Overview of age-related changes in psychomotor and cognitive functions in a prosimian primate, the gray mouse lemur (Microcebus murinus): Recent advances in risk factors and antiaging interventions

Aging is not homogeneous in humans and the determinants leading to differences between subjects are not fully understood. Impaired glucose homeostasis is a major risk factor for cognitive decline in middle-aged humans, pointing at the existence of early markers of unhealthy aging. The gray mouse lemur (Microcebus murinus), a small lemuriform Malagasy primate, shows relatively slow aging with decreased psychomotor capacities at middle-age (around 5-year old). In some cases (similar to 10%), it spontaneously leads to pathological aging. In this case, some age-related deficits, such as severe cognitive decline, brain atrophy, amyloidosis, and glucoregulatory imbalance are congruent with what is observed in humans. In the present review, we inventory the changes occurring in psychomotor and cognitive functions during healthy and pathological aging in mouse lemur. It includes a summary of the cerebral, metabolic, and cellular alterations that occur during aging and their relation to cognitive decline. As nutrition is one of the major nonpharmacological antiaging strategies with major potential effects on cognitive performances, we also discuss its role in brain functions and cognitive decline in this species. We show that the overall approach of aging studies in the gray mouse lemur offers promising ways of investigation for understanding, prevention, and treatments of pathological aging in humans.

Automated summary

Gray mouse lemur, a species with relatively slow aging, presents similarities to human pathological aging in terms of cognitive decline, brain atrophy, amyloidosis, and glucoregulatory imbalance. Studying aging in mouse lemurs offers promising insights for understanding, preventing, and treating pathological aging in humans, with potential focus on nutrition as a nonpharmacological antiaging strategy.