Lead impairs long-term memory by disrupting mitochondrial redox homeostasis in Drosophila.

Lead exposure in Drosophila melanogaster selectively disrupts protein-synthesis-dependent long-term memory, linked to elevated mitochondrial oxidative stress in cholinergic and DAL neurons.

• Why it matters: The cellular mechanism by which Pb causes cognitive dysfunction is unclear, limiting targeted strategies to prevent memory consolidation deficits.
• What they did: Developmental and adult-onset Pb exposure were tested for memory specificity, alongside mito-roGFP2-Orp1 imaging of mitochondrial redox in cholinergic and DAL neurons. Pb suppressed training-induced de novo protein synthesis in DAL neurons, and epigallocatechin gallate restored redox balance and reinstated activity-dependent protein synthesis.
• The result: Antioxidant treatment with epigallocatechin gallate rescues Pb-impaired LTM by reestablishing mitochondrial redox homeostasis and protein synthesis in DAL neurons. This supports mitochondrial redox dysregulation as a mechanism for Pb-related consolidation impairment and enables evaluation of antioxidant mitigation strategies.

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