Glutamatergic dysregulation is one of the leading theories regarding the pathoaetiolopy of schizophrenia. Meta-analysis of magnetic resonance spectroscopy studies in schizophrenia shows increased levels of glutamate and glutamine (Glx) in the medial frontal cortex and basal ganglia in clinical high-risk groups for psychosis and increased glutamine levels in the thalamus, but it is unclear if this is also the case in people at genetic high risk for psychosis. The aim of this study was to investigate glutamatergic function in the anterior cingulate cortex, striatum and thalamus in carriers of a genetic variant (22q11.2 deletion) associated with a high risk for psychosis. 53 volunteers (23 22q11.2 deletion carriers and 30 controls) underwent proton magnetic resonance spectroscopy imaging and neuropsychological assessments for prodromal psychotic symptoms, schizotypy, anxiety, depression and FSIQ. We did not find any difference between groups in Glx in the anterior cingulate cortex, striatum or thalamus (Glx: t(50)=-1.26, p = 0.21; U = 251, z = -0.7, p = 0.49; U = 316, z= -0.26, p = 0.79, respectively). No correlation was detected between Glx levels in any region and symptomatology or FSIQ. Our findings indicate that glutamatergic function is not altered in people at genetic high risk of psychosis due to the 22q11.2 deletion, which could suggest that this is not the mechanism underlying psychosis risk in 22q11.2 deletion carriers.

中文翻译：

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精神病遗传高危人群的谷氨酸能功能：22q11.2 缺失个体的质子磁共振波谱研究

谷氨酸能失调是关于精神分裂症病理学的主要理论之一。对精神分裂症磁共振波谱研究的荟萃分析显示，临床精神病高危人群内侧额叶皮层和基底神经节中谷氨酸和谷氨酰胺 (Glx) 水平升高，丘脑中谷氨酰胺水平升高，但尚不清楚这是否具有精神病遗传高风险的人群也是如此。本研究的目的是调查与精神病高风险相关的遗传变异（22q11.2 缺失）携带者的前扣带回皮层、纹状体和丘脑的谷氨酸能功能。53 名志愿者 (23 22q11. 2 名缺失携带者和 30 名对照者）接受了质子磁共振波谱成像和神经心理学评估，以评估前驱精神病症状、分裂症、焦虑、抑郁和 FSIQ。我们没有发现前扣带回皮层、纹状体或丘脑的 Glx 组之间有任何差异（Glx：t(50)=-1.26, p = 0.21; U = 251, z = -0.7, p = 0.49; U = 316 , z= -0.26, p = 0.79, 分别）。在任何区域的 Glx 水平与症状或 FSIQ 之间未检测到相关性。我们的研究结果表明，由于 22q11.2 缺失，具有精神病遗传高风险人群的谷氨酸能功能没有改变，这可能表明这不是 22q11.2 缺失携带者精神病风险的潜在机制。我们没有发现前扣带回皮层、纹状体或丘脑的 Glx 组之间有任何差异（Glx：t(50)=-1.26, p = 0.21; U = 251, z = -0.7, p = 0.49; U = 316 , z= -0.26, p = 0.79, 分别）。在任何区域的 Glx 水平与症状或 FSIQ 之间未检测到相关性。我们的研究结果表明，由于 22q11.2 缺失，具有精神病遗传高风险人群的谷氨酸能功能没有改变，这可能表明这不是 22q11.2 缺失携带者精神病风险的潜在机制。我们没有发现前扣带回皮层、纹状体或丘脑的 Glx 组之间有任何差异（Glx：t(50)=-1.26, p = 0.21; U = 251, z = -0.7, p = 0.49; U = 316 , z= -0.26, p = 0.79, 分别）。在任何区域的 Glx 水平与症状或 FSIQ 之间未检测到相关性。我们的研究结果表明，由于 22q11.2 缺失，具有精神病遗传高风险人群的谷氨酸能功能没有改变，这可能表明这不是 22q11.2 缺失携带者精神病风险的潜在机制。