Mitochondrial complex I and III mRNA levels in bipolar disorder

2015 ◽  
Vol 184 ◽  
pp. 160-163 ◽  
Author(s):  
Süleyman Akarsu ◽  
Deniz Torun ◽  
Murat Erdem ◽  
Salih Kozan ◽  
Hatice Akar ◽  
...  
2004 ◽  
Vol 56 (7) ◽  
pp. 483-489 ◽  
Author(s):  
Shinsuke Washizuka ◽  
Kazuya Iwamoto ◽  
An-a Kazuno ◽  
Chihiro Kakiuchi ◽  
Kanako Mori ◽  
...  

2017 ◽  
Vol 3 (3) ◽  
pp. 157-169 ◽  
Author(s):  
Brandi L. Rollins ◽  
Ling Morgan ◽  
Brooke E. Hjelm ◽  
Adolfo Sequeira ◽  
Alan F. Schatzberg ◽  
...  

2006 ◽  
Vol 15 (8) ◽  
pp. 504-507 ◽  
Author(s):  
Claudia Mehler-Wex ◽  
J. Catharina Duvigneau ◽  
Romana T. Hartl ◽  
Dorit Ben-Shachar ◽  
Andreas Warnke ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Helena Kyunghee Kim ◽  
Wenjun Chen ◽  
Ana Cristina Andreazza

Mitochondrial dysfunction and activation of the inflammatory system are two of the most consistently reported findings in bipolar disorder (BD). More specifically, altered levels of inflammatory cytokines and decreased levels of mitochondrial complex I subunits have been found in the brain and periphery of patients with BD, which could lead to increased production of mitochondrial reactive oxygen species (ROS). Recent studies have shown that mitochondrial production of ROS and inflammation may be closely linked through a redox sensor known as nod-like receptor pyrin domain-containing 3 (NLRP3). Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade. In this review, we discuss the potential role of the NLRP3 inflammasome as a link between complex I dysfunction and inflammation in BD and its therapeutic implications.


2014 ◽  
Vol 2 (1) ◽  
Author(s):  
Süleyman Akarsu ◽  
Deniz Torun ◽  
Abdullah Bolu ◽  
Murat Erdem ◽  
Salih Kozan ◽  
...  

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