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RESEARCH PRODUCT
Magnesium and Alzheimer’s Disease
Ligia J. DominguezMario BelvedereMario BarbagalloDelia Sprinisubject
medicine.medical_specialtyAntioxidantChemistrymedicine.medical_treatmentchemistry.chemical_elementInflammationMitochondrionCalciummedicine.disease_causePathogenesisEndocrinologyInternal medicineSynaptic plasticitymedicinemedicine.symptomCognitive declineOxidative stressdescription
Environmental factors, including nutrition and metal elements, are implicated in the pathophysiology of Alzheimer’s disease (AD). Several in vitro and in vivo data indicate a role for magnesium (Mg) in many biological and clinical aspects of AD. Mg deficiency, aside from having a negative impact on the energy production pathways required by the mitochondria to generate adenosine triphosphate, also affects many biochemical mechanisms vital for neuronal properties and synaptic plasticity, including the response of N-methyl- d -aspartate receptors to excitatory amino acids, stability, and viscosity of the cell membrane. Mg also has an action as a mild calcium antagonist, and as an antioxidant against free-radical damage of the mitochondria. Total and ionized Mg levels in plasma, as well as Mg concentrations in various tissues, were found to be decreased in AD patients and negatively associated with clinical deterioration. Chronic Mg deficiency results in excessive production of oxygen-derived free radicals and low-grade inflammation, these also being possible pathogenic factors in AD. Moreover, Mg was shown to have a role in the processing of amyloid-beta precursor protein, which plays a central role in the pathogenesis of AD. Whether Mg supplementation may help in preventing cognitive decline in the elderly remains to be demonstrated.
year | journal | country | edition | language |
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2015-01-01 |