Abstract
Senile plaques (SP) are characteristic histopathological manifestations of Alzheimer's disease (AD), but are also found in normal aging (NA). Recent studies have demonstrated that beta amyloid (Aβ) proteins that have been truncated at the N-terminal position 3 (AβpN3) are the predominant component of SP in AD, but not in NA. The present study revealed that AβpN3 was deposited in an age-dependent manner in canine brains. Moreover, AβpN3 was the main component of the SP that developed in very old dogs. The deposition of AβpN3 increased in accordance with the number of SP, but that of N-terminally intact Aβ (AβN1) did not. In addition, AβpN3 was also deposited in the SP of a Japanese macaque and an American black bear, but not in a feline brain. Focal microvascular cerebral amyloid angiopathy was also observed in the deep cortices and the white matter of the dogs and a woodpecker. Those were always composed of both AβpN3 and AβN1. In conclusion, though non-human animals do not develop full pathology of AD of the human type, AβpN3 is widely deposited in the brains of senescent vertebrates.
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