Bo Liu1, Huan Yang2, Fei Gao2, Qing Wang1, Bin Zhao2, Tao Gong2, Zhensong Wang3, Weibo Chen4, Guangbin Wang2, Richard A E Edden5. 1. Department of Radiology, Qilu Hospital of Shandong University, Jinan, China. 2. Shandong Medical Imaging Research Institute affiliated to Shandong University, Jinan, China. 3. Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China. 4. Philips Healthcare, Shanghai, China. 5. Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Abstract
OBJECTIVE: Evidence indicates that thyroid hormones have effects on the inhibitory GABAergic system. The aim of this study was to investigate whether brain GABA levels are altered in patients with hypothyroidism compared with healthy controls. DESIGN/ METHODS: Fifteen patients with primary hypothyroidism and 15 matched healthy controls underwent single-voxel MEGA-PRESS magnetic resonance spectroscopy at 3T, to quantify GABA levels in the median prefrontal cortex (mPFC) and posterior cingulate cortex (PCC). 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: The patients with hypothyroidism had significantly lower GABA+ levels in the mPFC compared with healthy controls (P = 0·016), whereas no significant difference (P = 0·214) was observed in the PCC. Exploratory analyses revealed that 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 (all P > 0·05). CONCLUSION: This study suggests that alteration of GABAergic neurotransmission may play an important role in the pathophysiology of primary hypothyroidism, providing intriguing neurochemical clues to understand thyroid-brain interactions.
OBJECTIVE: Evidence indicates that thyroid hormones have effects on the inhibitory GABAergic system. The aim of this study was to investigate whether brain GABA levels are altered in patients with hypothyroidism compared with healthy controls. DESIGN/ METHODS: Fifteen patients with primary hypothyroidism and 15 matched healthy controls underwent single-voxel MEGA-PRESS magnetic resonance spectroscopy at 3T, to quantify GABA levels in the median prefrontal cortex (mPFC) and posterior cingulate cortex (PCC). 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: The patients with hypothyroidism had significantly lower GABA+ levels in the mPFC compared with healthy controls (P = 0·016), whereas no significant difference (P = 0·214) was observed in the PCC. Exploratory analyses revealed that 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 (all P > 0·05). CONCLUSION: This study suggests that alteration of GABAergic neurotransmission may play an important role in the pathophysiology of primary hypothyroidism, providing intriguing neurochemical clues to understand thyroid-brain interactions.
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