TY - JOUR
T1 - Role of amyloid peptides in vascular dysfunction and platelet dysregulation in Alzheimer’s disease
AU - Canobbio, Ilaria
AU - Abubaker, Aisha Alsheikh
AU - Visconte, Caterina
AU - Torti, Mauro
AU - Pula, Giordano
PY - 2015/3/3
Y1 - 2015/3/3
N2 - 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.
AB - 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.
KW - Alzheimer’s disease
KW - Amyloid peptides
KW - Cerebrovascular disease
KW - Platelets
KW - Vascular cells
UR - http://www.scopus.com/inward/record.url?scp=84925061509&partnerID=8YFLogxK
UR - http://dx.doi.org/10.3389/fncel.2015.00065
U2 - 10.3389/fncel.2015.00065
DO - 10.3389/fncel.2015.00065
M3 - Article
AN - SCOPUS:84925061509
VL - 9
JO - Frontiers in Cellular Neuroscience
JF - Frontiers in Cellular Neuroscience
SN - 1662-5102
IS - 65
ER -