- Perinatal Pb exposure significantly increased diffuse amyloid beta and Aβ-positive cells in the 18-month murine cortex.
- Pb-associated metabolite changes observed in plasma and cortex at 3 weeks and 18 months implicate oxidative stress, inflammation, and lipid metabolism.
- Developmental Pb exposure linked to molecular and metabolic features characteristic of dementia, suggesting mechanisms by which early exposure may increase dementia risk.
Alzheimers Dement. 2026 Sep;22(9):e71791. doi: 10.1002/alz.71791.
ABSTRACT
INTRODUCTION: Developmental neurotoxicant exposures (e.g., lead [Pb]) are suspected contributors to dementia. Dementia is characterized by amyloid beta (Aβ) plaques and dysregulated metabolism. To better understand the relationship between environment and dementia risk, we assessed the impact of perinatal Pb exposure on dementia-related outcomes in the murine brain.
METHODS: Female mice were exposed to 32 ppm Pb or control water during gestation and lactation. Offspring were aged out to 3 weeks or 18 months. We measured Aβ in the 18-month cortex and performed untargeted metabolomics in plasma and cortex at 3 weeks and 18 months of age.
RESULTS: Diffuse Aβ and Aβ-positive cells were significantly elevated with Pb exposure. Pb-associated metabolites were enriched for those implicated in oxidative stress, inflammation, and lipid metabolism.
DISCUSSION: Pb was associated with molecular and metabolic features of dementia. Important biochemical classes provide insights into possible mechanisms by which developmental Pb exposure may contribute to dementia risk.
PMID:42669632 | DOI:10.1002/alz.71791
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