Magnesium and Alzheimer’s Disease

Carolyn Dean, MD., ND comments regarding Jan 2011 study below:

Recent studies show that calcium supplements cause inflammatory heart disease in women. This particular tissue culture study tested the inflammatory response of calcium to tissue damage and the effects of magnesium. These results indicate that increased magnesium inhibits calcium and may be a strategy for reducing the damaging consequences of calcium-induced neuroinflammation in degenerative neurological disorders such as Alzheimer disease and Parkinson disease.

Mg2+ Ions Reduce Microglial and THP-1 Cell Neurotoxicity by Inhibiting Ca2+ Entry Through Purinergic Channels

Source:

Brain Res. 2011 Jan 19;1369:21-35.                                                                                                                                                                                                                                        Lee M, Jantaratnotai N, McGeer E, McLarnon JG, McGeer PL.Kinsmen Laboratory of Neurological Research, 2255 Wesbrook Mall, University of British Columbia, Vancouver, BC, Canada.

Abstract:

Mg(2+) is a known antagonist of some Ca(2+) ion channels. It may therefore be able to counteract the toxic consequences of excessive Ca(2+) entry into immune-type cells. Here we examined the effects of Mg(2+) on inflammation induced by Ca(2+) influx into microglia and THP-1 cells following activation of purinergic receptors. Using tissue culture, an inflammatory response was induced by treatment with either the P2X7 purinergic receptor agonist 2′,3′-[benzoyl-4-benzoyl]-ATP (BzATP) or the P2Y2,4 receptor agonist uridine 5′-triphosphate (UTP). Both microglia and THP-1 cells expressed the mRNAs for these receptors. Treatment produced a rapid rise in intracellular Ca(2+) which was significantly reduced by Mg(2+) or the calcium chelator BAPTA-AM. Purinergic receptor stimulation activated the intracellular inflammatory pathway P38 MAP kinase and NF?B. This caused release of TNF?, IL-6, nitrite ions and other materials that are neurotoxic to SH-SY5Y cells. These effects were all ameliorated by Mg(2+). They were also partly ameliorated by the P2X7R antagonists, oxATP and KN-62, the P2YR antagonist MRS2179, and the store operated Ca(2+) channel blocker, SK96365. These results indicate that elevated Mg(2+) is a broad spectrum inhibitor of Ca(2+) entry into microglia or THP-1 cells. Mg(2+) administration may be a strategy for reducing the damaging consequences Ca(2+) induced neuroinflammation in degenerative neurological disorders such as Alzheimer disease and Parkinson disease.

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