Lee Junghee, Green Michael F
Department of Psychiatry and Biobehavioral Science, David Geffen School of Medicine at University of California, Los Angeles, CA, USA; Veterans Affairs Desert Pacific Mental Illness Research, Education and Clinical Center, Los Angeles, CA, USA.
Department of Psychiatry and Biobehavioral Science, David Geffen School of Medicine at University of California, Los Angeles, CA, USA; Veterans Affairs Desert Pacific Mental Illness Research, Education and Clinical Center, Los Angeles, CA, USA.
Trends Neurosci. 2016 Sep;39(9):587-596. doi: 10.1016/j.tins.2016.06.005. Epub 2016 Jul 29.
Impaired social functioning is pervasive in schizophrenia. Unfortunately, existing treatments have limited efficacy, and possible psychological or neurobiological mechanisms underlying social dysfunction in this disorder remain obscure. Here, we evaluate whether social preference, one key aspect of social processing that has been largely overlooked in schizophrenia research, and N-methyl-d-aspartate receptor (NMDAR) dysfunction can provide insights into the mechanism underlying social dysfunction in schizophrenia. Based on evidence from developmental psychology, and behavioral and clinical neuroscience, we propose a heuristic model in which reduced NMDAR function may induce disrupted social preference that can subsequently lead to social cognitive impairment and social disability. We discuss its implications in terms of the pathophysiology of schizophrenia, other disorders with marked social disability, and potential treatments.
社会功能受损在精神分裂症中普遍存在。不幸的是，现有治疗方法疗效有限，该疾病中社交功能障碍潜在的心理或神经生物学机制仍不清楚。在此，我们评估社交偏好（这一在精神分裂症研究中很大程度上被忽视的社交处理关键方面）和N-甲基-D-天冬氨酸受体（NMDAR）功能障碍是否能为精神分裂症社交功能障碍的潜在机制提供见解。基于发展心理学、行为和临床神经科学的证据，我们提出一个启发式模型，其中NMDAR功能降低可能导致社交偏好紊乱，进而导致社会认知障碍和社交残疾。我们从精神分裂症的病理生理学、其他有明显社交残疾的疾病以及潜在治疗方法等方面讨论其意义。
