Background and Purpose--The present study assessed -amyloid (A) 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 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, A40, and A42 aggregates in the cortex and thalamus by immunohistochemical techniques.

Results--The load of A aggregates did not display a significant association with cerebrovascular lesions. The load of A, A40, and A42 aggregates increased with age, and there was a tendency toward higher odds ratios for A 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 aggregates, the load of thalamic A42 was significantly higher than the load of A40.

Conclusions--Our findings indicate that cerebrovascular disease does not influence the load of A, whereas a shift of aggregation from the A40 to the A42 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 production, its insufficient elimination, or other susceptibility factors.