopenia which maybe makes
amyloidosis complicated (8) .
Furthermore, platelets convert soluble Aß into fibrillar elements that were absorbed by apoptotic 


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