A team of Japanese scientists says it has confirmed a possible link between mitochondrial dysfunction in brain nerve cells and bipolar disorder. The team, which includes scientists at the RIKEN Brain Science Institute based in Wako, Saitama Prefecture, published their findings in the online edition of the US scientific journal Molecular Psychiatry on Tuesday.
There are different hypotheses on the cause of bipolar disorder, with some indicating the involvement of neurotransmitters, but the disease's exact mechanism is unknown. Bipolar disorder, also known as manic-depressive disorder, is characterised by recurrent depressive and manic phases.
In their experiment, the team created a mouse whose mitochondria in brain nerve cells were set to dysfunction through genetic engineering.
Normal mice became active in the dark and stopped their activity as it turned brighter, but the disabled mice continued to be active in the bright environment for a while, showing insomnia-like symptoms seen among bipolar patients. The team has long pointed out the link between mitochondrial dysfunction and bipolar disorder. "There is a possibility to help resolve the disease's mechanism and to develop new drugs,'" said the team's leader, Tadafumi Kato.
http://www.medicalnewstoday.com/healthnews.php?newsid=41906More on the mice from Molecular PsychiatryThe mutant mice exhibited characteristic behavioral phenotypes, a distorted day–night rhythm and a robust periodic activity pattern associated with estrous cycle. These abnormal behaviors resembling mood disorder were worsened by tricyclic antidepressant treatment and improved by lithium, a mood stabilizer.
We also observed antidepressant-induced mania-like behavior and long-lasting irregularity of activity in some mutant animals. Our data suggest that accumulation of mtDNA defects in brain caused mood disorder-like mental symptoms with similar treatment responses to bipolar disorder.
These findings are compatible with the mitochondrial dysfunction hypothesis of bipolar disorder.
http://www.nature.com/mp/journal/vaop/ncurrent/abs/4001824a.html