The Neurobiology and Pharmacotherapy of Posttraumatic Stress Disorder.

The Neurobiology and Pharmacotherapy of Posttraumatic Stress Disorder.
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DOI:
10.1146/annurev-pharmtox-010818-021701
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发表时间:
2019-01-06
影响因子:
12.5
通讯作者:
Krystal JH
Krystal JH
中科院分区:
医学1区
文献类型:
--
作者:
Abdallah CG;Averill LA;Akiki TJ;Raza M;Averill CL;Gomaa H;Adikey A;Krystal JH

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创伤后应激障碍(PTSD)的神经生物学的新方法,需要解决报告的危机,在PTSD药物开发。这些新方法可能需要该领域超越狭隘的基于恐惧的观点,因为基于恐惧的药物尚未表现出令人信服的疗效。抗抑郁药,特别是最近的速效抗抑郁药,对脑功能和结构产生复杂的影响,这些影响建立在创伤后应激障碍生物学的新方面,包括应激相关突触连接障碍在神经生物学和创伤后应激障碍治疗中的作用。在这里,我们将这一观点纳入一个更广泛的框架,即,(1)由基于氨基酸的病理引起的应激相关的突触损失,和(2)与基于单胺的病理相关的应激相关的突触增益的双重病理模型。然后,我们总结了标准和实验(例如,氯胺酮)的药物治疗PTSD的选择,并讨论其假定的作用机制和临床疗效。
New approaches to the neurobiology of posttraumatic stress disorder (PTSD) are needed to address the reported crisis in PTSD drug development. These new approaches may require the field to move beyond a narrow fear-based perspective, as fear-based medications have not yet demonstrated compelling efficacy. Antidepressants, particularly recent rapid-acting antidepressants, exert complex effects on brain function and structure that build on novel aspects of the biology of PTSD, including a role for stress-related synaptic dysconnectivity in the neurobiology and treatment of PTSD. Here, we integrate this perspective within a broader framework, i.e., a dual pathology model of (1) stress-related synaptic loss arising from amino acid-based pathology, and (2) stress-related synaptic gain related to monoamine-based pathology. Then, we summarize the standard and experimental (e.g., ketamine) pharmacotherapeutic options for PTSD, and discuss their putative mechanism of action and clinical efficacy.
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发表时间: 2018-10
影响因子: 13.5
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发表时间: 2016-01
期刊: The Behavioral and brain sciences
影响因子: --
作者:
Abdallah CG;Averill LA;Krystal JH;Southwick SM;Arnsten AF
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发表时间: 2017-05-01
影响因子: 7.6
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