Abstract
Alzheimer Disease (AD) is the most common neurodegenerative disorder worldwide, and account for 60% to 70% of all cases of progressive cognitive impairment in elderly patients. At the microscopic level distinctive features of AD are neurons and synapses degeneration, together with extensive amounts of senile plaques and neurofibrillars tangles. The degenerative process probably starts 20–30 years before the clinical onset of the disease. Senile plaques are composed of a central core of amyloid β peptide, Aβ, derived from the metabolism of the larger amyloid precursor protein, APP, which is expressed not only in the brain, but even in non neuronal tissues. More than 30 years ago, some studies reported that human platelets express APP and all the enzymatic activities necessary to process this protein through the same pathways described in the brain. Since then a large number of evidence has been accumulated to suggest that platelets may be a good peripheral model to study the metabolism of APP, and the pathophysiology of the onset of AD. In this review, we will summarize the current knowledge on the involvement of platelets in Alzheimer Disease. Although platelets are generally accepted as a suitable model for AD, the current scientific interest on this model is very high, because many concepts still remain debated and controversial. At the same time, however, these still unsolved divergences mirror a difficulty to establish constant parameters to better defined the role of platelets in AD.
Highlights
Molecular features and pathogenesis of alzheimer disease Alzhemeir’s Disease (AD) is a chronic progressive neurodegenerative disorder characterized by a devastating cognitive and memory decline
Nowday researchers have recognized that platelets are the principal components of human blood to be affected in the onset but even in the progression of AD
Platelets seem to mirror what happens in nervous tissue during the evolution of AD, and represent the cellular type where to identified the early events in the onset of the disorder
Summary
Molecular features and pathogenesis of alzheimer disease Alzhemeir’s Disease (AD) is a chronic progressive neurodegenerative disorder characterized by a devastating cognitive and memory decline. Bermejo and coworkers, reported an increased platelets levels of COX2 in AD and MCI patients compared to elderly controls, indicating that platelet inflammatory pathways are activated, and that this could be considered an early event in AD development [133]. Studies reported that platelets of patients carrying the mutation Met293Val in PS2 protein did not show altered expression of APP isoforms ratio pattern to what reported for sporadic AD patients [142] It was demonstrated an association between early stages of AD, or of Mild Cognitive Impairment, MCI, with a reduction in platelet APP isoforms ratio, and suggested that, since alteration of APP processing may be an early event in AD, the characterization of APP ratio in platelet could have a great diagnostic power [8,143,144,145]. Platelet APP isoforms ratio may be a very important AD biomarker, as its evaluation is reliable and simple test to be performed
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