# Lead impairs long-term memory in Drosophila via mitochondrial oxidative stress in DAL neurons

- Published: 2026-11-05 23:25 UTC
- Section: Life & Health › Neurotechnology
- Tags: lead exposure, Drosophila melanogaster, long-term memory, mitochondrial redox homeostasis, DAL neurons, epigallocatechin gallate, memory consolidation, protein synthesis, neurotoxicity
- URL: https://realtech.media/news/rt-226ccc5b68e4719b7abb50a2_lead_impairs_long/

**In fruit flies, lead exposure in development and adulthood selectively impaired long-term memory, and the antioxidant epigallocatechin gallate restored it in the experiments.**

![Lead impairs long-term memory in Drosophila via mitochondrial oxidative stress in DAL neurons](https://sgzwpqqelzmajkcubgkl.supabase.co/storage/v1/object/public/rt-media/2026/11/1de008873472750c.jpg)
*USDAgov, Wikimedia Commons, Public domain*

Researchers report in Proceedings of the National Academy of Sciences that lead (Pb) exposure, both during development and in adulthood, selectively disrupts protein-synthesis-dependent long-term memory (LTM) in the fruit fly Drosophila melanogaster, while other memory forms are spared [1]. Lead remains a major environmental risk factor for cognitive dysfunction, but the cellular mechanisms of Pb-induced memory impairment are poorly understood.

Using a mitochondria-targeted redox biosensor, mito-roGFP2-Orp1, the authors found that lead elevates mitochondrial oxidative stress and disrupts redox homeostasis in cholinergic neurons and in dorsal-anterior-lateral (DAL) neurons, a critical locus for LTM consolidation [1]. This redox imbalance suppressed training-induced de novo protein synthesis in DAL neurons, which impaired memory consolidation [1].

Treatment with the antioxidant epigallocatechin gallate restored mitochondrial redox balance and rescued LTM by reinstating activity-dependent protein synthesis in DAL neurons, according to the authors [1]. The work was done in flies. The authors describe the model as a genetically tractable platform for studying neurotoxic mechanisms and for evaluating antioxidant-based strategies against Pb-induced cognitive dysfunction.

## Sources

1. [Proceedings of the National Academy of Sciences](https://doi.org/10.1073/pnas.2612578123)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-226ccc5b68e4719b7abb50a2_lead_impairs_long/