Abstract
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.
References
- Andrási, E., Igaz, S., Molnár, Z., & Makó, S. (2000). Disturbances of magnesium concentrations in various brain areas in Alzheimer’s disease. Magnesium Research, 13(3), 189–196.
- Askarova, S., Yang, X., & Lee, J. C.-M. (2011). Impacts of Membrane Biophysics in Alzheimer′s Disease: From Amyloid Precursor Protein Processing to A β Peptide‐Induced Membrane Changes. International Journal of Alzheimer’s Disease, 2011(1). https://doi.org/10.4061/2011/134971
Details
| Primary Language | English |
|---|---|
| Subjects | Central Nervous System |
| Journal Section | Review |
| Authors | |
| Submission Date | January 9, 2026 |
| Acceptance Date | January 21, 2026 |
| Publication Date | January 30, 2026 |
| Published in Issue | Year 2026 Volume: 2 Issue: 1 |