The Neuroanatomy, Etiopathogenesis, and Novel Therapeutic Targets in Depressive Disorders

Indu Arora, Kunal Khurana, Manish Kumar
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Abstract

Depression has a high prevalence and associated comorbidities. It is still unknown what the molecular basis of depression is, regardless of many theories that have been put up to explain it. Many researchers investigate that present-day therapies for depression are ineffective due to their low efficacy, delayed onset of action (typically two weeks), and adverse effects. Novel medications that operate more quickly and effectively are thus needed. Several novel molecules (e.g., ketamine, buprenorphine) have been proven to produce quick and dependable antidepressant benefits in depressive patients who are resistant to treatment; yet, questions about their effectiveness, possible abuse, and adverse effects persist. The molecular basis and pharmacological interventions for depression were included in this study. Even if pharmaceutical treatments for depression have mostly failed to alleviate the condition, identifying and addressing possible risk factors in an effort to reduce the prevalence of this psychiatric disease is beneficial for public health. We emphasized the neuroanatomy and etiopathogenesis of depression, along with a discussion of the putative pharmacological mechanisms, novel targets, research hurdles, and prospective therapeutic futures.
抑郁障碍的神经解剖、发病机制和新型治疗靶点
抑郁症的发病率很高,并伴有多种并发症。许多研究人员调查发现,目前治疗抑郁症的药物疗效不佳,起效时间较晚(通常为两周),且存在不良反应。因此,我们需要更快、更有效的新型药物。有几种新型分子药物(如氯胺酮、丁丙诺啡)已被证实能对耐药的抑郁症患者产生快速、可靠的抗抑郁疗效;然而,有关其有效性、可能的滥用和不良反应的问题依然存在。本研究包括抑郁症的分子基础和药物干预。尽管抑郁症的药物治疗大多无法缓解病情,但识别和解决可能的风险因素,努力降低这种精神疾病的患病率,对公共健康是有益的。我们强调了抑郁症的神经解剖学和发病机理,并讨论了推测的药理机制、新靶点、研究障碍和治疗前景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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