Can Magnesium Supplementation Help Reduce Brain Damage and Cytoskeletal Protein Alterations?

Several studies have shown that central nervous system injury results in changes in blood and brain magnesium (Mg) levels. Decreases in intracellular magnesium ion levels resulting from brain injuries can compromise critical cellular functions. In a recent study, researchers looked at how pre brain injury magnesium deficiency and post-injury magnesium treatment affected cell cytoskeletal protein alterations after brain injury. Cytoskeletal protein alterations have been shown to lead to abnormal structural changes and neuronal cell death. They have also been linked to pathological alterations in brain plasticity, which may be a key player in neuronal regeneration or continued degeneration after stroke. The potential for magnesium supplementation to affect brain damage was looked at through calcium sensitive pathways that can activate calpains which can degrade microtubule-associated protein-2 (MAP-2) and spectrin. The degradation of cytoskeletal proteins MAP-2 and spectrin were looked at as markers of neuronal injury.

To test this idea, rats were fed a magnesium deficient diet for two weeks prior to induced brain injury or supplemented with a magnesium chloride solution 10 minutes post injury. It was found that magnesium treatment post injury reduced brain cell loss and reduced the amount MAP-2 and spectrin alterations. The magnesium deficient rats had a greater level of cell death and were observed to have cytoskeletal protein alterations in the cortex and hippocampus not observed in the control or magnesium treated groups. This experimentation revealed both a possible treatment and mechanism behind traumatic brain injury. Magnesium administration in the acute post-traumatic phase of brain injury helps maintain cytoskeletal integrity and reduces cortical cell loss and the cytoskeletal alterations responsible for cell death may be modulated by calpains.

The results of this study show that it may be beneficial to supplement one's diet with magnesium from a source such as a daily multi-vitamin. I am curious toward the idea of magnesium supplementation as means to treat stroke patients. It would be interesting to see if magnesium administration to stroke patients in the acute phase of stroke would lead to a decreased level acute phase and/or long-term cell death.


Reference:
K. Sattman, F. Bareyre, M.S Grady, T. McIntosh. "Acute Cytoskeletal Alterations and Cell Death Induced by Experimental Brain Injury Are Attenuated by Magnesium Treatment and Exacerbated by Magnesium Deficiency." Journal of Neuropathy and Experimental Neuroscience; Vol 60, No. 2. February 2001, pp. 183-194.