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