Lack of limbic-predominant age-related TDP-43 encephalopathy (LATE) neuropathological changes in aged macaques with memory impairment

• Published in: Neurobiology of aging 2021-11, Vol.107, p.53-56
• Main Authors: Darricau, Morgane, Canron, Marie-Hélène, Bosc, Marion, Arotçarena, Marie-Laure, Quang, Mégane Le, Dehay, Benjamin, Bezard, Erwan, Planche, Vincent
• Format: Article
• Language: English
• Subjects: Aging; Aging - metabolism; Aging - pathology; Aging - psychology; Animals; Brain Diseases - complications; Brain Diseases - pathology; DNA-Binding Proteins - metabolism; LATE; Life Sciences; Limbic System - metabolism; Limbic System - pathology; Macaca mulatta; Memory Disorders - etiology; Memory Disorders - pathology; Negative Results; Non–human primate; TDP-43; TDP-43 Proteinopathies - complications; TDP-43 Proteinopathies - pathology
• ISSN: 0197-4580; 1558-1497
• DOI: 10.1016/j.neurobiolaging.2021.07.009

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 memory-impaired 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.