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While conventional antidepressant therapies aim to modulate monoamine neurotransmitter levels, their clinical efficacy is limited due to their inability to effectively regulate MAO activity and their challenges in crossing the BBB

J Neurochem 1998

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In the first no-polymorphism phenotype, low folate intake or low FAD availability with normal MTHFR activity, lack of folate-substrate and FAD-cofactor for the MTHFR enzyme, retards both folate and methionine cycles creating an under-methylation setting