Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative cause of dementia in the elderly. AD is accompanied by the accumulation of amyloid peptides in the brain parenchyma and in the cerebral vessels. The sporadic form of AD accounts for about 95% of all cases. It is characterized by a late onset, typically after the age of 65, with a complex and still poorly understood aetiology. Several observations point towards a central role of cerebrovascular dysfunction in the onset of sporadic AD (SAD). According to the “vascular hypothesis”, AD may be initiated by vascular dysfunctions that precede and promote the neurodegenerative process. In accordance to this, AD patients show increased hemorrhagic or ischemic stroke risks. It is now clear that multiple bidirectional connections exist between AD and cerebrovascular disease, and in this new scenario, the effect of amyloid peptides on vascular cells and blood platelets appear to be central to AD. In this review, we analyze the effect of amyloid peptides on vascular function and platelet activation and its contribution to the cerebrovascular pathology associated with AD and the progression of this disease.
Highlights
Reviewed by: Dmitry Lim, Università del Piemonte Orientale “Amedeo Avogadro”, Italy Tiziana Casoli, Istituto Nazionale di Riposo e Cura per Anziani, Italy
It is clear that multiple bidirectional connections exist between Alzheimer’s disease (AD) and cerebrovascular disease, and in this new scenario, the effect of amyloid peptides on vascular cells and blood platelets appear to be central to AD
ANIMAL MODELS OF AD AND PLATELET AND VASCULAR (DYS)FUNCTIONS Since the formulation of the “amyloid cascade hypothesis” and the discovery of mutations correlated with familial AD (FAD), several AD transgenic mice have been developed to study the pathophysiological role of amyloid precursor protein (APP) and Aβ peptides
Summary
Role of amyloid peptides in vascular dysfunction and platelet dysregulation in Alzheimer’s disease. We analyze the effect of amyloid peptides on vascular function and platelet activation and its contribution to the cerebrovascular pathology associated with AD and the progression of this disease. Aβ peptides that accumulate in cerebral senile plaques and vessel walls derive from the metabolism of the larger glycoprotein called amyloid precursor protein (APP), which is a type 1 membrane glycoprotein expressed ubiquitously in the cells. Aβ oligomers have the ability to permeabilize the plasma membrane of different cell types, which triggers a series of cellular event leading to cell dysfunction and death This mechanism of action is common to different amyloidogenic peptides, including Aβ peptides, α-synuclein, polyglutamine and APP (Glabe, 2006)
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