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 r
hesus monkeys (Macaca mulatta). In a total of 81 brains from animals r
anging from 16 to 39 years old, beta-amyloid plaques were found in 38,
10 of which were associated with amyloid angiopathy. Brains from eigh
t adults, 16 to 19 years, had no lesions. In aged groups, the rates we
re 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 l
iver, the adrenal, or the pancreatic islets: and 7 of 12 had amyloid p
laques (5) and plaques associated with cerebral angiopathy (2). No neu
rofibrillary tangles were detected in these brain lesions. Amyloid in
both plaques and cerebral angiopathy showed immunocytochemical crossre
activity with human amyloid beta (beta/A4) and precursor proteins (APP
-A4), but visceral amyloid was negative. Ultrastructurally, amyloid in
itially appears as loose filaments in the perivascular or Disse space:
and they further aggregate to produce dense interlacing bundles. Cere
bral amyloid angiopathy associated with plaque appears to be a subclas
s of senile plaque lesions in aged monkeys as well as in aged humans,
and it appears to have no pathogenetic correlation with visceral amylo
idosis.