High Caloric Diet Induces Memory Impairment and Disrupts Synaptic Plasticity in Aged Rats

Sara L. Paulo, Catarina Miranda-Lourenço, Rita F. Belo, Rui S. Rodrigues, João Fonseca-Gomes, Sara R. Tanqueiro, Vera Geraldes, Isabel Rocha, Ana M. Sebastião, Sara Xapelli, Maria J. Diógenes
Current Issues in Molecular Biology. 2021-12-18; 43(3): 2305-2319
DOI: 10.3390/cimb43030162


The increasing consumption of sugar and fat seen over the last decades and the consequent overweight and obesity, were recently linked with a deleterious effect on cognition and synaptic function. A major question, which remains to be clarified, is whether obesity in the elderly is an additional risk factor for cognitive impairment. We aimed at unravelling the impact of a chronic high caloric diet (HCD) on memory performance and synaptic plasticity in aged rats. Male rats were kept on an HCD or a standard diet (control) from 1 to 24 months of age. The results showed that under an HCD, aged rats were obese and displayed significant long-term recognition memory impairment when compared to age-matched controls. Ex vivo synaptic plasticity recorded from hippocampal slices from HCD-fed aged rats revealed a reduction in the magnitude of long-term potentiation, accompanied by a decrease in the levels of the brain-derived neurotrophic factor receptors TrkB full-length (TrkB-FL). No alterations in neurogenesis were observed, as quantified by the density of immature doublecortin-positive neurons in the hippocampal dentate gyrus. This study highlights that obesity induced by a chronic HCD exacerbates age-associated cognitive decline, likely due to impaired synaptic plasticity, which might be associated with deficits in TrkB-FL signaling.

Auteurs Bordeaux Neurocampus