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Although previous studies have largely assigned depressive symptoms to the three monoamine neurotransmitters (dopamine, norepinephrine, or serotonin), we describe a specific peripheral glutamatergic dysfunction (decreased GDH activity in K2 relatively control) that accompanies distinct clinical DE phenotypes with a predominance of parkinsonian neurological symptoms

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Beyond GSH, structures of Cys-GSTs with physiological substrates have been obtained in rare cases

It also modulates nitric oxide pathways, helping regulate inflammation and blood flow

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