Memory dysfunction in type 2 diabetes mellitus correlates with reduced hippocampal CA1 and subiculum volumes.
Memory dysfunction in type 2 diabetes mellitus correlates with reduced hippocampal CA1 and subiculum volumes.
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2 型糖尿病的记忆功能障碍与海马 CA1 和下丘脑体积减少相关
DOI：
10.4103/0366-6999.151082
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发表时间：
2015-02-20
影响因子：
6.1
通讯作者：
Wang J
中科院分区：
文献类型：
--
作者：
Zhang YW;Zhang JQ;Liu C;Wei P;Zhang X;Yuan QY;Yin XT;Wei LQ;Cui JG;Wang J
皮质下深灰质（SDGM）结构在2型糖尿病（T2DM）所致认知功能损害中的作用，特别是海马亚区的作用，目前还没有引起足够的关注。我们的目的是使用磁共振成像（MRI）评估SDGM结构和海马子区域的体内体积，并测试它们与T2DM认知表现的相关性。本研究共入组了80例T2DM患者和80例神经系统未受损的健康对照，年龄、性别和教育水平相匹配。我们使用一种新的技术，使自动容积法评估的SDGM结构和七个海马子领域的MRI的体积。我们使用简易精神状态检查和蒙特利尔认知评估（莫卡）评分作为认知表现的衡量标准。通过偏相关分析评估2型糖尿病患者糖化血红蛋白（HbA1c）与SDGM结构和神经心理学测试的相关性，以及海马子区域与神经心理学测试之间的相关性。双侧海马体积在T2DM患者中较小，主要在CA1和下托亚区。偏相关分析表明，莫卡评分，特别是那些关于延迟记忆，与海马CA1和下托体积减少T2DM患者显着正相关。此外，较高的HbA1c水平与T2DM患者记忆力差和海马萎缩显著相关。这些数据表明，海马可能是2型糖尿病SDGM结构中的主要受累区域。海马CA1和下托区的这些结构变化可能是海马功能障碍的潜在神经生物学机制的核心，表明这些区域的变性可能是T2DM患者记忆障碍的原因。
Little attention has been paid to the role of subcortical deep gray matter (SDGM) structures in type 2 diabetes mellitus (T2DM)-induced cognitive impairment, especially hippocampal subfields. Our aims were to assess the in vivo volumes of SDGM structures and hippocampal subfields using magnetic resonance imaging (MRI) and to test their associations with cognitive performance in T2DM. A total of 80 T2DM patients and 80 neurologically unimpaired healthy controls matched by age, sex and education level was enrolled in this study. We assessed the volumes of the SDGM structures and seven hippocampal subfields on MRI using a novel technique that enabled automated volumetry. We used Mini-Mental State Examination and Montreal Cognitive Assessment (MoCA) scores as measures of cognitive performance. The association of glycosylated hemoglobin (HbA1c) with SDGM structures and neuropsychological tests and correlations between hippocampal subfields and neuropsychological tests were assessed by partial correlation analysis in T2DM. Bilaterally, the hippocampal volumes were smaller in T2DM patients, mainly in the CA1 and subiculum subfields. Partial correlation analysis showed that the MoCA scores, particularly those regarding delayed memory, were significantly positively correlated with reduced hippocampal CA1 and subiculum volumes in T2DM patients. Additionally, higher HbA1c levels were significantly associated with poor memory performance and hippocampal atrophy among T2DM patients. These data indicate that the hippocampus might be the main affected region among the SDGM structures in T2DM. These structural changes in the hippocampal CA1 and subiculum areas might be at the core of underlying neurobiological mechanisms of hippocampal dysfunction, suggesting that degeneration in these regions could be responsible for memory impairments in T2DM patients.