The cholinergic deficit in Alzheimer’s disease (AD) remains the cornerstone for the understanding of chemical signal transfer. Hypofunctions of cholinergic systems are significantly involved in the signs and symptoms of senile dementia of the Alzheimer type. Cognitive deficits in AD have been widely associated with dysfunction of the cholinergic system. As a diagnostic marker of AD the activity of choline esterase is evident in blood cells and serum. A decrease in the activity of choline esterase is a supporting indicator of the clinical diagnosis of AD. Magnesium is the second most abundant intracellular cation and plays an essential role as a cofactor in many enzymatic reactions. There are some reports indicating a relationship between neurotransmitter release and intracellular magnesium concentration. Magnesium is directly involved in numerous important biochemical reactions and is particularly a necessary cofactor in more than 300 enzymatic reactions and specifically in all those processes involving the utilization and transfer of adenosine triphosphate. A study in patients with different diagnoses showed low enzyme activity of choline esterase in erythrocytes. Administration of magnesium resulted in normal catalytic activity of choline esterase. The measurement of the enzyme activity of choline esterase is a possibility to prove magnesium deficiency and to verify the efficacy of magnesium administration. Magnesium deficiency, resulting from low magnesium dietary intake, is more common and may be corrected by magnesium supplementation.

Keywords:
Alzheimer’s disease Magnesium, Cholinergic hypothesis, Choline esterase in erythrocytes, Acetylcholinesterase, Butyrylcholinesterase
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2012
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