Glutamate levels in the anterior cingulate cortex in un-medicated first episode psychosis: a proton magnetic resonance spectroscopy study
Glutamate levels in the anterior cingulate cortex in un-medicated first episode psychosis: a proton magnetic resonance spectroscopy study
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DOI：
10.1038/s41598-019-45018-0
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发表时间：
2019-07-02
影响因子：
4.6
通讯作者：
Howes, Oliver D.
中科院分区：
文献类型：
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作者：
Borgan, Faith R.;Jauhar, Sameer;Howes, Oliver D.
越来越多的证据表明，多巴胺能功能障碍可能与首发精神病的病理生理学有关。我们调查了没有接受任何药物治疗和服用违禁药物的首发精神病患者是否表现出皮质神经元能改变。111名志愿者，包括65名健康志愿者和46名未接受任何药物治疗的首次发作精神病患者（28名未接受药物治疗），接受了质子磁共振波谱扫描，测量双侧前扣带回皮质中的谷氨酸水平。采用阳性和阴性症状量表（PANSS）测量症状严重程度，采用韦氏成人智力量表（WAIS）数字符号测试测量认知能力。患者和对照组之间的谷氨酸水平没有差异。当调整年龄、性别和种族的影响时，或当将分析限制在对所有药物治疗和非法药物均未接受过药物治疗的患者时，这些结果保持不变。虽然这些发现并不排除精神病中的谷氨酸能改变，但我们需要方法学的进步来研究患者是否表现出谷氨酸功能其他方面的改变，如突触前谷氨酸或释放。
Converging lines of evidence suggest that glutamatergic dysfunction may contribute to the pathophysiology of first episode psychosis. We investigated whether first episode psychosis patients free from all pharmacological treatments and illicit substances show cortical glutamatergic alterations. One-hundred and eleven volunteers including 65 healthy volunteers and 46 first episode psychosis patients free from all pharmacological treatments (28 drug naive) underwent a proton magnetic resonance spectroscopy scan measuring glutamate levels in the bilateral anterior cingulate cortex. Symptom severity was measured using the Positive and Negative Syndrome Scale (PANSS) and cognition was measured using the Wechsler Adult Intelligence Scale (WAIS) digit symbol test. There were no differences in glutamate levels between patients and controls. These findings remained unchanged when adjusting for the effects of age, sex and ethnicity or when restricting the analyses to patients who were both medication naive to all pharmacological treatments and illicit substances. Whilst these findings do not preclude glutamatergic alterations in psychosis, methodological advances are needed for us to investigate whether patients show alterations in other aspects of glutamate function, such as pre-synaptic glutamate or release.