Neuroinflammation in Alzheimer’s Disease: The Emerging Modulatory Role of Magnesium

Alzheimer’s disease (AD) is a progressive and fatal neurodegenerative disorder and represents the most common form of dementia in the elderly population. In addition to amyloid-beta (Aβ) plaque accumulation and neurofibrillary tangle formation, growing evidence highlights neuroinflammation as a critical contributor to AD pathogenesis. Although neuroinflammation initially serves as a protective mechanism by promoting pathogen clearance and tissue repair, chronic and unresolved inflammatory responses may exacerbate neuronal damage and disease progression. Magnesium (Mg+2), an essential mineral involved in numerous enzymatic and cellular processes, has been shown to play an important role in neuronal function, synaptic transmission, and inflammatory regulation. Experimental studies suggest that Mg+2 deficiency may enhance neuroinflammatory signaling, whereas adequate Mg+2 levels may attenuate inflammatory responses through mechanisms involving N-methyl-D-aspartate (NMDA) receptor modulation and suppression of pro-inflammatory pathways such as nuclear factor kappa B (NF-κB). This review summarizes current knowledge on neuroinflammation in AD and discusses the potential modulatory role of magnesium in neuroinflammatory processes associated with AD.