METHODS: We recruited 35 patients with T2DM and 40 healthy control subjects (HCs). They underwent resting-state functional MRI (rs-fMRI), arterial spin labeling (ASL) scans, and a series of cognitive tests. Then, we compared the differences of two groups in the cerebral blood flow (CBF) value, amplitude of low-frequency fluctuation (ALFF) value, and regional homogeneity (ReHo) value of the bilateral hippocampus subfields.
RESULTS: The CBF values of cornu ammonis area 1 (CA1), dentate gyrus (DG), and subiculum in the right hippocampus of T2DM group were significantly lower than those of HCs. The ALFF values of left hippocampal CA3, subiculum, and bilateral hippocampus amygdala transition area (HATA) were higher than those of HCs in T2DM group. The ReHo values of CA3, DG, subiculum, and HATA in the left hippocampus of T2DM group were higher than those of HCs. In the T2DM group, HbAc1 and FINS were negatively correlated with imaging characteristics in some hippocampal subregions.
CONCLUSIONS: This study indicates that T2DM patients had decreased perfusion in the CA1, DG, and subiculum of the right hippocampus, and the right hippocampus subiculum was associated with chronic hyperglycemia. Additionally, we observed an increase in spontaneous neural activity within the left hippocampal CA3, subiculum, and bilateral HATA regions, as well as an enhanced local neural coordination in the left hippocampal CA3, DG, HATA, and subiculum among patients with type 2 diabetes, which may reflect an adaptive compensation for cognitive decline. However, this compensation may decline with the exacerbation of metabolic disorders.
方法:我们招募了35名T2DM患者和40名健康对照受试者。他们接受了静息状态功能磁共振成像(rs-fMRI),动脉自旋标记(ASL)扫描,和一系列认知测试。然后,比较两组脑血流量(CBF)值的差异,低频波动幅度(ALFF)值,和双侧海马子场的区域同质性(ReHo)值。
结果:氨面积1(CA1)的CBF值,齿状回(DG),2型糖尿病组右侧海马下膜明显低于HCs。左侧海马CA3,下丘的ALFF值,2型糖尿病组双侧海马杏仁核过渡区(HATA)均高于HCs。CA3、DG、下膜,T2DM组左侧海马HATA高于HCs。在T2DM组中,HbAc1和FINS与某些海马亚区的影像学特征呈负相关。
结论:本研究表明,T2DM患者在CA1、DG、和右侧海马下丘,右侧海马下膜与慢性高血糖有关。此外,我们观察到左海马CA3,下膜的自发神经活动增加,和双边HATA地区,以及左侧海马CA3,DG的局部神经协调增强,HATA,在2型糖尿病患者中,这可能反映了对认知能力下降的适应性补偿。然而,这种补偿可能随着代谢紊乱的加重而下降.