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Abnormal cellular energy and phospholipid metabolism in the left dorsolateral prefrontal cortex of medication‐free individuals with bipolar disorder: an in vivo 1 H MRS study
Author(s) -
Frey Benício N,
Stanley Jeffrey A,
Nery Fabiano G,
Serap Monkul E,
Nicoletti Mark A,
Chen HuaHsuan,
Hatch John P,
Caetano Sheila C,
Ortiz Oswaldo,
Kapczinski Flávio,
Soares Jair C
Publication year - 2007
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1111/j.1399-5618.2007.00454.x
Subject(s) - dorsolateral prefrontal cortex , bipolar disorder , prefrontal cortex , phospholipid , neuroscience , medicine , endocrinology , psychology , psychiatry , lithium (medication) , chemistry , cognition , biochemistry , membrane
Objectives: While the pathophysiology of bipolar disorder (BD) remains to be elucidated, postmortem and neuroimaging studies have suggested that abnormalities in the dorsolateral prefrontal cortex (DLPFC) are implicated. We compared the levels of specific brain chemicals of interest measured with proton magnetic resonance spectroscopy ( 1 H MRS) in medication‐free BD subjects and age‐ and gender‐matched healthy controls. We hypothesized that BD subjects would present abnormal cellular metabolism within the DLPFC, as reflected by lower N ‐acetyl‐aspartate (NAA) and creatine + phosphocreatine (Cr + PCr). Methods: Thirty‐two medication‐free BD subjects (33.8 ± 10.2 years) and 32 matched controls (33.8 ± 9.0 years) underwent a short echo‐time (TE = 30 ms) 1 H MRS. An 8‐cm 3 single voxel was placed in the left DLPFC, and individual concentrations of NAA, Cr + PCr, choline‐containing compounds (GPC + PC), myo ‐inositol, and glutamate were obtained, using the water signal as an internal reference. Results: BD subjects had lower Cr + PCr [ F (1,62) = 5.85; p = 0.018; one‐way analysis of variance (ANOVA)] and lower GPC + PC [ F (1,62) = 5.79; p = 0.019; one‐way ANOVA] levels in the left DLPFC. No significant differences were observed for other brain metabolites. Conclusions: These findings provide further evidence that the pathophysiology of BD involves impairment in the DLPFC. Our findings can be interpreted as evidence for reduced cellular energy and phospholipid metabolism, consistent with the hypothesis of mitochondrial dysfunction in BD.