The Brain Finally Gets Into the Act

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. KEYWORDS—serotonin; adult brain neurogenesis; stress; clinical depression When the history of mental illness is written, the 20th century will be remembered primarily not for its biomedical advances, but as the period when depression (along with the other major psychopathologies) was finally considered to be a disease and not a failure of character or a weakness of will. In part, this change is attributable to putting to rest, at least in the scientific community, the dogma of Cartesian duality of mind and body. Given that the mind is the manifestation of the brain, depression could be considered to be a somatic disorder, along with pathologies of the heart, kidney, and other organs.