At early stages of Alzheimer’s disease, before symptoms are present, accumulation of abnormal protein deposits (called amyloid plaques) and tangles of fibers (called neurofibrillary tangles) cause nerve cells in the brain to work less efficiently.
In cell and animal model systems, lead, cadmium, and manganese are neurotoxicants that contribute to canonical Alzheimer’s disease pathologies. Adult human epidemiologic studies have consistently shown lead, cadmium, and manganese are associated with impaired cognitive function and cognitive decline.
Manganese is one of the most abundant metals in the tissues of mammals and has been shown to function in many key biological processes. Manganese is an essential trace metal in the human body and has important biochemical and physiological functions as it is a cofactor for several important enzymes, such as glutamine synthetase, pyruvate carboxylase, arginase, and manganese superoxide dismutase.
However, it is toxic at low levels or in excess. Excess manganese in brain can be neurotoxic, implicated in several neurodegenerative disorders such as sporadic Alzheimer's disease.
Study published in Journal of Alzheimer’s Disease (42 (2014) 865–878), manganese was shown significantly higher levels in the parietal cortex of the Alzheimer’s disease brain, and there was a significant inverse correlation of cerebrospinal fluid (CSF) amyloid-β (Aβ) with Mn. Together, these studies suggest that high Mn could be a potential risk for Alzheimer's disease.
Manganese and Alzheimer’s Disease
