Cyclic AMP response element binding protein and brain-derived neurotrophic factor: molecules that modulate our mood?
Cyclic AMP response element binding protein and brain-derived neurotrophic factor: molecules that modulate our mood?
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DOI：
10.1007/bf02704114
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发表时间：
2006-09
影响因子：
2.9
通讯作者：
Vaidya VA
中科院分区：
文献类型：
--
作者：
Nair A;Vaidya VA
抑郁症是我们这个时代的主要精神疾病，困扰着大约 20% 的人口。尽管这种复杂疾病很普遍，但其病理生理学尚不清楚。此外，尽管抗抑郁药已经存在了几十年，但其治疗作用的机制仍然难以捉摸。越来越多的证据表明特定神经回路的可塑性在抑郁症的病理生理学和治疗中发挥着作用。边缘区域的损伤被认为是导致抑郁症的病因，据报道抗抑郁药可以逆转这种损伤并促进适应性可塑性。导致抑郁症和抗抑郁药介导的可塑性相关损害的分子途径是科学研究的主要焦点。转录因子环AMP反应元件结合蛋白（CREB）和神经营养蛋白脑源性神经营养因子（BDNF）是多种抗抑郁药的靶标，并且已知在动物模型和患有抑郁症的患者中受到调节。鉴于它们在神经元可塑性中的作用，CREB 和 BDNF 已成为可能在调节情绪中发挥重要作用的分子。本综述的目的是讨论 CREB 和 BDNF 在抑郁症中的作用以及作为抗抑郁作用的目标/介质。
Depression is the major psychiatric ailment of our times, afflicting ~20% of the population. Despite its prevalence, the pathophysiology of this complex disorder is not well understood. In addition, although antidepressants have been in existence for the past several decades, the mechanisms that underlie their therapeutic effects remain elusive. Building evidence implicates a role for the plasticity of specific neuro-circuitry in both the pathophysiology and treatment of depression. Damage to limbic regions is thought to contribute to the etiology of depression and antidepressants have been reported to reverse such damage and promote adaptive plasticity. The molecular pathways that contribute to the damage associated with depression and antidepressant-mediated plasticity are a major focus of scientific enquiry. The transcription factor cyclic AMP response element binding protein (CREB) and the neurotrophin brain-derived neurotrophic factor (BDNF) are targets of diverse classes of antidepressants and are known to be regulated in animal models and in patients suffering from depression. Given their role in neuronal plasticity, CREB and BDNF have emerged as molecules that may play an important role in modulating mood. The purpose of this review is to discuss the role of CREB and BDNF in depression and as targets/mediators of antidepressant action.