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Objective: Accumulated evidence from preclinical studies has indicated that thyroid hormones have effects on the inhibitory γ-aminobutyric acid (GABA) neurotransmitter system. The aim of the study was to investigate whether brain GABA levels are altered in hypothyroid patients compared with healthy controls. Methods: 15 patients with hypothyroidism and 15 matched controls participated in this study. Scans were performed on a 3.0 Tesla Philips scanner. For each subject, a T1-weighted 3D TFE scan was acquired for MRS voxel placement and tissue segmentation. Spectra were recorded from median prefrontal cortex (mPFC) and posterior cingulate cortex (PCC) using MEGAPRESS sequence (TR= 2000 ms; TE =68 ms; 256 averages) . Post-processing of the MEGA-PRESS data was carried out using Gannet v 2.0 toolkit2. Unsuppressed water signal was used as a reference for absolute quantification. Since GABA levels differ between gray matter (GM) and white matter (WM), tissue segmentation was performed using an automatic segmentation program, FAST in the FSL package. All participants underwent thyroid function test. Neuropsychological performances were evaluated by administration of the Montreal Cognitive Assessment (MoCA) and the 21-item Beck Depression Inventory-Ⅱ (BDI-Ⅱ). Results: There were no significant group differences in tissue composition in either voxel (all p-values > 0.32). The mPFC GABA levels were significantly lower (p = 0.016) in hypothyroid group (1.34 ± 0.09 IU) compared to healthy controls (1.42 ± 0.08 IU), whereas no significant difference (p=0.214) was observed in the PCC. The mPFC GABA levels were negatively correlated with the BDI-Ⅱ scores in patient group (r = -0.60, p = 0.018). No correlations were found between GABA levels and TSH or fT3 or fT4 levels in either region. Conclusion: This study is the first to report decreased brain GABA in hypothyroidism. The altered GABAergic neurotransmission may be an important neurological mechanism contributing to neuropsychiatric and cognitive changes in hypothyroidism, providing intriguing neurochemical clues to understand thyroid–brain interactions.