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Abstract Glutathione (GSH), the brain’s primary antioxidant, confers a critical first line of defense against oxidative-stress-induced cellular damage, with some evidence supporting compensatory upregulation of anterior cingulate cortex (ACC) GSH in bipolar disorder (BD).
Abstract Forty percent of people with bipolar disorder (BD) develop alcohol use disorder (AUD), with co-occurring AUD substantially worsening the course of BD. Though efficacious treatments remain elusive, frontal glutamate and GABA dysregulation represent promising targets for intervention.
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