Resolving the heterogeneity of dopamine subsystems dysfunction in schizophrenia: a PET meta-analysis

解决精神分裂症多巴胺子系统功能障碍的异质性:一项PET荟萃分析

阅读:1

Abstract

The "dopamine hypothesis" of schizophrenia suggests the imbalance of the brain dopamine system plays a crucial role in the development of this disorder. Although this hypothesis has been partly supported by early studies, the brain region-specific abnormalities of different dopamine subsystems, and the influential factors on the heterogeneity of dopamine dysfunction of schizophrenia are still unknown. To address these issues, we carried out random-effect meta-analyses by collecting 49 in vivo PET studies (692 patients and 730 controls). Patients exhibited significant regional and population heterogeneity in D(2/3) receptor availability, primarily manifesting as a moderate increased in the striatum of only drug-off patients (Cohen's d = 0.56, 95%CI [0.16; 0.97]), whereas only drug-on patients showed a large decrease in D(2/3) receptor availability in the thalamus, limbic lobe, substantia nigra, and temporal lobe (Cohen's d < -1.40). Drug-off patients also had a small increase in dopamine synthesis in the striatum (Cohen's d = 0.38, 95%CI[0.06; 0.69]), with no replicable dysfunctions in drug-on patients or other brain regions. D(1) receptor availability and DAT showed high heterogeneity but no consistent significances. Finally, Meta-regression indicated that elevated striatal D(2/3) levels correlated with a higher proportion of males, older patients, longer duration and worse symptoms predicted more severe D(1) deficits in the striatum and prefrontal cortex. This study suggests that different dopamine subsystems in schizophrenia are selectively involved across brain regions; moreover, medication status, sex, age, illness duration and symptom diversity have significant impacts on the dysfunctions of dopamine subsystems in schizophrenia.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。