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    元认知损害主观认知下降患者灰质体积及神经递质变化特征研究

    Characteristics of gray matter volume and neurotransmitter changes in SCD patients with metacognitive impairment

    • 摘要: 目的 研究伴元认知损害主观认知下降(SCD)患者灰质体积和神经递质缺陷的特征模式及与认知表现的相关性。方法 通过阿尔茨海默病神经影像学计划(ADNI)数据库纳入了SCD患者和健康对照者(HCs)各100例。依据是否伴有元认知损害,将SCD患者分为元认知正常组和元认知损害组。采用VBM和JuSpace工具箱分析各组体素灰质体积和神经递质变化情况。结果 与HCs组相比,元认知损害组额、颞、顶叶灰质萎缩,元认知正常组中央后回灰质萎缩。与元认知正常组相比,元认知损害组颞中回灰质萎缩,中央后回灰质增加。元认知损害SCD患者的颞中回萎缩与5-羟色胺受体1b(5HT1b)、多巴胺D1、N-甲基-D-天冬氨酸(NMDA)和代谢型谷氨酸受体第5亚型(mGluR5)分布在空间上密切相关。结论 伴元认知损害的SCD患者存在特定神经递质缺陷相关的颞中回萎缩,并与认知功能密切相关。

       

      Abstract: Objective To investigate the characteristic patterns of gray matter volume and neurotransmitter deficits in subjective cognitive decline (SCD) patients with metacognitive impairment, and their correlation with cognitive performance. Methods A total of 100 SCD patients and 100 healthy controls (HCs) were included into the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Based on the presence of metacognitive impairment, these SCD patients were divided into two groups (n=50): a normal metacognition group and an impaired metacognition group. The voxel-based gray matter volume and neurotransmitter changes in each group were analyzed by voxel-based morphometry (VBM) and JuSpace toolbox. Results Compared with the HCs group, the impaired metacognition group showed gray matter atrophy in the frontal, temporal, and parietal lobes, while the normal metacognition group presented gray matter atrophy in the postcentral gyrus. Compared with the normal metacognition group, the impaired metacognition group exhibited gray matter atrophy in the middle temporal gyrus and increased gray matter in the postcentral gyrus. The atrophy of the middle temporal gyrus in SCD patients with metacognitive impairment was spatially closely related to the distribution of 5HT1b, D1, NMDA, and mGluR5. Conclusions SCD patients with metacognitive impairment have specific middle temporal gyrus atrophy related to neurotransmitter deficits, which is closely associated with cognitive function.

       

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