Neurobiological basis of bipolar disorder: Mitochondrial dysfunction hypothesis and beyond.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing mechanistic hypotheses and preclinical animal data
PubMed 27839913 · doi:10.1016/j.schres.2016.10.037
What was done
The authors reviewed the mitochondrial dysfunction hypothesis of bipolar disorder, focusing on the role of mitochondrial DNA deletions (ΔmtDNA) and the behavioral and pharmacological characteristics of mutant polymerase γ transgenic mice that accumulate brain ΔmtDNA.
What was found
No quantitative data, sample sizes, or effect sizes are reported in the abstract. The authors state that ΔmtDNA deletions contribute to pathophysiology in some bipolar disorder patients, potentially by altering intracellular calcium regulation. Transgenic mice accumulating ΔmtDNA in the brain displayed recurrent spontaneous depression-like episodes that were prevented by a selective serotonin reuptake inhibitor and exacerbated by lithium withdrawal.
Why it matters
This framework links mitochondrial genetics to mood disorder pathophysiology and presents a potential preclinical animal model for screening mood-stabilizing therapeutics.
Limits
The abstract presents a narrative review and preclinical animal model with no quantitative data, human trial evidence, or sample sizes reported.
Cited by
- supports Tadafumi Kato published research linking mitochondrial dysfunction to the pathophysiology of bipolar disorder.