Relative paucity of tau accumulation in the small areas with abundant Abeta42-positive capillary amyloid angiopathy within a given cortical region in the brain of patients with Alzheimer pathology.

Cerebral amyloid angiopathy (CAA) is a manifestation of amyloid beta-protein (Abeta) accumulation in the elderly as well as in patients with Alzheimer's disease (AD). Two types of CAA have been noted, based on the type of vasculature in which Abeta is deposited: cerebral capillary amyloid angiopathy (capCAA) and non-capCAA. Non-capCAA is a common form of CAA that consists of Abeta deposited in arteries and arterioles. Recent information on Abeta metabolism in the brain suggests that non-capCAA is associated with Abeta secretion into the cerebrospinal fluid via the perivascular space, whereas capCAA is associated with Abeta removal to blood plasma via the capillary endothelium. Abeta40, a major and relatively soluble Abeta isoform, is deposited predominantly in non-capCAA, and Abeta42, which is insoluble and associated more closely than Abeta40 with AD, is deposited predominantly in capCAA. Studying small areas of microscopic size within a given cortical region, we found an inverse association of capCAA and senile plaques. We also found a relative paucity of tau pathology in the small areas with abundant capCAA compared with the small areas with abundant senile plaques within a cortical region with the same cytoarchitecture. We suppose that both capCAA and senile plaques indicate high Abeta42 in the neuropil but that only Abeta42 in the form of insoluble deposits in senile plaques promotes tau abnormality.