Does the concept of "Sensitization" provide a plausible mechanism for the putative link between the environment and schizophrenia?
Does the concept of "Sensitization" provide a plausible mechanism for the putative link between the environment and schizophrenia?
复制标题
DOI：
10.1093/schbul/sbm163
复制
发表时间：
2008-03-01
影响因子：
6.6
通讯作者：
Van Os, Jim
中科院分区：
文献类型：
--
作者：
Collip, Dina;Myin-Germeys, Inez;Van Os, Jim
精神分裂症公报回顾的先前证据表明，一系列不同的环境因素在精神病发展中的重要性。然而，与精神分裂症相关的环境影响的多样性不太可能与许多不同的潜在机制有关。有证据表明，环境暴露可能会诱导，在相互作用（epi）遗传因素，心理或生理变化，可以追溯到最终的共同途径的认知偏见和/或改变多巴胺神经传递，广义上称为“敏化”，促进精神病症状的发作和持续。在群体水平上，可以通过量化暴露于与应激或多巴胺激动剂药物相关的环境风险因素的群体中的（1）亚临床精神病经历的正常短暂发育表达的持续性（表明持久致敏）增加的速率和（2）随后向临床精神病性障碍转变的增加的速率来检查致敏的行为表型。
Previous evidence reviewed in Schizophrenia Bulletin suggests the importance of a range of different environmental factors in the development of psychotic illness. It is unlikely, however, that the diversity of environmental influences associated with schizophrenia can be linked to as many different underlying mechanisms. There is evidence that environmental exposures may induce, in interaction with (epi)genetic factors, psychological or physiological alterations that can be traced to a final common pathway of cognitive biases and/or altered dopamine neurotransmission, broadly referred to as "sensitization," facilitating the onset and persistence of psychotic symptoms. At the population level, the behavioral phenotype for sensitization may be examined by quantifying, in populations exposed to environmental risk factors associated with stress or dopamine-agonist drugs, (1) the increased rate of persistence (indicating lasting sensitization) of normally transient developmental expressions of subclinical psychotic experiences and (2) the subsequent increased rate of transition to clinical psychotic disorder.