ArticlePLoS genetics2025
High-fat diet impairs intermediate-term memory by autophagic-lysosomal dysfunction in Drosophila.
Article in PLoS genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Synaptic proteomics identifies cathepsin B as a regulator of synapse remodelling during learning.bioRxiv : the preprint server for biology · 2026Article
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5 authors.
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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.
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