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Beyond its classical function in myelin synthesis which is critical for preventing demyelination-associated hyperexcitability, VB12 deficiency disrupts homocysteine metabolism which is associated with an increased risk of neurological disorders, cardiovascular diseases, and cognitive decline [136]
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It has a complicated pathogenesis associated with environmental modifications, genetic predispositions, deregulated dopamine metabolism, neuroinflammation, oxidative stress, and mitochondrial dysfunction (Gke okal et al., 2017
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