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Linking cognition to age and amyloid-β burden in the brain of a nonhuman primate (Microcebus murinus)
Neurobiol Aging. 2020 Oct;94:207-216. doi: 10.1016/j.neurobiolaging.2020.03.025.
Daniel Schmidtke 1, Elke Zimmermann 2, Stéphanie G Trouche 3, Pascaline Fontès 3, Jean-Michel Verdier 3, Nadine Mestre-Francés 3
Abstract:
The gray mouse lemur (Microcebus murinus) is a valuable model in research on age-related proteopathies. This nonhuman primate, comparable to humans, naturally develops tau and amyloid-β proteopathies during aging. Whether these are linked to cognitive alterations is unknown. Here, standardized cognitive testing in pairwise discrimination and reversal learning in a sample of 37 aged (>5 years) subjects was combined with tau and amyloid-β histochemistry in individuals that died naturally. Correlation analyses in successfully tested subjects (n = 22) revealed a significant relation between object discrimination learning and age, strongly influenced by outliers, suggesting pathological cases. Where neuroimmunohistochemistry was possible, as subjects deceased, the naturally developed cortical amyloid-β burden was significantly linked to pretraining success (intraneuronal accumulations) and discrimination learning (extracellular deposits), showing that cognitive (pairwise discrimination) performance in old age predicts the natural accumulation of amyloid-β at death. This is the first description of a direct relation between the cortical amyloid-β burden and cognition in a nonhuman primate.