�The news about antidepressant drug medications over the past several years has been mixed. The bad news from tumid multicenter studies such as STAR*D is that current antidepressant medications are in force, but non as effective as one might hope. Thus, in that respect is a significant pauperization for new treatment mechanisms for depression. On that front, thither has been mixed news as comfortably. One of the most exciting new drugs to reach human clinical trials, one that blocks the corticotrophin cathartic factor-1 (CRF1) receptor, did not process in a large clinical trial sponsored by Pfizer Pharmaceuticals. Is it meter to give up CRF1 antagonists as antidepressants or should we revisit these agents from a new linear perspective? It is in this context that a new paper by Alexandre Surget and colleagues, scheduled for publication in the August 15th issue of Biological Psychiatry, is particularly interesting.
Through prior work, it has been shown that the power to blow the stress-related disruption of hippocampal neurogenesis, the ability of the brain to make modern nerve cells in adulthood, was important to the actions of our available antidepressant medications. In this new study, the researchers affirm the prior findings, but suggest that deuce experimental approaches to the treatment of depression, block off of the CRF1 sensory receptor or the vasopressin-1B (V1B) receptor, retain their efficacy in reversing the shock of stress on demeanour even when neurogenesis is disrupted. Catherine Belzung, Ph.D., corresponding author on this article, further explains that "we now report evidence that restoration of the functioning of the stress axis may be the key to how these new antidepressant approaches might work."
How can unrivalled reconcile these interesting enquiry findings in animals with the lack of antidepressant drug efficacy of a CRF1 receptor antagonist in the Pfizer study? Is this approach just ineffective in humans or might at that place be subgroups of patients who power be more likely to respond to a CRF1 antagonist? The Surget et al. data raise the possibility that CRF1 sense organ antagonists might be effective in treating stress-related behavioral disturbances regular in a context where other antidepressants do non work, perhaps due to disruption of neurogenesis. John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments: "These findings loan weight to the hope that CRF1 antagonists might play a role in the handling of antidepressant-resistant symptoms of depression or posttraumatic accent disorder. If so, CRF1 antagonists could fulfill an important unmet need." He adds that "we do not pauperism another Prozac, but we urgently need to find ways to help the large number of patients who fail to respond adequately to our available treatments."
Elsevier
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