• Bo Cao, Jeffrey A Stanley, Sudhakar Selvaraj, Benson Mwangi, Ives Cavalcante Passos, Giovana B Zunta-Soares, and Jair C Soares.
• UT Center of Excellence on Mood Disorders, Department of Psychiatry and Behavioral Sciences, University of Texas Health Science Center at Houston, TX 77054, USA. Electronic address: cloudbocao@gmail.com.
• J Psychiatr Res. 2016 Oct 1; 81: 48-55.

BackgroundPrevious proton magnetic resonance spectroscopy ((1)H MRS) studies have reported elevated glycerophosphocholine plus phosphocholine (GPC+PC) in the basal ganglia of patients with bipolar disorders (BD), which implicates an imbalance between synthesis and degradation activity of neuronal and glia membrane phospholipids (MPLs). However, the full extent of altered metabolites of MPLs in subareas within the basal ganglia, such as caudate and putamen, as well as anterior cingulate cortex (ACC) of BD patients is poorly understood.MethodsMulti-voxel (1)H MRS measurements were acquired in 50 type-one BD (BD-I) and 44 healthy controls (HC) on a 3-T MRI scanner. Four different anatomically defined voxels covering ACC, caudate and putamen were systematically extracted and quantified using LCModel. Group differences in absolute GPC+PC and other metabolites were tested with age and gender as covariates.ResultsBD-I patients had higher GPC+PC levels in the anterior-dorsal ACC (p = 0.037), caudate (p = 0.005) and putamen (p = 0.004) compared to HC. GPC+PC levels in the caudate were elevated most significantly in currently unmediated BD-I patients (p = 0.022) and were positively correlated with HAM-D scores (r = 0.51, p = 0.005). PCr+Cr and myo-inositol levels were also significantly higher in the caudate head (F(1,45) = 6.010, p = 0.018) of patients compared to HC. NAA and glutamate levels were not significantly different between BD-I and HC in these regions (p > 0.05).ConclusionThe increased GPC+PC in BD-I patients may reflect an imbalance in the MPL metabolism. Caudate GPC+PC levels may be a potential biomarker for depressive symptoms in BD.Copyright © 2016 Elsevier Ltd. All rights reserved.

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