Emerging risk of environmental factors: insight mechanisms of Alzheimer's diseases

Environ Sci Pollut Res Int. 2020 Dec;27(36):44659-44672. doi: 10.1007/s11356-020-08243-z. Epub 2020 Mar 23.

Abstract

Neurodegenerative disorders are typically sporadic in nature in addition to usually influenced through an extensive range of environmental factors, lifestyle, and genetic elements. Latest observations have hypothesized that exposure of environmental factors may increase the prospective risk of Alzheimer's diseases (AD). However, the role of environmental factors as a possible dangerous issue has extended importance concerned in AD pathology, although actual etiology of the disorder is still not yet clear. Thus, the aim of this review is to highlight the possible correlation between environmental factors and AD, based on the present literature view. Environmental risk factors might play an important role in decelerating or accelerating AD progression. Among well-known environmental risk factors, prolonged exposure to several heavy metals, for example, aluminum, arsenic, cadmium, lead, and mercury; particulate air, and some pesticides as well as metal-containing nanoparticles have been participated to cause AD. These heavy metals have the capacity to enhance amyloid β (Aβ) peptide along with tau phosphorylation, initiating amyloid/senile plaques, as well as neurofibrillary tangle formation; therefore, neuronal cell death has been observed. Furthermore, particulate air, pesticides, and heavy metal exposure have been recommended to lead AD susceptibility and phenotypic diversity though epigenetic mechanisms. Therefore, this review deliberates recent findings detailing the mechanisms for a better understanding the relationship between AD and environmental risk factors along with their mechanisms of action on the brain functions.

Keywords: Alzheimer’s diseases; Amyloid β; Environmental factors; Tau phosphorylation.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease*
  • Amyloid beta-Peptides / metabolism
  • Epigenesis, Genetic
  • Humans
  • Phosphorylation
  • Prospective Studies

Substances

  • Amyloid beta-Peptides