{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yue T"],"funding":["JSPS KAKENHI","AMED","JST SPRING"],"pagination":["e1011818"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12370196"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(8)"],"pubmed_abstract":["High-fat diet (HFD) is considered a risk factor for age-related memory impairments such as Alzheimer's disease. However, how HFD affects memory formation remains unclear. In this study, we established a model of memory defects caused by HFD in Drosophila. Our results revealed that the HFD impaired intermediate-term memory (ITM), but not short-term memory (STM), produced by classical aversive olfactory conditioning, and decreased autophagic activity in the heads of the HFD-fed flies. Transient reduction in autophagic activity also impaired ITM, but not STM. Genetic enhancement of autophagic activity in neurons effectively restored ITM performance in the HFD-fed flies. Mechanistically, HFD impairs lysosomal function by downregulating the expression of lysosome-related genes, leading to impaired fusion of autophagosomes with lysosomes. These findings suggest that HFD impairs ITM by reducing autophagic activity and lysosomal dysfunction in the neurons."],"journal":["PLoS genetics"],"pubmed_title":["High-fat diet impairs intermediate-term memory by autophagic-lysosomal dysfunction in Drosophila."],"pmcid":["PMC12370196"],"funding_grant_id":["JP24K22013","JP21H02621","JP22H05485","JP22gm6710006h0001","JP22gm6110024h0004","JPMJSP2109","JP22H02715"],"pubmed_authors":["Yue T","Tonoki A","Itoh M","Onuki K","Jiang M"],"additional_accession":[]},"is_claimable":false,"name":"High-fat diet impairs intermediate-term memory by autophagic-lysosomal dysfunction in Drosophila.","description":"High-fat diet (HFD) is considered a risk factor for age-related memory impairments such as Alzheimer's disease. However, how HFD affects memory formation remains unclear. In this study, we established a model of memory defects caused by HFD in Drosophila. Our results revealed that the HFD impaired intermediate-term memory (ITM), but not short-term memory (STM), produced by classical aversive olfactory conditioning, and decreased autophagic activity in the heads of the HFD-fed flies. Transient reduction in autophagic activity also impaired ITM, but not STM. Genetic enhancement of autophagic activity in neurons effectively restored ITM performance in the HFD-fed flies. Mechanistically, HFD impairs lysosomal function by downregulating the expression of lysosome-related genes, leading to impaired fusion of autophagosomes with lysosomes. These findings suggest that HFD impairs ITM by reducing autophagic activity and lysosomal dysfunction in the neurons.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-04-08T05:32:43.471Z","creation":"2026-04-07T22:33:23.202Z"},"accession":"S-EPMC12370196","cross_references":{"pubmed":["40825051"],"doi":["10.1371/journal.pgen.1011818"]}}