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Climate Change, the Exposome and the Rising Burden of Neurodegenerative Diseases: A Review
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This review examines how climate change-driven events such as wildfires, flooding, and heat waves alter human exposure to environmental neurotoxicants including microplastics, heavy metals, and air pollutants, contributing to rising rates of neurodegenerative disease. It argues for an exposome-based framework that integrates climate and chemical risk assessment.
Dynamic shifts in global temperatures have increased the intensity of extreme weather events over many decades, leading to an increase in wildfires, drought, floods, intense hurricanes, longer hurricane seasons, damaging dust storms, humidity changes, decreasing foliage canopy, and altering crop patterns. Accelerated environmental changes can cause negative impacts on everyday human activities and living conditions leading to an increase in the likelihood of human exposure to anthropogenic chemicals: i.e., microplastics; insecticides, fungicides, and herbicides; and biological chemicals: i.e., algal toxins, these exposures are defined collectively as the “exposome”. Every human being is unique in their genetic makeup; therefore, individuals will respond differently to those chemical exposures. Intersecting with climate change is a global increase in neurodegenerative disorders. Exposure to specific compounds has been linked to various neurological diseases, such as dementia, Alzheimer’s, and Parkinson’s.
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This review synthesizes evidence from 2017 to 2024 on how climate change is accelerating the release, distribution, and toxicity of environmental contaminants including microplastics, heavy metals, and PFAS. The study suggests that rising temperatures, altered precipitation, permafrost thaw, and extreme weather events are amplifying contaminant mobility and creating new combined exposure risks for both ecosystems and human health.
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Researchers reviewed how microplastics cross the blood-brain barrier and accumulate in the central nervous system, cataloguing the mechanistic pathways — oxidative stress, neuroinflammation, protein aggregation — through which they may contribute to Alzheimer's, Parkinson's, and ALS, while proposing that environmental microplastic detection and removal technologies could be adapted for CNS applications.
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This review summarizes existing research on how pollutants, including air pollution, heavy metals, pesticides, and micro- and nanoplastics, may enter the brain and contribute to processes linked to Alzheimer's disease, such as protein buildup and inflammation. The authors note that most evidence comes from lab and animal studies, with limited research so far in humans.
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