To assess whether amyloid plaque accumulation in the monkey brain can
account for age-related cognitive impairment that begins at about 20 y
ears of age, we measured plaque content in the brains of 14 rhesus mon
keys aged 5-30 years. We used immunohistochemistry employing the monoc
lonal antibody 6E10, which is specific to amino acids 1-17 of the amyl
oid beta peptide to identify amyloid plaques in serial coronal section
s of the forebrain. Amyloid plaques accumulate with age, starting at 2
5 years of age and escalating after 30 years. Until the age of 30, pla
ques are only found in a few monkeys and are relatively sparse. Result
s from our group and others show that plaque content and the proportio
n of individuals afflicted with amyloid plaques increase with age. Alt
hough both cognitive dysfunction and plaque content increase with age,
amyloid plaque content does not correlate with the cognitive dysfunct
ion observed in elderly monkeys since even in very old subjects some c
ognitively impaired animals have few amyloid plaques and others with a
bundant plaques show only minor cognitive impairments. in summary, amy
loid plaques appear to accumulate significantly only in monkeys over 2
5 years of age but do not appear to be a causal factor in age-related
cognitive decline of the normal aging rhesus monkey.