Alzheimer’s Disease (AD) is a debilitating neurodegenerative disease that is diagnosed by gradual memory loss and certain cognitive impairments involving attention, reasoning, and language. Most of the research on Alzheimer’s disease focuses on the correlation of its neuropathological changes in the neurofibrillary tangles caused by hyper-phosphorylated tau protein and β-amyloid plaques with respect to cognitive impairment. Its pathology, however, remains incompletely understood. Currently, research has demonstrated that environmental factors such as biometals play a crucial role in exacerbating AD progression.
The present review examines the role of metals in AD progression and how metal dyshomeostasis attributes to AD pathogenesis. It was found that certain metals possess both beneficial and harmful properties in terms of AD progression. Depending upon the concentration of the metal of interest, copper, zinc, iron, and selenium have general beneficial properties. However, when present in excess, they can lead to oxidative stress and hyperphosphorylation of tau protein, amongst other harmful effects, while calcium and magnesium were seen to have beneficial effects by regulating biometal uptake.
In this review, we have provided evidential studies that focus on the involvement of certain metals in antioxidant pathways leading to the formation of reactive species indicative of neurodegeneration.