Evidence is mounting that low levels of magnesium contribute to the heavy metal deposition in the brain that precedes Alzheimer’s.
Mg values are found to be significantly decreased in brain regions of (Alzheimer’s) patients compared to the controls. Dr. E Andrasi
Andrasi E, Igaz S, Molnar Z, Mako S. Disturbances of magnesium concentrations in various brain areas in Alzheimer's disease. L. Eotvos University , Budapest , Hungary
Dr. J.L. Glick in 1990 showed a significant decrease in the frequency of intracellular magnesium deposits in neurons of Alzheimer disease patients as compared with control patients
Normalizing brain levels of magnesium may help fight deposition of aggregated beta-amyloid (Abeta) as seen in Alzheimer’s disease and related dementias
Evidence is presented indicating that dementias are associated with a relative insufficiency of Magnesium (Mg) in the brain.
Med Hypotheses 1990 Dec;33(4):preceding 301.
Our data suggest that there is a relationship between serum Mg levels and the degree of Alzheimer’s disease and that the determination of the Mg level at various stages may provide valuable information in further understanding the progression and treatment of Alzheimer’s disease.
Undoubtedly the trigger mechanism of Altzheimer’s is the accumulation of heavy metals in the nervous system causing free radical damage leading to DNA and Mitochondrial DNA (mtDNA) damage.
Mercury:
In a human autopsy study, brain tissues from people with AD at death were compared with an age-matched group of control brains from subjects without AD. Mercury content was considerably higher in the AD group. Mercury concentration was prominent in the brain structures involved in memory function.
Many researchers feel that the actual cause of Alzheimer’s disease is due to toxic metal that leaches from mercury-silver amalgam dental fillings. Mercury vapor from amalgam fillings is absorbed into the sinuses and goes through the blood stream directly to the brain.
Vaccines as well as the air, water and food we eat all contain mercury.
Aluminum:
Is neurotoxic even in minute quantities. Normally, the brain is protected form toxic substances by a membrane, the blood-brain barrier. However, because aluminum seems to be concentrated in brain tissue of Alzheimer's victims, it is assumed that there must be a defect in the barrier system permitting aluminum to enter.
Dr. Jean Durlach recognized fifteen years ago the importance of magnesium in the development of Alzheimer’s saying. “Numerous studies have revealed the increased presence of aluminum (Al) in brain tissue obtained from autopsies of Alzheimer disease patients.”
Mg depletion, particularly in the hippocampus, appears to represent an important pathogenic factor in Alzheimer's disease. It is associated with high aluminum incorporation into brain neurons - Dr.Jean Durlach
Dr. Glick suggests that Alzheimer's disease involves a defective transport process characterized by both an abnormally low Mg incorporation and an abnormally high Al incorporation into brain neurons.
Aluminum given to a healthy subject will bring on symptoms of tremors, forgetfulness, disorientation, a very dry, or weeping eczema and skin rashes, as well as other nerve and brain tissue disorders.
Magnesium protects cells from aluminium ,mercury, lead, cadmium, beryllium and nickel. Low magnesium is associated with glutathione depletion. This is vital since glutathione is one of the few antioxidant molecules known to neutralize mercury.
In an article recently published in the Journal of Orthomolecular Medicine, an Ontario
Blood brain barrier permeability:
The integrity and function of the BBB is critical for overall brain function. Changes in permeability often reflect alterations in BBB transport systems. Causes of generalized changes in BBB permeability include organic solvents, enzymes, heavy metals and free radicals.
Magnesium has an important role at the BBB and is the crucial nutrient that makes a big difference in prevention and treatment of Alzheimer’s disease
More benefits of Magnesium
Memory and the overall functioning of our brains depend on proteins in our brains called NMDA receptors, which allow our neurons to communicate with each other.
An understanding of the strategic importance of magnesium at these crucial NMDA receptor sites confirms the medical view that heavy magnesium supplementation would lead to better treatments for schizophrenia, Alzheimer’s disease, and stroke.
Magnesium permits calcium to enter a nerve cell to allow electrical transmission along the nerves to and from the brain. Even our thoughts, via brain neurons, are dependent on magnesium.
Dr. Carolyn Dean
Dr. Carolyn Dean
Magnesium is essential in regulating central nervous system excitability. It calms the brain and people do not need to become severely deficient in magnesium for the brain to become hyperactive.
One study confirmed earlier reports that a marginal magnesium intake overexcites the brain's neurons and results in less coherence--creating cacophony rather than symphony--according to (EEG) measurements.
Of all the macronutrient minerals in the human body,
magnesium is the one most likely to be deficient.
magnesium is the one most likely to be deficient.
Even a mild deficiency of magnesium can cause sensitiveness to noise, nervousness, irritability, mental depression, confusion, twitching, trembling, apprehension, and insomnia.
The two most basic requirements for the normal operation of our brain are a sufficient energy supply and an optimal presence of biochemicals involved in transmitting messages. Magnesium is crucial in both the production of energy and neurotransmitters and the integrity of the blood brain barrier. It is solid science that connects magnesium to neurological disorders.
Magnesium Research (1990) 3, 3, 217-218
ReplyDeleteLetter to the Editor
Magnesium depletion and pathogenesis of Alzheimer's disease
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Jean Durlach
SDRM, Hôpital Saint-Vincent-de-Paul, 74-82 Avenue Denfert-Rochereau F-75674, Paris Cedex 14, France
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Summary: Mg depletion, particularly in the hippocampus, appears to represent an important pathogenic factor in Alzheimer's disease. It is associated with high aluminium incorporation into brain neurones. This type of Mg deficit cannot respond to mere Mg supplementation, but requires correction of the dysregulation inducing this Mg depletion. Further research should seek to control the alterations of albumin, which may induce this brain Mg depletion.
Key words: Alzheimer's disease, aluminium, hippocampus, magnesium, Mg depletion.
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Among the recent studies concerning the difficult problem of the pathogenesis of Alzheimer's disease numerous studies have revealed the increased presence of aluminium (Al) in brain tissue obtained from autopsies of Alzheimer disease patients. However, while Perl et al. stressed the significance of their findings concerning Al in hippocampal tissue, they ignored practically any discussion of their findings concerning magnesium (Mg)1,2. Glick3 subjects the Mg data of Perl and colleagues to a statistical analysis which shows a significant decrease in the frequency of intracellular Mg deposits in neurones of Alzheimer disease patients as compared with control patients. These data agree with more recent observations by Korf et al. who report decreases in Mg, K, and glutamic acid in hippocampal atissue of Alzheimer patients4 while the Mg content of the whole brain remains normal5. Mg has been shown in vitro to gate cation channels opened by glutamate, and particularly those on the N-methyl-D-asparte (NMDA) receptors6. Glutamate binding to NMDA receptors was reduced by 75-80% in the hippocampus of Alzheimer disease brains7. The hypothesis of a link between this loss of glutamatergic transmission and Mg depletion in the hippocampus in Alzheimer's disease has been proposed. Glick3 goes further and suggests that Alzheimer's disease involves a defective transport process characterized by both an abnormally low Mg incorporation and an abnormally high Al incorporation into brain neurones. The origin of this disturbance rests on an alteration of serum albumin, forming a species which has a greater affinity for Al than for Mg, in contrast to the normal protein which binds Mg better than Al. The altered albumin crosses the blood-brain barrier more efficiently than the normal protein and competes with it in binding to brain neurones. Binding of the altered albumin to the target neurones would both impede Mg uptake and facilitate Al uptake.
The brilliant hypothesis of Glick should stimulate further therapeutic research on the control of albumin alteration considered as the basic disturbance in the Mg depletion found in Alzheimer's disease. Other studies agree on the presence of Mg depletion rather than of Mg deficiency in Alzheimer's disease. First the nervous consequences of Mg deficiency are usually merely diffuse nervous hyperexcitability and not dementia accompanied by reduced Mg concentration in the hippocampus 10,11. Secondly, in patients affected by Alzheimer's disease, plasma, red blood cell, and lymphocyte Mg concentrations are not significantly different from those of healthy old people. The only marker of Mg dysregulation is a significant increase in Mg/K ratio measured in granulocytes12.
In summary, Mg depletion appears to be an important pathogenic factor in Alzheimer's disease. Further research should seek to control the alterations of albumin which may constitute the origin of this hippocampal Mg depletion.
EDITED VERSION