Molecular and genetic basis of depression

Abstract

Joyousness or sadness is normal reaction to state of life. If any of these lead to certain semi-permanent changes in daily life, then it is termed as mental disorder. Depression is one of the mental disorders with a state of low mood and aversion to activities that exerts a negative effect on a person's thoughts and behaviour. Adolescent group is probably the world's largest active group of people, who are getting prone to this state of mind leading to their diminished mental and physical abilities. Depression is closely linked to stress and thus a chronic stressful life can increase the risk of depression. Depression is a complex disease having both genetic and environmental components as contributing factors. In this study an attempt has been made to put forward the understanding of the known genes and their functional relationships with depression and stress with special reference to BDNF and 5-HTTLPR. Analysis of common genetic variants associated with depression, especially in the members of a family who had a previous history, might help in identifying the individuals at risk prior to the onset of depression.

BDNF and COX-2 participate in anti-depressive mechanisms of catalpol in rats undergoing chronic unpredictable mild stress

“…As previously mentioned, increasing evidence indicates that BDNF also plays essential roles in the pathogenesis of depression, regardless of experimental research or clinical trials [4][5][6][7][8][9][11][12][13]15,16]. The present study found that BDNF expression was reduced in the hippocampus and frontal cortex of CUMS-exposed rats, which was consistent with previous reports [57].…”

“…The data above have led to the proposal of "neurotrophin hypothesis of depression" [10]. Recent genetic studies also supported the link between BDNF and depressive behavior [11]. BDNF and abnormalities in its cognate receptor tropomycin-related kinase B (TrkB) have been previously reported in depressed patients [12].…”

“…Epigenetic modulation of the BDNF and TrkB genes may contribute to their altered expression and function [13]. Overall, these studies suggest that BDNF and its mediated signaling may participate in the pathophysiology of depressive behavior [11,[13][14][15][16]. Increasing evidence also demonstrates that COX-2 may play a vital role in several pathological conditions, such as epilepsy, ischemia, anxiety, depression, and other degenerative diseases of the central nervous system (CNS) [17][18][19][20].…”

Epigenetics and major depression disorder

“…Napredak u molekularnoj biologiji omogućio je uvid u epigenetičke mehanizme djelovanja koji su, kako se pokazalo, izuzetno osjetljivi na utjecaje iz okoliša. Iznimno važna posljedica epigenetičkog modeliranja promjena je aktivnosti gena 14 , koja, u kontekstu izloženosti utjecajima okoliša, predstavlja dio prilagodbe. Ova se prilagodba odražava i na funkciji neurona, i, posljedič-no, na promjene u ponašanju.…”

Duality of Antidepressants and Neuroprotectants

“…It is now well recognized that more often than not, a number of factors, particularly genetic and environmental, act together to bring about the disorder (Roy et al 2014; Lopizzo et al 2015). In general, genes provide the susceptibility or vulnerability component and the environment, either internal or external, provides the knockout punch.…”