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High-fat diet impairs intermediate-term memory by autophagic-lysosomal dysfunction in Drosophila
Tong Yue1, Minrui Jiang1, Kotomi Onuki1
1Department of Biochemistry, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan.
Plos Genetics
|August 18, 2025
Summary
High-fat diets impair intermediate-term memory (ITM) by reducing neuronal autophagy and lysosomal function. Enhancing autophagy in neurons can restore memory function, suggesting a therapeutic target for diet-induced memory deficits.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- High-fat diets (HFD) are linked to age-related memory decline, including Alzheimer's disease.
- The precise mechanisms by which HFD impacts memory formation are not fully understood.
Purpose of the Study:
- To investigate the effects of HFD on memory formation in a Drosophila model.
- To elucidate the molecular pathways involved in HFD-induced memory impairment.
Main Methods:
- Utilized Drosophila melanogaster as a model organism for memory studies.
- Employed classical aversive olfactory conditioning to assess short-term memory (STM) and intermediate-term memory (ITM).
- Investigated autophagic activity and lysosomal function in fly brains.
Main Results:
- HFD selectively impaired ITM, but not STM.
- HFD reduced autophagic activity and impaired lysosomal function in fly heads.
- Genetic enhancement of neuronal autophagy rescued ITM deficits in HFD-fed flies.
- HFD downregulated lysosome-related genes, hindering autophagosome-lysosome fusion.
Conclusions:
- HFD negatively impacts intermediate-term memory formation.
- Reduced autophagic activity and lysosomal dysfunction are key mechanisms underlying HFD-induced memory impairment.
- Targeting neuronal autophagy presents a potential strategy to mitigate cognitive deficits associated with HFD.
