%0 Journal Article
%T Brains of rhesus monkeys display A¦Â deposits and glial pathology while lacking A¦Â dimers and other Alzheimer's pathologies
%A Baian Chen
%A Jianping Jia
%A Jing Lu
%A Jing Zhang
%A Liming Zhu
%A Qiao Zhao
%A Quan Sun
%A Shubo Wang
%A Wei Qin
%A Yanhua Qiao
%A Yi Wu
%A Zitong Yao
%J Archive of "Aging Cell".
%D 2019
%R 10.1111/acel.12978
%X Cerebral amyloid beta (A¦Â) deposits are the main early pathology of Alzheimer's disease (AD). However, abundant A¦Â deposits also occur spontaneously in the brains of many healthy people who are free of AD with advancing aging. A crucial unanswered question in AD prevention is why AD does not develop in some elderly people, despite the presence of A¦Â deposits. The answer may lie in the composition of A¦Â oligomer isoforms in the A¦Â deposits of healthy brains, which are different from AD brains. However, which A¦Â oligomer triggers the transformation from aging to AD pathogenesis is still under debate. Some researchers insist that the A¦Â 12©\mer causes AD pathology, while others suggest that the A¦Â dimer is the crucial molecule in AD pathology. Aged rhesus monkeys spontaneously develop A¦Â deposits in the brain with striking similarities to those of aged humans. Thus, rhesus monkeys are an ideal natural model to study the composition of A¦Â oligomer isoforms and their downstream effects on AD pathology. In this study, we found that A¦Â deposits in aged monkey brains included 3©\mer, 5©\mer, 9©\mer, 10©\mer, and 12©\mer oligomers, but not 2©\mer oligomers. The A¦Â deposits, which were devoid of A¦Â dimers, induced glial pathology (microgliosis, abnormal microglia morphology, and astrocytosis), but not the subsequent downstream pathologies of AD, including Tau pathology, neurodegeneration, and synapse loss. Our results indicate that the A¦Â dimer plays an important role in AD pathogenesis. Thus, targeting the A¦Â dimer is a promising strategy for preventing AD
%K aging
%K Alzheimer's disease
%K amyloid beta (A¦Â) deposits
%K A¦Â oligomer
%K gliosis
%K tau pathology
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6612634/