首页> 外文期刊>BMC Psychiatry >Neurometabolic characteristics in the anterior cingulate gyrus of Alzheimer’s disease patients with depression: a 1 H magnetic resonance spectroscopy study
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Neurometabolic characteristics in the anterior cingulate gyrus of Alzheimer’s disease patients with depression: a 1 H magnetic resonance spectroscopy study

机译:阿尔茨海默氏病抑郁患者的前扣带回中的神经代谢特征:1 H磁共振波谱研究

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Depression is a common comorbid psychiatric symptom in patients with Alzheimer’s disease (AD), and the prevalence of depression is higher among people with AD compared with healthy older adults. Comorbid depression in AD may increase the risk of cognitive decline, impair patients’ function, and reduce their quality of life. However, the mechanisms of depression in AD remain unclear. Here, our aim was to identify neurometabolic characteristics in the brain that are associated with depression in patients with mild AD. Thirty-seven patients were evaluated using the Neuropsychiatric Inventory (NPI) and Hamilton Depression Rating Scale (HAMD-17), and divided into two groups: 17?AD patients with depression (D-AD) and 20 non-depressed AD patients (nD-AD). Using proton magnetic resonance spectroscopy, we characterized neurometabolites in the anterior cingulate gyrus (ACG) of D-AD and nD-AD patients. Compared with nD-AD patients, D-AD patients showed lower N-acetylaspartate/creatine (NAA/Cr) and higher myo-inositol/creatine (mI/Cr) in the left ACG. NPI score correlated with NAA/Cr and mI/Cr in the left ACG, while HAMD correlated with NAA/Cr. Our findings show neurometabolic alterations in D-AD patients. Thus, D-AD pathogenesis may be attributed to abnormal activity of neurons and glial cells in the left ACG.
机译:抑郁症是阿尔茨海默氏病(AD)患者的常见合并症精神症状,与健康的老年人相比,AD患者的抑郁症患病率更高。 AD合并症的抑郁症可能增加认知能力下降的风险,损害患者的功能并降低其生活质量。但是,AD抑郁的机制仍不清楚。在这里,我们的目的是确定与轻度AD患者抑郁相关的大脑神经代谢特征。使用神经精神病学量表(NPI)和汉密尔顿抑郁量表(HAMD-17)对37例患者进行了评估,分为两组:17?AD抑郁症患者(D-AD)和20例非抑郁AD患者(nD -广告)。使用质子磁共振波谱,我们表征了D-AD和nD-AD患者的前扣带回(ACG)中的神经代谢物。与nD-AD患者相比,D-AD患者左ACG的N-乙酰天门冬氨酸/肌酸(NAA / Cr)降低,肌醇/肌酸(mI / Cr)升高。 NPI评分与左ACG中的NAA / Cr和mI / Cr相关,而HAMD与NAA / Cr相关。我们的发现显示D-AD患者的神经代谢改变。因此,D-AD发病机制可能归因于左ACG中神经元和神经胶质细胞的异常活动。

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