1Lack of Limbic-predominant Age-related TDP-43 Encephalopathy (LATE) neuropathological changes in agedmacaques with memory impairmentMorgane Darricau1,Marie-Hélène Canron1, Marion Bosc2, Marie-Laure Arotçarena1, Mégane Le Quang1,3,Benjamin Dehay1,Erwan Bezard1,2and Vincent Planche1,31. Univ. Bordeaux, CNRS, IMN, UMR 5293, F-33000Bordeaux, France. 2. Motac Neuroscience, F-33000 Bordeaux, France3. Centre Mémoire Ressources Recherches, Pôle de Neurosciences Cliniques, CHU de Bordeaux, F-33000 Bordeaux, FranceAbstractThe neuropathological changes of limbic-predominant age-related TDP-43 encephalopathy (LATE) arefrequent inthe agedpopulationand arenow 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 agedmemory-impaired rhesus macaques (Macacamulatta,18 to 32years old) from two different cohorts. While present in anFTLD-TDP case used as a positive control for immunostaining, we found no TDP-43 or phosphorylated TDP-43immunoreactive neuronal cytoplasmic inclusion in the amygdala or the hippocampus of these aged animals (as well as in young and mature macaquesused as negative controls). We concluded that LATE is probablya human-specific condition, such as many other proteinopathies, and does not participate in age-related memory impairment in non-human primates.