β-amyloid aggregation in human brains with cerebrovascular lesions

Background and Purpose - The present study assessed beta-amyloid (A beta) protein aggregates in postmortem human brains in subjects who had experienced stroke to examine the proposed association between ischemic stress and the accumulation of A beta reported in rodents. Methods - A sample of 484 postmortem brains from nondemented subjects, lacking isocortical neurodegenerative pathology with verified cerebrovascular lesions, and 57 age-matched controls were assessed with respect to A beta, A beta 40, and A beta 42 aggregates in the cortex and thalamus by immunohistochemical techniques. Results - The load of A beta aggregates did not display a significant association with cerebrovascular lesions. The load of A beta, A beta 40, and A beta 42 aggregates increased with age, and there was a tendency toward higher odds ratios for A beta aggregates, though not statistically significant, in subjects with acute cerebrovascular lesions. In the oldest subjects with cerebrovascular lesions and with both thalamic and cortical A beta aggregates, the load of thalamic A beta 42 was significantly higher than the load of A beta 40. Conclusions - Our findings indicate that cerebrovascular disease does not influence the load of A beta, whereas a shift of aggregation from the A beta 40 to the A beta 42 residue is noted in the thalamus but only in aged subjects. It is impossible, however, to state whether this result is attributable to increased A beta production, its insufficient elimination, or other susceptibility factors.