The neural plasticity theory of depression: assessing the roles of adult neurogenesis and PSA-NCAM within the hippocampus.
The neural plasticity theory of depression: assessing the roles of adult neurogenesis and PSA-NCAM within the hippocampus.
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DOI：
10.1155/2013/805497
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发表时间：
2013
影响因子：
3.1
通讯作者：
Galea LA
中科院分区：
文献类型：
--
作者：
Wainwright SR;Galea LA
抑郁症是一种破坏性和流行性疾病，对神经结构和功能有深远的影响;然而，抑郁症的病因和神经病理学仍然知之甚少。虽然有抗抑郁药物存在，但它们并不理想，因为只有一部分患者得到有效治疗，治疗起效延迟，这些药物的确切机制仍有待阐明。抑郁症的几种理论确实存在，包括单胺能神经传递的调制，神经营养因子的改变，以及成人海马神经发生的上调，并在综述中简要提及。然而，这些理论都不能充分解释抑郁症本身的病理和治疗。最近，抑郁症的神经可塑性理论假设，大脑可塑性的多个方面，超越神经发生，可能会弥合流行的理论。术语“神经可塑性”包括一系列机制，从新神经元的出生、存活、迁移和整合到神经突生长、突触发生和成熟突触的调节。这篇综述批判性地评估了成年海马神经发生和细胞粘附分子PSA-NCAM（已知参与神经可塑性的许多方面）在抑郁症和抗抑郁药治疗中的作用。
Depression is a devastating and prevalent disease, with profound effects on neural structure and function; however the etiology and neuropathology of depression remain poorly understood. Though antidepressant drugs exist, they are not ideal, as only a segment of patients are effectively treated, therapeutic onset is delayed, and the exact mechanism of these drugs remains to be elucidated. Several theories of depression do exist, including modulation of monoaminergic neurotransmission, alterations in neurotrophic factors, and the upregulation of adult hippocampal neurogenesis, and are briefly mentioned in the review. However none of these theories sufficiently explains the pathology and treatment of depression unto itself. Recently, neural plasticity theories of depression have postulated that multiple aspects of brain plasticity, beyond neurogenesis, may bridge the prevailing theories. The term “neural plasticity” encompasses an array of mechanisms, from the birth, survival, migration, and integration of new neurons to neurite outgrowth, synaptogenesis, and the modulation of mature synapses. This review critically assesses the role of adult hippocampal neurogenesis and the cell adhesion molecule, PSA-NCAM (which is known to be involved in many facets of neural plasticity), in depression and antidepressant treatment.
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影响因子：
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影响因子：
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