S. E. Oriaifo, E. O. Okogbenin and E. K. I. Omogbai
The compelling and evolving nature of depressive disorders, one of a family of related conditions referred to as the “affective spectrum disorders’ and one of the most prevalent psychiatric disorders, may be underscored by the numerous hypotheses enunciated in the last three decades concerning the nature of the disorder. Depressive disorders are a group of illnesses associated with significant neurobiological changes involving structural, functional and molecular alterations in several areas of the brain. Since no single cause of depression has been identified, understanding the neurobiologic substrates or biomarkers underlying the disease will help unravel the complexity of the disease as well as provide mechanistic explanation for the action of antidepressants and new insights on the latency of action of antidepressants, a latency of action which is at present undesirable considering the serious social and economic cost of the disease. These new insights, such as histone deacetylase (HDAC) inhibitors, isoform 2 of the potassium-chloride co-transporter (KCC2) blockers, N-Methyl-D-aspartate (NMDA) modulators and anti-apoptotics, endogenous enkephalin and cocaine-amphetamine regulated transcript (CART) peptides, melanin concentrating hormone (MCH) receptor antagonists, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) potentiators and mitochondrial-targeted treatments like small-molecule inhibitors of glycogen synthase kinase (GSK)-3, may help provide drugs with a higher rate of responders than presently-available medications, since recent studies suggest that alteration in neuroplasticity and cellular resiliency may be more closely related to the pathogenesis and pathophysiology of depression as well as the mechanism of action related to affective treatments.
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