title: Disrupted Structural Brain Network in AD and aMCI: A Finding of Long Fiber Degeneration.
abstract: Although recent evidence has emerged that Alzheimer's disease (AD) and amnestic mild cognitive impairment (aMCI) patients show both regional brain abnormalities and topological degeneration in brain networks, our understanding of the effects of white matter fiber aberrations on brain network topology in AD and aMCI is still rudimentary. In this study, we investigated the regional volumetric aberrations and the global topological abnormalities in AD and aMCI patients. The results showed a widely distributed atrophy in both gray and white matters in the AD and aMCI groups. In particular, AD patients had weaker connectivity with long fiber length than aMCI and normal control (NC) groups, as assessed by fractional anisotropy (FA). Furthermore, the brain networks of all three groups exhibited prominent economical small-world properties. Interestingly, the topological characteristics estimated from binary brain networks showed no significant group effect, indicating a tendency of preserving an optimal topological architecture in AD and aMCI during degeneration. However, significantly longer characteristic path length was observed in the FA weighted brain networks of AD and aMCI patients, suggesting dysfunctional global integration. Moreover, the abnormality of the characteristic path length was negatively correlated with the clinical ratings of cognitive impairment. Thus, the results therefore suggested that the topological alterations in weighted brain networks of AD are induced by the loss of connectivity with long fiber lengths. Our findings provide new insights into the alterations of the brain network in AD and may indicate the predictive value of the network metrics as biomarkers of disease development.
authors.forename: Rong
authors.initials: R
authors.lastname: Fang
authors.forename: Xiao-Xiao
authors.initials: XX
authors.lastname: Yan
authors.forename: Zhi-Yuan
authors.initials: ZY
authors.lastname: Wu
authors.forename: Yu
authors.initials: Y
authors.lastname: Sun
authors.forename: Qi-Hua
authors.initials: QH
authors.lastname: Yin
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.forename: Hui-Dong
authors.initials: HD
authors.lastname: Tang
authors.forename: Jun-Feng
authors.initials: JF
authors.lastname: Sun
authors.forename: Fei
authors.initials: F
authors.lastname: Miao
authors.affiliation: Department of Neurology & Institute of Neurology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200025 China; School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200030 China. chen_sd@medmail.com.cn.
authors.forename: Sheng-Di
authors.initials: SD
authors.lastname: Chen
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000473:pathology*; D000704:Analysis of Variance; D001921:Brain / Q000473:pathology*; D001931:Brain Mapping; D016022:Case-Control Studies; D060825:Cognitive Dysfunction / Q000473:pathology*; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008609:Mental Status Schedule; D008875:Middle Aged; D009434:Neural Pathways / Q000473:pathology*; D066127:White Matter / Q000473:pathology*