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  • Title: Cerebral amyloid angiopathy and plaques, and visceral amyloidosis in aged macaques.
    Author: Uno H, Alsum PB, Dong S, Richardson R, Zimbric ML, Thieme CS, Houser WD.
    Journal: Neurobiol Aging; 1996; 17(2):275-81. PubMed ID: 8744409.
    Abstract:
    In the present study, we report our extended data on the incidence of two types of cerebral amyloidosis (plaques and plaques associated with angiopathy) and visceral amyloidosis in late adult and aged captive rhesus monkeys (Macaca mulatta). In a total of 81 brains from animals ranging from 16 to 39 years old, beta-amyloid plaques were found in 38, 10 of which were associated with amyloid angiopathy. Brains from eight adults, 16 to 19 years, had no lesions. In aged groups, the rates were 20.8% in the 20- to 25-year group (24), 60.9% in the 26- to 31-year group (41), and 100% in the 33- to 39-year group (8). Twelve monkeys in these aged groups had an involvement of amyloidosis in either the liver, the adrenal, or the pancreatic islets, and 7 of 12 had amyloid plaques (5) and plaques associated with cerebral angiopathy (2). No neurofibrillary tangles were detected in these brain lesions. Amyloid in both plaques and cerebral angiopathy showed immunocytochemical crossreactivity with human amyloid beta (beta/A4) and precursor proteins (APP-A4), but visceral amyloid was negative. Ultrastructurally, amyloid initially appears as loose filaments in the perivascular or Disse space, and they further aggregate to produce dense interlacing bundles. Cerebral amyloid angiopathy associated with plaque appears to be a subclass of senile plaque lesions in aged monkeys as well as in aged humans, and it appears to have no pathogenetic correlation with visceral amyloidosis.
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