Magnesium
 

from The Magnesium Miracle, Carolyn Dean (2nd edition 2017)

MIT: Magnesium May Reverse Middle-age Memory Loss 12-27-2004

..."Our study shows…maintaining proper magnesium in the cerebrospinal fluid is essential for maintaining the plasticity of synapses," the authors wrote. "Since it is estimated that the majority of American adults consume less than the estimated average requirement of magnesium, it is possible that such a deficit may have detrimental effects…resulting in potential declines in memory function."

Plasticity, or the ability to change, is key to the brain's ability to learn and remember. Synapses, the connections among brain cells, undergo physical changes in response to brain activity. While the mechanisms underlying these changes remain elusive, it is known that synapses are less plastic in the aging or diseased brain. Loss of plasticity in the hippocampus, where short-term memories are stored, causes the forgetfulness common in older people.

Short-term magnesium deficiency downregulates telomerase, upregulates neutral sphingomyelinase and induces oxidative DNA damage in cardiovascular tissues: relevance to atherogenesis, cardiovascular diseases and aging 3-15-2014

The present work tested the hypotheses that: 1) short-term dietary deficiency of magnesium (Mg; 21 days) in rats (MgD) would result in a downregulation of telomerase in cardiac and aortic smooth muscle cells, 2) low levels of Mg2+ added to drinking water (DW) would either prevent or greatly reduce the downregulation of telomerase in MgD, 3) MgD in rats would cause an upregulation of neutral-sphingomyelinase (N-SMAse) and p53, 4) short-term MgD would result in oxidation of DNA in diverse cardiac muscle and aortic smooth muscle cells as exemplified by measurement of 8-hydroxydeoxyguanosine (8-OH-dG), and 5) cross-talk between telomerase, N-SMase, p53, and 8-OH-dG would be evident in left ventricular (LV), right ventricular (RV), atrial and aortic smooth muscle obtained from rats subjected to short-term MgD. The data indicated that short-term MgD (10% normal dietary intake) resulted in downregulation of telomerase in LV, RV, atrial and aortic muscle cells; even very low levels of water-bourne Mg2+ (e.g., 15-40 mg/lday) either prevented or ameliorated the downregulation of telomerase. Our experiments also showed that MgD resulted in a 7-10 fold increased formation of 8-OH-dG in the cardiac and aortic muscle cells. The experiments also confirmed that short-term dietary deficiency of Mg resulted in greatly increased upregulation of N-SMAse and p53 in the cardiac and aortic muscle tissues. These new experiments point to a sizeable cross-talk among telomerase, N-SMAse, and p53 in rat cardiac and peripheral vascular muscle exposed to a short-term MgD. These studies would be compatible with the idea that even short-term MgD could cause alterations of the genome in diverse cell types leading to mutations of cardiac, vascular, and endothelial cells seen in aging and atherogenesis. Since we have shown, previously, that activation of N-SMAse in MgD leads to synthesis and release of ceramide in cardiovascular tissues and cells, we believe this pathway, most likely, helps to result in downregulation of telomerase, upregulation of transcription factors (e.g., p53; NF-kB), cytokine release, mutations, transformations, and dysfunctional growth seen in the cardiac and vascular cells observed in the normal aging process, atherogenesis, hypertension, and cardiac failure. Lastly, we suggest ways in which this hypothesis can be tested.

Will need to read in the morning. Yes plasticity is an awesome thing--actually takes time to make the new connections, and requires adequate sleep to maintain them. Or a nap.

Hoping the Mg will improve the short term memory. One son struggles with memory and other son can remember everything forever. He had become our memory.