Andrew W Johnson, Gregory J Zipfel, and Byung H Han
Cerebral amyloid angiopathy (CAA) occurs sporadically in elderly populations or in familial forms of Alzheimer’s disease (AD) and is characterized by insoluble deposition of amyloid-beta peptides (Aβ), within arterial vessels of the central nervous system. Amyloid precursor protein is processed by β- and γ-secretases generating Aβ1-40 and Aβ1-42 species that exist as soluble monomers, soluble oligomers (toxic intermediate species), and insoluble fibrils (principle component of CAA) [1]. Of interest, the co-morbidity and relationship between vascular compromise and neurodegenerative processes are not fully understood. CAA is an associated risk factor for intracerebral hemorrhage and ischemic stroke and also may contribute to the cognitive decline observed in aging, AD, or both [1]. Most AD cases feature early decreases in cerebral perfusion that may arise as a consequence of peripheral vascular disease (e.g., type II diabetes, hypertension) and/or loss of basalocortical cholinergic innervation that regulates cerebral blood flow (CBF) among other neurological functions [2]. Much remains to be understood concerning CAA-induced vasomotor impairment and its impact toward the occurrence and/or progression of impaired cognitive function within neurodegenerative disease.
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