{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Paulo SL"],"funding":["Santa Casa da Misericórdia","Fundação para a Ciência e Tecnologia"],"pagination":["2305-2319"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8929079"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["43(3)"],"pubmed_abstract":["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."],"journal":["Current issues in molecular biology"],"pubmed_title":["High Caloric Diet Induces Memory Impairment and Disrupts Synaptic Plasticity in Aged Rats."],"pmcid":["PMC8929079"],"funding_grant_id":["MB37-2017","IF/01227/2015"],"pubmed_authors":["Tanqueiro SR","Paulo SL","Rocha I","Rodrigues RS","Geraldes V","Miranda-Lourenco C","Belo RF","Sebastiao AM","Diogenes MJ","Fonseca-Gomes J","Xapelli S"],"additional_accession":[]},"is_claimable":false,"name":"High Caloric Diet Induces Memory Impairment and Disrupts Synaptic Plasticity in Aged Rats.","description":"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.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2025-04-04T09:41:25.33Z","creation":"2025-04-04T09:41:25.33Z"},"accession":"S-EPMC8929079","cross_references":{"pubmed":["34940136"],"doi":["10.3390/cimb43030162"]}}