Mar 19, 2015

Role of amyloid peptides in vascular dysfunction and platelet dysregulation in Alzheimer's disease

Frontiers in Cellular Neuroscience
Ilaria CanobbioG Pula

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.

Mentioned in this Paper

Ischemic Cerebrovascular Accident
Vascular Motor Function
Parenchyma
APP protein, human
Cerebrovascular System
Blood Vessel
Brain
Alzheimer's Disease
Etiology
Amyloid Deposition

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