Date of Award
Master of Science in Biomedical Sciences
Depression is a complex disorder influenced by biological, psychological, and environmental factors (Santarelli et al., 2016). Depression is one of the most common forms of mental illness worldwide (WHO, 2021), yet the pathogenesis of depression and the mechanism of how antidepressants reverse depression remain unclear (Liu et al., 2017). The symptoms of depression are evident to most individuals, but the symptoms’ persistent nature remains a mystery to most. The four primary regions of the brain involved in depression are the Prefrontal Cortex (PFC), hippocampus, amygdala, and Anterior Cingulate Cortex (ACC) (Hayley et al., 2013). This review presents the prevailing literature on how antidepressants and Cognitive Behavior Therapy (CBT) can reverse depression. More specifically, this paper will examine the pathogenesis of depression (chronic stress model of depression); how the combination of antidepressants and CBT can help reverse depression (neuroplasticity theory of depression) and minimize relapse associated with depression. The neuroplasticity theory of depression is supported by evidence of decreased neuroplasticity in the hippocampus and PFC; decreased concentration of BDNF; and antidepressants increasing the concentration of BDNF and improving neuroplasticity in the hippocampus and PFC (Liu et al., 2017). The increase in BDNF promoting neurogenesis in the hippocampus and PFC also promotes neurogenesis in the amygdala, Ventral Tegmental Area (VTA), and Nucleus Accumbens (NAc) (Liu et al., 2017). The increase in neurogenesis in the amygdala exasperates depressive-like symptoms and is a primary reason for relapse (Hayley et al., 2013).
The first section of the paper reviews the stress model of depression and the disruption in structural neuroplasticity (Liu et al., 2017). The second section entails the neuroplasticity theory of depression in explaining how antidepressants and CBT can reverse depression by elevating the concentration of neurotrophic factors such as Brain-Derived Neurotrophic Factor (BDNF) and promoting positive neuroplasticity in the PFC and hippocampus (Liu et al., 2017). The third section examines the efficacy of combining antidepressants and CBT, and how CBT can help reduce relapses in depression caused by hyperactivity of the amygdala (Arnau-Soler et al., 2016). Finally, the last section presents recommendations for future studies, such as advancing the correlation between genetics and depression; the molecular mechanisms involved in depression; and treatment approaches utilizing precision medicine for clinical use.
Harbi, Vahid, "The Neuroplasticity of Depression: How Antidepressants and Cognitive Behavior Therapy (CBT) can Reverse Depression" (2021). PCOM Capstone Projects. 30.