ArticleBipolar disorders2006
Decrease in creatine kinase messenger RNA expression in the hippocampus and dorsolateral prefrontal cortex in bipolar disorder.
Article in Bipolar disorders, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Systematic review of genome-wide gene expression studies of bipolar disorder.BMC psychiatry · 2013Pooled it
- Coenzyme Q10 effects on creatine kinase activity and mood in geriatric bipolar depression.Journal of geriatric psychiatry and neurology · 2012Trial
- The Role of the Ketogenic Diet in Modulating Biochemical Pathophysiology in Psychiatric and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Reconceptualizing bipolar disorder through an integrative biological lens: synthesis, convergence, and emerging directions.Frontiers in integrative neuroscience · 2026Review
- Diminished Compensatory Energy Production Following Hypoxic Stress in the Prefrontal and Anterior Cingulate Cortex Among Individuals With Schizophrenia.Psychiatry investigation · 2025Article
- Neuronal Synaptic Communication and Mitochondrial Energetics in Human Health and Disease.Advances in experimental medicine and biology · 2025Review
- Mitochondrial Dysfunction as a Biomarker of Illness State in Bipolar Disorder: A Critical Review.Brain sciences · 2024Review
- The major biogenic amine metabolites in mood disorders.Frontiers in psychiatry · 2024Review
- Mitochondria dysfunction and bipolar disorder: From pathology to therapy.IBRO neuroscience reports · 2023Article
- Mitochondrial dysfunction as a critical event in the pathophysiology of bipolar disorder.Mitochondrion · 2021Review
- The Role of Mitochondria in Mood Disorders: From Physiology to Pathophysiology and to Treatment.Frontiers in psychiatry · 2021Review
- Targeting Mitochondrial Dysfunction for Bipolar Disorder.Current topics in behavioral neurosciences · 2021Review
- Abnormal Brain Bioenergetics in First-Episode Psychosis.Schizophrenia bulletin open · 2021Article
- Abnormalities in High-Energy Phosphate Metabolism in First-Episode Bipolar Disorder Measured UsingBiological psychiatry · 2018Article
- The Relationship between the Number of Manic Episodes and Oxidative Stress Indicators in Bipolar Disorder.Psychiatry investigation · 2018Article
- Article
- Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia: Possible Interactions with Cellular Processes.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2016Review
- Decreased brain PME/PDE ratio in bipolar disorder: a preliminary (31) P magnetic resonance spectroscopy study.Bipolar disorders · 2015Article
- Abnormal high-energy phosphate molecule metabolism during regional brain activation in patients with bipolar disorder.Molecular psychiatry · 2015Article
- A preliminary evaluation of the correlation between regional energy phosphates and resting state functional connectivity in depression.NeuroImage. Clinical · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesBipolar disorder (BPD) affects more than 2 million adults in the USA and ranks among the top 10 causes of worldwide disabilities. Despite its prevalence, very little is known about the etiology of BPD. Recent evidence suggests that cellular energy metabolism is disturbed in BPD. Mitochondrial function is altered, and levels of high-energy phosphates, such as phosphocreatine (PCr), are reduced in the brain. This evidence has led to the hypothesis that deficiencies in energy metabolism could account for some of the pathophysiology observed in BPD. To further explore this hypothesis, we examined levels of creatine kinase (CK) mRNA, the enzyme involved in synthesis and metabolism of PCr, in the hippocampus (HIP) and dorsolateral prefrontal cortex (DLPFC) of control, BPD and schizophrenia subjects.
methodsTissue was obtained from the Harvard Brain Tissue Resource Center. Real-time quantitative polymerase chain reaction (HIP, DLPFC) and gene expression microarrays (HIP) were employed to compare the brain and mitochondrial 1 isoforms of CK.
resultsBoth CK isoforms were downregulated in BPD. Furthermore, mRNA transcripts for oligodendrocyte-specific proteins were downregulated in the DLPFC, whereas the mRNA for the neuron-specific protein microtubule-associated protein 2 was downregulated in the HIP.
conclusionAlthough some of the downregulation of CK might be explained by cell loss, a more general mechanism seems to be responsible. The downregulation of CK transcripts, if translated into protein levels, could explain the reduction of high-energy phosphates previously observed in BPD.
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