期刊论文详细信息
SCHIZOPHRENIA RESEARCH 卷:187
Neurobiological basis of bipolar disorder: Mitochondrial dysfunction hypothesis and beyond
Review
Kato, Tadafumi1 
[1] RIKEN Brain Sci Inst, Lab Mol Dynam Mental Disorders, 2-1 Hirosawa, Wako, Saitama 3510198, Japan
关键词: Bipolar disorder;    Mitochondrial DNA;    Calcium;    Paraventricular thalamic nucleus;    Animal model;   
DOI  :  10.1016/j.schres.2016.10.037
来源: Elsevier
PDF
【 摘 要 】

Bipolar disorder is one of two major psychotic disorders together with schizophrenia and causes severe psychosocial disturbance. Lack of adequate animal models hampers development of new mood stabilizers. We proposed a mitochondrial dysfunction hypothesis and have been studying the neurobiology of bipolar disorder based on this hypothesis. We showed that deletions of mitochondrial DNA (Delta mtDNA) play a pathophysiological role at least in some patients with bipolar disorder possibly by affecting intracellular calcium regulation. Mutant polymerase gamma transgenic mice that accumulate Delta mtDNA in the brain showed recurrent spontaneous depression-like episodes which were prevented by a serotonin-selective reuptake inhibitor and worsened by lithium withdrawal. The animal model would be useful to develop new mood stabilizers. (C) 2016 The Author. Published by Elsevier B.V.

【 授权许可】

Free   

【 预 览 】
附件列表
Files Size Format View
10_1016_j_schres_2016_10_037.pdf 501KB PDF download
  文献评价指标  
  下载次数:1次 浏览次数:0次