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Review
. 2015 Apr 10:9:124.
doi: 10.3389/fncel.2015.00124. eCollection 2015.

Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases

Miguel Chin-Chan  1 , Juliana Navarro-Yepes  1 , Betzabet Quintanilla-Vega  1
Affiliations
Review

Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases

Miguel Chin-Chan et al. Front Cell Neurosci. .

Abstract

Neurodegenerative diseases including Alzheimer (AD) and Parkinson (PD) have attracted attention in last decades due to their high incidence worldwide. The etiology of these diseases is still unclear; however the role of the environment as a putative risk factor has gained importance. More worryingly is the evidence that pre- and post-natal exposures to environmental factors predispose to the onset of neurodegenerative diseases in later life. Neurotoxic metals such as lead, mercury, aluminum, cadmium and arsenic, as well as some pesticides and metal-based nanoparticles have been involved in AD due to their ability to increase beta-amyloid (Aβ) peptide and the phosphorylation of Tau protein (P-Tau), causing senile/amyloid plaques and neurofibrillary tangles (NFTs) characteristic of AD. The exposure to lead, manganese, solvents and some pesticides has been related to hallmarks of PD such as mitochondrial dysfunction, alterations in metal homeostasis and aggregation of proteins such as α-synuclein (α-syn), which is a key constituent of Lewy bodies (LB), a crucial factor in PD pathogenesis. Common mechanisms of environmental pollutants to increase Aβ, P-Tau, α-syn and neuronal death have been reported, including the oxidative stress mainly involved in the increase of Aβ and α-syn, and the reduced activity/protein levels of Aβ degrading enzyme (IDE)s such as neprilysin or insulin IDE. In addition, epigenetic mechanisms by maternal nutrient supplementation and exposure to heavy metals and pesticides have been proposed to lead phenotypic diversity and susceptibility to neurodegenerative diseases. This review discusses data from epidemiological and experimental studies about the role of environmental factors in the development of idiopathic AD and PD, and their mechanisms of action.

Keywords: Alzheimer’s diseases; Parkinson’s disease; alpha-synuclein; beta-amyloid; metals; neurodegenerative disorders; pesticides; tau protein.

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Figures

Figure 1
Figure 1
Environmental factors associated with Alzheimer’s disease (AD) development through different mechanisms. Several factors including metals, pesticides, nanoparticles, and diet can affect the two targets of AD such as Aβ generation and Tau phosphorylation. The figure depicts the molecular targets than can be modified at different levels following the amyloid hypothesis that ends in Aβ senile plaques formation (upper part) or the hyperphosphorylation of Tau protein and its subsequent deposition as neurofibrillary tangles (NFTs) (lower part). For more detail see the text.
Figure 2
Figure 2
Molecular mechanisms altered by environmental factors related to increased Parkinson’s disease risk. Exposure to environmental toxicants mainly pesticides, metals and solvents may lead to the selective loss of dopaminergic neurons on the substantia nigra pars compacta (SNpc) through the dysregulation/alteration of the molecular mechanisms implicated on PD development such as mitochondrial dysfunction, impairment of protein quality pathways, microglia activation and inflammation, which converge in the production of oxidative stress as the main factor in PD. For more detail see the text.
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