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Aging in a highly polluted world: challenges and solutions to prevent Alzheimer's disease
Original title: Aging in a highly polluted world: challenges and solutions to prevent Alzheimer’s disease
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This review pulls together existing research showing that pollution—including air pollution, heavy metals, pesticides, and even microplastics—may contribute to Alzheimer's disease by damaging the brain over decades, sometimes starting as early as childhood in people who grow up in heavily polluted areas. This matters because it suggests some Alzheimer's risk isn't just genetic or age-related, but tied to environmental exposures we can potentially reduce through personal choices and public policy, making prevention possible earlier in life than previously thought.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder globally and a leading cause of disability and death among the elderly. As populations age worldwide, the epidemiological burden of AD is expected to more than double by 2050, surpassing 150 million affected individuals. While genetic susceptibility, particularly the apolipoprotein E ε4 (APOE4) allele, modulates individual risk, most AD cases are late-onset and shaped by complex interactions between genetic background and modifiable environmental exposures. Environmental pollution has emerged as a critical and potentially preventable contributor to this burden. The 2024 Lancet Commission on Dementia Prevention, Intervention, and Care has identified 14 modifiable risk factors, with air pollution explicitly included. Drawing on evidence from human epidemiological cohorts, experimental animal models, and in vitro neuronal/glial systems, the present review aims to synthesize mechanistic evidence linking environmental pollutant classes to AD-relevant neuropathology. The review examines the growing body of evidence linking major categories of environmental pollutants (ambient particulate matter, heavy metals, pesticides, PFAS, and emerging contaminants including microplastics and nanoplastics) to AD risk and pathogenesis. Special attention is given to studies showing that the characteristic neuropathological features of AD may emerge in children and young adults chronically exposed to heavily polluted urban environments, which highlights critical concerns about when and how these changes develop throughout life. Shared mechanistic pathways through which environmental pollutants promote neurodegeneration are discussed, including neuroinflammation, oxidative stress, blood-brain barrier disruption, tau kinase dysregulation, epigenetic reprogramming, and gut-brain axis dysbiosis. The review also examines the amplifying role of biological aging on neurotoxic vulnerability and proposes a comprehensive, multi-level prevention framework addressing individual exposure reduction, clinical risk identification, and population-level policy interventions.
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This review examines how common environmental pollutants — including heavy metals, pesticides, and microplastics — contribute to Alzheimer's disease risk by damaging neurons, triggering inflammation, and promoting the hallmark protein buildups (amyloid-beta and tau) seen in the disease. Microplastics are identified as an emerging neurotoxic pollutant alongside more established chemicals. The evidence adds to growing concern that everyday environmental exposures, not just genetics, play a meaningful role in driving dementia.
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