ArticleFrontiers in toxicology2026
ALDH1/2 deficiency modulates dieldrin-induced dopaminergic neurodegeneration and reactive glial morphometry in male mice.
Article in Frontiers in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The etiology of Parkinson's disease (PD) is associated with exposure to environmental contaminants, including the organochlorine pesticide dieldrin. This is thought to occur through induction of oxidative damage and dysregulation of dopamine homeostasis via impairment of aldehyde dehydrogenase (ALDH) enzymes, resulting in neuronal stress that may contribute to glial-mediated neurotoxicity. We postulated that sub-chronic murine dieldrin exposure would induce PD-relevant histopathologic changes in the substantia nigra (SN) which would be exacerbated in ALDH-deficient mice. To test this hypothesis, six-month-old wildtype and Aldh1a1
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