Anhedonia in depression: biological mechanisms and computational models.

Anhedonia in depression: biological mechanisms and computational models.
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DOI:
10.1016/j.cobeha.2018.01.024
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发表时间:
2018-08
影响因子:
5
通讯作者:
Treadway MT
Treadway MT
中科院分区:
心理学2区
文献类型:
--
作者:
Cooper JA;Arulpragasam AR;Treadway MT

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快感缺乏是一种严重的状况,描述了几乎完全没有享受,动机和兴趣。作为抑郁症的一个核心特征,快感缺失的临床表现可能包括体验快乐、与接近相关的动机行为以及学习如何将期望与环境相匹配方面的缺陷。迄今为止,抑郁症快感缺乏的确切神经生物学机制仍知之甚少。我们以前曾认为,矛盾的结果和无法确定特定的神经生物学底物的快感缺乏症状可能会导致样本异质性,次优的评估方法,以及不同成分的快感缺乏之间的分离的挑战。然而,最近,计算的精神症状的操作化的进步,提高了能力,以评估该症状域的组成元素的神经生物学。在本文中,我们回顾(1)在行为和计算方法评估奖励处理和动机的进展和(2)新的自我报告,神经学和生物学方法的亚型,可能是有用的,在未来的追求,以扩大我们的理解,在抑郁症的快感缺乏的神经生物学的发展。
Anhedonia is a severe condition that describes a near-complete absence of enjoyment, motivation, and interest. A core feature of depression, clinical manifestations of anhedonia can include deficits in experiencing pleasure, approach-related motivated behavior, and learning how to match expectations to the environment. To date, the precise neurobiological mechanisms of anhedonia in major depression are still poorly understood. We have previously argued that contradictory findings and the inability to identify specific neurobiological substrates for anhedonic symptoms may result from sample heterogeneity, suboptimal methods of assessment, and the challenge of dissociating between different components of anhedonia. Recently, however, computational advances to the operationalization of psychiatric symptoms have enhanced the ability to evaluate the neurobiology of constituent elements of this symptom domain. In this paper, we review (1) advances in behavioral and computational methods of assessing reward processing and motivation and (2) the development of new self-report, neurological, and biological methods of subtyping that may be useful in future pursuits to expand our understanding of the neurobiology of anhedonia in depression.
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