Magnesium (Mg) is a crucial divalent cation with more than 300 cellular functions. This ion shows therapeutic properties in several neurological diseases. Although there are numerous basic evidences showing that Mg can inhibit pathological processes involved in neuroglial degeneration, this low-cost option is not well-considered in clinical research and practice for now. Nevertheless, none of the expensive drugs currently recommended by the classic guidelines (in addition to physiological rehabilitation) had shown exceptional effectiveness. Herein, focusing on Alzheimer's disease (AD), we analyze the therapeutic pathways that support the use of Mg for neurogenesis and neuroprotection. According to experimental findings reviewed, Mg shows interesting abilities to facilitate toxin clearance, reduce neuroinflammation, inhibit the pathologic processing of amyloid protein precursor (APP) as well as the abnormal tau protein phosphorylation, and to reverse the deregulation of N-methyl-D-aspartate receptors. Currently, some crucial details of the mechanisms involved in these proved effects remain elusive and clinical background is poor. Therefore, further studies are required to enable a better overview on pharmacodynamic targets of Mg and thus, to find optimal pharmacologic strategies for clinical use of this ion.
Keywords: Alzheimer's disease; Magnesium; NMDA; Neurodegeneration; β-Amyloid.
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