Autor(es): Paulo, Sara L ; Miranda-Lourenço, Catarina ; Belo, Rita F. ; Rodrigues, Rui S. ; Fonseca-Gomes, João ; Tanqueiro, Sara ; Geraldes, Vera ; Rocha, Isabel ; Sebastião, Ana M ; Xapelli, Sara ; Diógenes, Maria José
Data: 2021
Identificador Persistente: http://hdl.handle.net/10451/50686
Origem: Repositório da Universidade de Lisboa
Assunto(s): Aging; Brain-derived neurotrophic factor (BDNF); High caloric diet; Hippocampal plasticity; Memory; Neurogenesis; Obesity
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.
