Alzheimer's disease pathology influences severity and topographical distribution of cerebral amyloid angiopathy

Cerebral amyloid angiopathy (CAA) is defined by beta-amyloid peptide (A beta) depositions in cerebral vessels and is associated with Alzheimer's disease (AD). The relationship between sporadic CAA and AD, and the origin of A beta in CAA are poorly understood. The aim of our study was to investigate the relationship between CAA and AD. Autopsy brains (n=113, 61.1% female, 55.8% clinically demented, age range 54-102 years, mean +/- SE 83.5 +/- 0.93 years) underwent standardized neuropathological assessment. CAA was evaluated in frontal, frontobasal, hippocampal, and occipital regions. Using immunohistochemistry, the severity of A beta deposition in vessels was assessed semiquantitatively for each region separately. Evaluation of APOE genotype in 53 cases using real-time PCR showed significant correlations with severe AD pathology and CAA. CAA was present in 77 cases (68.1%), with the occipital region being affected significantly more often and more severely than other regions (P<0.01). Of brains without AD pathology 23.5% revealed CAA, whereas 24% with AD pathology showed no CAA. In concordance with other studies, the severity of both AD pathology and CAA showed a low, but significant correlation. This correlation, however, was only caused by the significant increase of occipital CAA with increasing AD pathology (P<0.01), and was independent of APOE genotype. Our results suggest that progressing AD pathology not only increases the severity of CAA, but also shifts its topographical distribution towards the occipital cortex.