Journal
NEUROBIOLOGY OF AGING
Volume 107, Issue -, Pages 53-56Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2021.07.009
Keywords
TDP-43; LATE; Aging; Non-human primate
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Funding
- Foundation Bettencourt Schueller (CCA-Inserm-Bettencourt)
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Through studying the brain tissues of aged rhesus macaques, it was found that LATE may be a human-specific condition and does not contribute to age-related memory impairment in non-human primates.
The neuropathological changes of limbic-predominant age-related TDP-43 encephalopathy (LATE) are frequent in the aged population and are now recognized as a cause of memory impairment. However, it remains unknown if this proteinopathy is also present in other primate species. We thus investigated the presence and distribution of TDP-43 pathology in the hippocampus and amygdala of 7 aged memoryimpaired rhesus macaques ( Macaca mulatta, 18-32 years old) from 2 different cohorts. While present in an FTLD-TDP case used as a positive control for immunostaining, we found no TDP-43 or phosphorylated TDP-43 immunoreactive neuronal cytoplasmic inclusion in the amygdala or the hippocampus of these aged animals (as well as in young and mature macaques used as negative controls). We concluded that LATE is probably a human-specific condition, such as many other proteinopathies, and does not participate in age-related memory impairment in non-human primates. (c) 2021 Elsevier Inc. All rights reserved.
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