背景:重度抑郁症(MDD)的特征是海马体积减少,影响认知功能。炎症,特别是升高的肿瘤坏死因子-α(TNF-α)水平,与MDD病理生理学有关。这项研究调查了TNF-α水平之间的关系,海马体积,β-淀粉样蛋白(Aβ)负荷,MDD患者的认知能力,旨在阐明炎症标志物之间复杂的相互作用,病理学指标,大脑结构改变,非痴呆MDD个体的认知表现。
方法:52例非痴呆MDD患者,包括25例轻度认知障碍(MCI),与10名对照受试者一起招募。每位参与者都进行了全面的评估,包括TNF-α血液检测,18F-florbetapir正电子发射断层扫描,磁共振成像扫描,和神经心理学测试。统计分析,根据年龄和教育程度进行调整,进行调查TNF-α水平之间的关联,调整海马体积(HVa),全球Aβ负荷,和认知表现。
结果:与对照组相比,MCIMDD患者的TNF-α水平升高,HVa降低。相关分析表明,MCIMDD中TNF-α水平与HVa呈负相关,所有MDD,和所有主题组。在所有MDD和所有受试者中,TNF-α水平和HVa均与处理速度显着相关。值得注意的是,全球18F-florbetapir标准化摄取值比率与TNF-α水平没有显着相关性,HVa,和认知措施。
结论:这项研究强调了MCIMDD患者TNF-α水平升高和海马体积减少,表明抑郁症患者外周炎症和脑结构性改变之间存在潜在关联。此外,我们的结果表明,某些MDD病例可能受非淀粉样蛋白介导的过程的影响,影响他们的TNF-α和海马体积。这些发现强调了进一步研究炎症之间复杂相互作用的重要性。神经变性,MDD中的认知功能。
BACKGROUND: Major depressive disorder (MDD) is characterized by hippocampal volume reduction, impacting cognitive function. Inflammation, particularly elevated tumor necrosis factor-alpha (TNF-α) levels, is consistently implicated in MDD pathophysiology. This study investigates the relationships between TNF-α levels, hippocampal volume, beta-amyloid (Aβ) burden, and cognitive abilities in MDD patients, aiming to illuminate the complex interplay among inflammatory markers, pathology indicators, structural brain alterations, and cognitive performance in non-demented MDD individuals.
METHODS: Fifty-two non-demented MDD patients, comprising 25 with mild cognitive impairment (MCI), were recruited along with 10 control subjects. Each participant underwent a thorough assessment encompassing TNF-α blood testing, 18F-florbetapir positron emission tomography, magnetic resonance imaging scans, and neuropsychological testing. Statistical analyses, adjusted for age and education, were performed to investigate the associations between TNF-α levels, adjusted hippocampal volume (HVa), global Aβ burden, and cognitive performance.
RESULTS: MCI MDD patients displayed elevated TNF-α levels and reduced HVa relative to controls. Correlation analyses demonstrated inverse relationships between TNF-α level and HVa in MCI MDD, all MDD, and all subjects groups. Both TNF-α level and HVa exhibited significant correlations with processing speed across all MDD and all subjects. Notably, global 18F-florbetapir standardized uptake value ratio did not exhibit significant correlations with TNF-α level, HVa, and cognitive measures.
CONCLUSIONS: This study highlights elevated TNF-α levels and reduced hippocampal volume in MCI MDD patients, indicating a potential association between peripheral inflammation and structural brain alterations in depression. Furthermore, our results suggest that certain cases of MDD may be affected by non-amyloid-mediated process, which impacts their TNF-α and hippocampal volume. These findings emphasize the importance of further investigating the complex interplay among inflammation, neurodegeneration, and cognitive function in MDD.