Neurofibrillary tangles and senile plaques in aged bears

LC Cork, RE Powers, DJ Selkoe… - … of Neuropathology & …, 1988 - academic.oup.com
LC Cork, RE Powers, DJ Selkoe, P Davies, JJ Geyer, DL Price
Journal of Neuropathology & Experimental Neurology, 1988academic.oup.com
In aged human beings and in individuals with age-associated degenerative disorders,
particularly Alzheimer's disease (AD), neurons develop cytoskeletal abnormalities, including
neurofibrillary tangles (NFT) and senile plaques (SP). Senile plaques occur in several
nonhuman species; however, NFT, with ultrastructural or immunocytochemical similarities to
those occurring in humans, have not been identified in other mammals. In this study of five
aged bears (Ursus, 20-30 years of age), we identified cytoskeletal abnormalities similar to …
Abstract
In aged human beings and in individuals with age-associated degenerative disorders, particularly Alzheimer's disease (AD), neurons develop cytoskeletal abnormalities, including neurofibrillary tangles (NFT) and senile plaques (SP). Senile plaques occur in several nonhuman species; however, NFT, with ultrastructural or immunocytochemical similarities to those occurring in humans, have not been identified in other mammals. In this study of five aged bears (Ursus, 20-30 years of age), we identified cytoskeletal abnormalities similar to those occurring in humans. An aged Asiatic brown bear had NFT, composed of straight 10-16-nm filaments, that were immunoreactive with antibodies directed against: phosphorylated epitopes of neurofilaments (NF); tau; A68 (a protein enriched in AD); and an antigen associated with paired helical filaments (PHF). An aged polar bear had numerous SP; neurites of these plaques were immunoreactive with antibodies against phosphorylated epitopes of NF, but NFT were not identified. These results indicate that nonprimate species develop age-related cytoskeletal abnormalities similar to those occurring in humans. Investigations of the comparative pathology of aged mammals may be useful in elucidating the pathogeneses of these abnormalities.
Oxford University Press