High-caloric diet Induces memory impairment and disrupts synaptic plasticity in aged rats

• Published in: Current issues in molecular biology Vol. 43; no. 3; pp. 2305 - 2319
• Main Authors: Paulo, Sara, Miranda Lourenço, Catarina, Belo, Rita, Rodrigues, Rui S, Fonseca-Gomes, João, Tanqueiro, Sara, Geraldes, Vera, rocha, isabel, Sebastião, Ana M, Xapelli, Sara, de Oliveira Diógenes Nogueira, Maria José
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI 18.12.2021; MDPI AG
• Subjects: Age Factors; Aging; Animals; Biomarkers; Brain - metabolism; brain-derived neurotrophic factor; Brief Report; Diet; Disease Models, Animal; Eating; High caloric diet; Hippocampal plasticity; Immunohistochemistry; Male; Memory; Memory Disorders - etiology; Neurogenesis; Neuronal Plasticity; Obesity; Rats; memory; high caloric diet; neurogenesis; aging; brain-derived neurotrophic factor; hippocampal plasticity; obesity
• ISSN: 1467-3045; 1467-3037; 1467-3045
• DOI: 10.3390/cimb43030162

© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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. This research was funded by Santa Casa da Misericórdia de Lisboa—MB37-2017; Fundação para a Ciência e a Tecnologia (FCT)—IF/01227/2015; and it received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 952455. Researchers were supported by the following: S.L.P.—FCT (PD/BD/150341/2019); C.M.-L.—FCT (SFRH/BD/118238/2016) and Universidade de Lisboa (BD2015); R.F.B.—FCT (PD/BD/114337/2016); R.S.R.—FCT (SFRH/BD/129710/2017); S.R.T.—FCT (SFRH/BD/128091/2016).