Mercury (Hg), which is a non-essential element, is considered a highly toxic pollutant for biological systems even when present at trace levels. Elevated Hg exposure with the growing release of atmospheric pollutant Hg and rising accumulations of mono-methylmercury (highly neurotoxic) in seafood products have increased its toxic potential for humans. This review aims to highlight the potential relationship between Hg exposure and Alzheimer's disease (AD), based on the existing literature in the field. Recent reports have hypothesized that Hg exposure could increase the potential risk of developing AD. Also, AD is known as a complex neurological disorder with increased amounts of both extracellular neuritic plaques and intracellular neurofibrillary tangles, which may also be related to lifestyle and genetic variables. Research reports on AD and relationships between Hg and AD indicate that neurotransmitters such as serotonin, acetylcholine, dopamine, norepinephrine, and glutamate are dysregulated in patients with AD. Many researchers have suggested that AD patients should be evaluated for Hg exposure and toxicity. Some authors suggest further exploration of the Hg concentrations in AD patients. Dysfunctional signaling pathways in AD and Hg exposure appear to be interlinked with some driving factors such as arachidonic acid, homocysteine, dehydroepiandrosterone (DHEA) sulfate, hydrogen peroxide, glucosamine glycans, glutathione, acetyl-L carnitine, melatonin, and HDL. This evidence suggests the need for a better understanding of the relationship between AD and Hg exposure, and potential mechanisms underlying the effects of Hg exposure on regional brain functions. Also, further studies evaluating brain functions are needed to explore the long-term effects of subclinical and untreated Hg toxicity on the brain function of AD patients.
Keywords: Alzheimer’s disease; Mercury; Tau; β-Amyloid.