Open Access Review Article

Basic Hypothesis and Therapeutics Targets of Depression: A Review

Monika Kadian, Hemprabha Tainguriya, Nitin Rawat, Varnika Chib, Jeslin Johnson and Anil Kumar*

Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh 160014, India

Corresponding Author

Received Date: May 11, 2021;  Published Date: June 07, 2021

Depression is a psychological disorder marked by emotional symptoms such as melancholy, anhedonia, distress mood, loss of interest in daily life activities, feeling of worthlessness, sleep disturbances and destructive tendencies. According to WHO, more than 264 million people from all age groups are suffering with depression thus, it is become a leading cause of disability and infirmity worldwide. It is estimated that 40% of risk for depression is genetic and the other 60% is non-genetic which involved acute & chronic stress, childhood trauma, viral infections and even random processes during brain development. Depression is mainly due to neurotransmitter imbalances, HPA disturbances, increased oxidative and nitrosative damage, impairment in glucose metabolism, and mitochondrial dysfunction, etc. The monoamine hypothesis is based on attenuation of monoamines such as serotonin (5-HT), norepinephrine (NE) and dopamine (DA) in the brain regions (hippocampus, limbic system and frontal cortex) that can cause depression like symptoms. Depression is also marked by increased level of corticotrophin-releasing hormone (CRH) and and impaired responsiveness to glucocorticoid hormone. The present review emits about its background knowledge, various pathophysiological pathways involved and current therapy for the depression.

Keywords:Depression, HPA axis, mitochondrial dysfunction, NMDA receptor, Serotonin, Glutamate

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