阿尔茨海默病和轻度认知障碍中抑郁症共病的破坏性静息状态网络特征。

IF 3.4 3区 医学 Q2 NEUROSCIENCES
Alessandro von Gal, Dario Papa, Marco D'Auria, Laura Piccardi
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引用次数: 0

摘要

研究表明,神经退行性疾病中的抑郁合并症可以预测从轻度认知障碍(MCI)到阿尔茨海默病(AD)的转变。然而,其病理生理机制尚不完全清楚。目的在此,我们描述了AD和MCI中抑郁症合并症的异常功能静息状态网络(rsn)。方法我们对Scopus、PubMed和Web of Science进行了系统的文献综述,提取了比较抑郁和非抑郁MCI或AD患者静息状态扫描的实验。我们采用激活似然估计(ALE)对搜索结果中符合条件的研究进行meta分析,以描述研究中显著的共激活区域。结果系统检索得到17个实验,共303名受试者。ALE产生了10个显著的共激活簇,分布在5个主要rsn和皮质-基底神经节-丘脑回路中。结论神经退行性疾病伴发抑郁表现为静息状态异常波动。了解这些网络内部和网络之间的变化可能对未来的诊断和治疗应用有用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Disruptive resting state networks characterizing depressive comorbidity in Alzheimer's disease and mild cognitive impairment.

BackgroundDepressive comorbidity in neurodegeneration has been shown to predict conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD). However, its pathophysiology is not completely understood.ObjectiveHere, we characterize aberrant functional resting state networks (RSNs) characterizing depressive comorbidity in both AD and MCI.MethodsWe conducted a systematic literature review on Scopus, PubMed, and Web of Science to extract experiments that compared resting state scans of depressed and non-depressed MCI or AD patients. We employed Activation Likelihood Estimation (ALE) meta-analysis on eligible studies resulting from the search, to describe regions of significant co-activation across studies.ResultsThe systematic search resulted in 17 experiments, with 303 participants in total. The ALE yielded 10 clusters of significant co-activation distributed in the five major RSNs and across cortico-basal ganglia-thalamic circuits.ConclusionsDepressive comorbidity in neurodegeneration presents signature aberrant resting-state fluctuations. Understanding these within- and between-network alterations may be useful for future diagnostic and therapeutic applications.

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来源期刊
Journal of Alzheimer's Disease
Journal of Alzheimer's Disease 医学-神经科学
CiteScore
6.40
自引率
7.50%
发文量
1327
审稿时长
2 months
期刊介绍: The Journal of Alzheimer''s Disease (JAD) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer''s disease. The journal publishes research reports, reviews, short communications, hypotheses, ethics reviews, book reviews, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer''s disease.
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