ArticleEnvironmental health perspectives2024
Lead Acetate Exposure and Cerebral Amyloid Accumulation: Mechanistic Evaluations in APP/PS1 Mice.
Article in Environmental health perspectives, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.Current opinion in neurobiology · 2026Review
- Iron toxicity potentiates cell-type specific amyloid beta proteotoxicity inbioRxiv : the preprint server for biology · 2026Article
- Endothelial PAI-1 Drives Lead-Induced Cerebral Amyloid Angiopathy via Activation of C3Biology · 2026Article
- Urate-lowering effect of delphinidin-3-glucoside in red kidney beans via binding to the FAD site of the XO enzyme.Journal of advanced research · 2026Article
- Neurotoxicity of heavy metals across the lifespan: The beneficial role of nutrition from fetus to the elderly.Advances in neurotoxicology · 2026Article
- Lead-induced hypertension and cognitive dysfunction: brain amyloid pathology.European journal of medical research · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundThe role of environmental factors in Alzheimer's disease (AD) pathogenesis remains elusive. Mounting evidence suggests that acute and past exposure to the environmental toxicant lead (Pb) is associated with longitudinal decline in cognitive function, brain atrophy, and greater brain
objectivesThis study investigates the role of Pb in the pathogenesis of cerebral amyloid angiopathy (CAA) and whether plasminogen activator inhibitor-1 (PAI-1) contributes to this process in the APP/PS1 mouse model.
methodsFemale APP/PS1 mice at 8 wk of age were administered either
resultsAPP/PS1 mice (an AD mice model) exposed to PbAc demonstrated more vascular amyloid deposition less neocortical myelination, and lower cognitive function, as well as greater vascular binding to DISCUSSION: Our findings suggest that PbAc induced CAA/AD pathogenesis via the PAI-1 signaling in the APP/PS1 mouse model, and the inhibition of PAI-1 could be a potential therapeutic target for PbAc-mediated CAA/AD disorders. https://doi.org/10.1289/EHP14384.
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