Review: sporadic cerebral amyloid angiopathy.

摘要: Cerebral amyloid angiopathy (CAA) may result from focal to widespread amyloid-β protein (Aβ) deposition within leptomeningeal and intracortical cerebral blood vessels. In addition, pericapillary Aβ refers depositions in the glia limitans adjacent neuropil, whereas capillary CAA are present wall. cause lobar intracerebral haemorrhages microbleeds. Hypoperfusion reduced vascular autoregulation due might infarcts white matter lesions. thus causes lesions that potentially lead (vascular) dementia further contribute by impeding clearance of solutes out brain transport nutrients across barrier. Severe is an independent risk factor for cognitive decline. The clinical diagnosis based on assessment associated cerebrovascular perivascular spaces concentrations both Aβ(40) Aβ(42) cerebrospinal fluid prove be suggestive CAA. Transgenic mouse models overexpress human precursor show parenchymal CAA, corroborating current concept pathogenesis: neuronal enters drainage pathway accumulate vessel walls increased amounts and/or decreased Aβ, respectively. We suggest represents early impairment while with transendothelial Aβ. plays important role multimorbid condition ageing but its contribution neurodegeneration remains elucidated.