Abstract: | Abstract— The theory of clinical depression presented here integrates etiological factors, changes in specific structural and cellular substrates, ensuing symptomatology, and treatment and prevention. According to this theory, important etiological factors, such as stress, can suppress the production of new neurons in the adult human brain, thereby precipitating or maintaining a depressive episode. Most current treatments for depression are known to elevate brain serotonin neurotransmission, and such increases in serotonin have been shown to significantly augment the ongoing rate of neurogenesis, providing the neural substrate for new cognitions to be formed, and thereby facilitating recovery from the depressive episode. This theory also points to treatments that augment neurogenesis as new therapeutic opportunities. |