Overview
Domingo and co-authors reviewed epidemiological and mechanistic evidence linking environmental toxic metals (lead, cadmium, arsenic, manganese, mercury), pesticides, air pollution particulates, and PFAS to Alzheimer’s disease pathogenesis. Each metal is discussed with respect to amyloid beta accumulation, tau hyperphosphorylation, neuroinflammation, and oxidative stress. Prevention strategies cited include dietary avoidance of contaminated foods and choosing organic produce and low-mercury fish. This is a mechanistic and epidemiological review without primary food concentration data.
Key findings
Lead, cadmium, arsenic, manganese, and mercury are each linked mechanistically to hallmark Alzheimer’s disease pathology in the reviewed epidemiological and animal model evidence. The review cites human cohort and animal model studies documenting metal accumulation in brain tissue and associations with cognitive decline endpoints. The review explicitly names dietary exposure as a primary route for most of these metals in the general population.
Prevention strategies in the review include choosing organic produce to reduce pesticide and cadmium exposure, selecting low-mercury fish, and reducing PFAS-containing cookware and food packaging use. These are framed as population-level prevention recommendations, not as clinical interventions.
Methods (brief)
Narrative review. No primary experiment. Evidence class: mechanistic and epidemiological review; no food occurrence data applicable to contamination profiling.
Evidence fitness
Supports: mechanistic context linking lead, cadmium, arsenic, manganese, and mercury to Alzheimer’s disease pathology; dietary exposure named as a primary exposure route. Does not support: food occurrence values, dose-response thresholds, or regulatory limit derivation.
Related evidence
Update history
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