Oxidative stress in anxiety and comorbid disorders

Abstract

Anxiety disorders, depression, and alcohol use disorder are common neuropsychiatric diseases that often occur together. Oxidative stress has been suggested to contribute to their etiology. Oxidative stress is a consequence of either increased generation of reactive oxygen species or impaired enzymatic or non-enzymatic defense against it. When excessive it leads to damage of all major classes of macromolecules, and therefore affects several fundamentally important cellular functions. Consequences that are especially detrimental to the proper functioning of the brain include mitochondrial dysfunction, altered neuronal signaling, and inhibition of neurogenesis. Each of these can further contribute to increased oxidative stress, leading to additional burden to the brain. In this review, we will provide an overview of recent work on oxidative stress markers in human patients with anxiety, depressive, or alcohol use disorders, and in relevant animal models. In addition, putative oxidative stress-related mechanisms important for neuropsychiatric diseases are discussed. Despite the considerable interest this field has obtained, the detailed mechanisms that link oxidative stress to the pathogenesis of neuropsychiatric diseases remain largely unknown. Since this pathway may be amenable to pharmacological intervention, further studies are warranted.