Alzheimer’s dis ease (AD) is a leading cause of mortality in the developed world with 70% risk
attributable to genetics. The remaining 30% of AD risk is hypothesized to include environmental factors and
human lifestyle patterns. Environmental factors possibly include inorganic and organic hazards, exposure to
toxic metals (aluminium, copper), pesticides (organochlorine and organophosphate insecticides), industrial
chemicals (flame retardants) and air pollutants (particulate matter). Long term exposures to these
environmental contaminants together with bioaccumulation over an individual’s life-time are speculated to
induce neuroinflammation and neuropathology paving the way for developing AD. Epidemiologic associations between
environmental contaminant exposures and AD are still limited. However, many in vitro and animal studies have identified
toxic effects of environmental contaminants at the cellular level, revealing alterations of pathways and metabolisms
associated with AD that warrant further investigations. This review provides an overview of in vitro, animal and
epidemiological studies on the etiology of AD, highlighting available data supportive of the long hypothesized link
between toxic environmental exposures and development of AD pathology.
Keywords: Adult-onset disease, Alzheimer’s disease, endocrine disruptors, environmental contaminants, metals, neuropathology,
Parkinson's disease, pesticides, synergistic effects, toxins.
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