NEUROBIOLOGICAL SIMILARITIES BETWEEN DEPRESSION AND PARKINSON’S DISEASE: ETIOLOGICAL AND THERAPEUTIC IMPLICATIONS

Abstract

This literature review discusses the comorbidity of depression and Parkinson’s disease and the possible implications for the etiology of depression given that it often occurs as a part of Parkinson’s disease progression. The review contains descriptions and analyses of three popular hypotheses about depression etiology, including the monoamine hypothesis, the inflammation hypothesis, and the neuroplasticity or glutamate hypothesis. Each of these proposed mechanisms is compared with the physiology of Parkinson’s disease to better understand why depression and Parkinson’s disease may be comorbid from a neurobiological standpoint. The monoamine hypothesis and the neuroplasticity hypothesis of depression seem to best fit the characteristics of Parkinson’s disease and provide the most cogent explanations of major depressive disorder. Furthermore, dopamine receptor agonists and ketamine are analyzed as interventions in depression and Parkinson’s disease.