Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review

Abstract

The environment has been implicated to be a strong determinant of brain health with higher risk of neurodegeneration. The drastic rise in the prevalence of neurodegenerative diseases (NDDs) including Alzheimer's disease (AD), Parkinson's disease (PD), autism spectrum disorder (ASD), multiple sclerosis (MS) etc., supports the idea that environmental factors may play a major role in NDDs aetiology. Nickel is one of the listed environmental metals reported to pose a serious threat to human health. This paper reported available studies on nickel level in NDDs covering both animal and human studies. Different databases were searched for articles reporting the main neurotoxicity mechanisms and the concentration of nickel in fluids and tissues of NDDs patients compared to controls. Data were extracted and synthesized by ensuring the articles were related to nickel and NDDs. Various mechanisms were reported as oxidative stress, disturbances in mitochondrial membrane potential, trace elements homeostasis destabilization, etc. Nickel was found elevated in biological fluids as blood, serum/plasma and CSF and in the brain of NDDs, as a consequence of unintentional exposure thorough nickel-contaminated air, food, water, and skin contact. In addition, after exposure to nickel, the concentration of markers of lipid peroxidation were increased, while some antioxidant defence systems decreased. Thus, the reduction in the exposure to nickel contaminant may hold a promise in reducing the incidence of NDDs.

Keywords: Biomarkers; Environmental exposure; Mitochondrial dysfunctions; Neurotoxicity; Nickel; Oxidative stress.

Fig. 1

Flow chart showing the number of selected articles.

Fig. 2

Potential mechanisms of nickel involvement in neurotoxicity ROS: reactive species oxygen; ATP: adenosine triphosphate; mtDNA: mitochondrial DNA; GABA: Gamma-aminobutyric acid; RNS: reactive nitrogen species; NCAD: N-cadherin; LPO: lipid peroxidation; NO: nitric oxide; SOD: superoxide dismutase; CAT: catalase; IL-1β: interleukin-1beta; IL-6:: interleukin-6; TNF-α: tumor necrosis factor-alpha.