Hippocampal dysfunction in the pathophysiology of schizophrenia: a selective review and hypothesis for early detection and intervention.

Hippocampal dysfunction in the pathophysiology of schizophrenia: a selective review and hypothesis for early detection and intervention.
复制标题

DOI:
10.1038/mp.2017.249
复制
发表时间:
2018-08
影响因子:
11
通讯作者:
Small SA
Small SA
中科院分区:
医学1区
文献类型:
--
作者:
Lieberman JA;Girgis RR;Brucato G;Moore H;Provenzano F;Kegeles L;Javitt D;Kantrowitz J;Wall MM;Corcoran CM;Schobel SA;Small SA

文献摘要

参考文献

被引文献

相似文献

长期以来,科学家们一直试图描述精神分裂症的病理生理学基础,并开发可以识别该疾病的生物标志物。广泛的尸检和体内神经影像学研究描述了海马体早期参与精神分裂症的病理生理学。在这种背景下,我们提出了一个假说,描述了精神分裂症从发病前到前驱阶段再到综合征性精神病的演变过程,并假设从海马 CA1 区开始的谷氨酸神经传递失调会诱发精神病症状减弱并开始向综合征性精神病的转变。随着病情的进展,这种病理过程扩展到海马回路的其他区域和包括额叶皮层在内的其他解剖区域的投射域,并诱发海马神经纤维减少和中间神经元丢失的萎缩过程。本文将描述我们小组和其他研究人员支持这一病理生理学假设的研究,及其对早期检测和治疗干预的影响。
Scientists have long sought to characterize the pathophysiologic basis of schizophrenia and develop biomarkers that could identify the illness. Extensive postmortem and in vivo neuroimaging research has described the early involvement of the hippocampus in the pathophysiology of schizophrenia. In this context, we have developed a hypothesis that describes the evolution of schizophrenia—from the premorbid through the prodromal stages to syndromal psychosis—and posits dysregulation of glutamate neurotransmission beginning in the CA1 region of the hippocampus as inducing attenuated psychotic symptoms and initiating the transition to syndromal psychosis. As the illness progresses, this pathological process expands to other regions of the hippocampal circuit and projection fields in other anatomic areas including the frontal cortex, and induces an atrophic process in which hippocampal neuropil is reduced and interneurons are lost. This paper will describe the studies of our group and other investigators supporting this pathophysiological hypothesis, as well as its implications for early detection and therapeutic intervention.
DOI: 10.1016/j.schres.2014.09.041
发表时间: 2015-09
影响因子: 4.5
作者:
Heckers, Stephan;Konradi, Christine
通讯作者: Konradi, Christine
DOI: 10.1146/annurev-neuro-062111-150444
发表时间: 2012
影响因子: 13.9
作者:
Buzsáki G;Wang XJ
通讯作者: Wang XJ
DOI: 10.1016/s0006-3223(99)00136-5
发表时间: 1999-09-01
影响因子: 10.6
作者:
Benes, FM
通讯作者: Benes, FM
精神病高风险状态:全面的最新评论。
DOI: 10.1001/jamapsychiatry.2013.269
发表时间: 2013-01
期刊: JAMA PSYCHIATRY
影响因子: 25.8
作者:
Fusar-Poli, Paolo;Borgwardt, Stefan;Bechdolf, Andreas;Addington, Jean;Riecher-Rossler, Anita;Schultze-Lutter, Frauke;Keshavan, Matcheri;Wood, Stephen;Ruhrmann, Stephan;Seidman, Larry J.;Valmaggia, Lucia;Cannon, Tyrone;Velthorst, Eva;De Haan, Lieuwe;Cornblatt, Barbara;Bonoldi, Ilaria;Birchwood, Max;McGlashan, Thomas;Carpenter, William;McGorry, Patrick;Klosterkotter, Joachim;McGuire, Philip;Yung, Alison
通讯作者: Yung, Alison
DOI: 10.1016/j.molbrainres.2004.12.005
发表时间: 2005-04-27
期刊: MOLECULAR BRAIN RESEARCH
影响因子: --
作者:
Coultrap, SJ;Nixon, KM;Browning, MD
通讯作者: Browning, MD