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Increased intrinsic default-mode network activity as a compensatory mechanism in aMCI: a resting-state functional connectivity MRI study

Numerous studies have investigated the differences in the mean functional connectivity (FC) strength between amnestic mild cognitive impairment (aMCI) patients and normal subjects using resting-state functional magnetic resonance imaging. However, whether the mean FC is increased, decreased or uncha...

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Detalles Bibliográficos
Autores principales: Liang, Jiali, Li, Yunfei, Liu, Hao, Zhang, Sisi, Wang, Meimei, Chu, Yonghua, Ye, Jianping, Xi, Qian, Zhao, Xiaohu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185142/
https://www.ncbi.nlm.nih.gov/pubmed/32238610
http://dx.doi.org/10.18632/aging.102986
Descripción
Sumario:Numerous studies have investigated the differences in the mean functional connectivity (FC) strength between amnestic mild cognitive impairment (aMCI) patients and normal subjects using resting-state functional magnetic resonance imaging. However, whether the mean FC is increased, decreased or unchanged in aMCI patients compared to normal controls remains unclear. Two factors might lead to inconsistent results: the determination of regions of interest and the reliability of the FC. We explored differences in FC and the degree centrality (Dc) constructed by the bootstrap method, between and within networks (default-mode network (DN), frontoparietal control network (CN), dorsal attention network (AN)), and resulting from a hierarchical-clustering algorithm. The mean FC within the DN and CN was significantly increased (P < 0.05, uncorrected) in patients. Significant increases (P < 0.05, uncorrected) in the mean FC were found in patients between DN and CN and between DN and AN. Five pairs of FC (false discovery rate corrected) and the Dc of six regions (Bonferroni corrected) displayed a significant increase in patients. Lower cognitive ability was significantly associated with a greater increase in the Dc of the left superior temporal sulcus. Our results demonstrate that the early dysfunctions in aMCI disease are mainly compensatory impairments.