TY - JOUR
T1 - Interactions Between Aging and Alzheimer’s Disease on Structural Brain Networks
AU - and The Alzheimer’s Disease Neuroimaging Initiative
AU - Wu, Zhanxiong
AU - Gao, Yunyuan
AU - Potter, Thomas
AU - Benoit, Julia
AU - Shen, Jian
AU - Schulz, Paul E.
AU - Zhang, Yingchun
N1 - Funding Information:
The research was supported in part by Natural Science Foundation of Zhejiang Province (LY20E070005, LY17E070007), National Natural Science Foundation of China (51207038), China Scholarship Council, and the University of Houston. Data collection and sharing for this project was funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI; National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the
Funding Information:
Funding. The research was supported in part by Natural Science Foundation of Zhejiang Province (LY20E070005, LY17E070007), National Natural Science Foundation of China (51207038), China Scholarship Council, and the University of Houston. Data collection and sharing for this project was funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI; National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer’s Association; Alzheimer’s Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research and Development, LLC.; Johnson and Johnson Pharmaceutical Research and Development LLC.; Lumosity; Lundbeck; Merck and Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health4. The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer’s Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California.
Publisher Copyright:
© Copyright © 2021 Wu, Gao, Potter, Benoit, Shen, Schulz, Zhang and The Alzheimer’s Disease Neuroimaging Initiative.
PY - 2021/6/10
Y1 - 2021/6/10
N2 - Normative aging and Alzheimer’s disease (AD) propagation alter anatomical connections among brain parcels. However, the interaction between the trajectories of age- and AD-linked alterations in the topology of the structural brain network is not well understood. In this study, diffusion-weighted magnetic resonance imaging (MRI) datasets of 139 subjects from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database were used to document their structural brain networks. The 139 participants consist of 45 normal controls (NCs), 37 with early mild cognitive impairment (EMCI), 27 with late mild cognitive impairment (LMCI), and 30 AD patients. All subjects were further divided into three subgroups based on their age (56–65, 66–75, and 71–85 years). After the structural connectivity networks were built using anatomically-constrained deterministic tractography, their global and nodal topological properties were estimated, including network efficiency, characteristic path length, transitivity, modularity coefficient, clustering coefficient, and betweenness. Statistical analyses were then performed on these metrics using linear regression, and one- and two-way ANOVA testing to examine group differences and interactions between aging and AD propagation. No significant interactions were found between aging and AD propagation in the global topological metrics (network efficiency, characteristic path length, transitivity, and modularity coefficient). However, nodal metrics (clustering coefficient and betweenness centrality) of some cortical parcels exhibited significant interactions between aging and AD propagation, with affected parcels including left superior temporal, right pars triangularis, and right precentral. The results collectively confirm the age-related deterioration of structural networks in MCI and AD patients, providing novel insight into the cross effects of aging and AD disorder on brain structural networks. Some early symptoms of AD may also be due to age-associated anatomic vulnerability interacting with early anatomic changes associated with AD.
AB - Normative aging and Alzheimer’s disease (AD) propagation alter anatomical connections among brain parcels. However, the interaction between the trajectories of age- and AD-linked alterations in the topology of the structural brain network is not well understood. In this study, diffusion-weighted magnetic resonance imaging (MRI) datasets of 139 subjects from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database were used to document their structural brain networks. The 139 participants consist of 45 normal controls (NCs), 37 with early mild cognitive impairment (EMCI), 27 with late mild cognitive impairment (LMCI), and 30 AD patients. All subjects were further divided into three subgroups based on their age (56–65, 66–75, and 71–85 years). After the structural connectivity networks were built using anatomically-constrained deterministic tractography, their global and nodal topological properties were estimated, including network efficiency, characteristic path length, transitivity, modularity coefficient, clustering coefficient, and betweenness. Statistical analyses were then performed on these metrics using linear regression, and one- and two-way ANOVA testing to examine group differences and interactions between aging and AD propagation. No significant interactions were found between aging and AD propagation in the global topological metrics (network efficiency, characteristic path length, transitivity, and modularity coefficient). However, nodal metrics (clustering coefficient and betweenness centrality) of some cortical parcels exhibited significant interactions between aging and AD propagation, with affected parcels including left superior temporal, right pars triangularis, and right precentral. The results collectively confirm the age-related deterioration of structural networks in MCI and AD patients, providing novel insight into the cross effects of aging and AD disorder on brain structural networks. Some early symptoms of AD may also be due to age-associated anatomic vulnerability interacting with early anatomic changes associated with AD.
KW - Alzheimer’s disease
KW - cognitive impairment
KW - diffusion-weighted magnetic resonance imaging
KW - nerve fiber tracking
KW - structural network
UR - http://www.scopus.com/inward/record.url?scp=85108650206&partnerID=8YFLogxK
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U2 - 10.3389/fnagi.2021.639795
DO - 10.3389/fnagi.2021.639795
M3 - Article
AN - SCOPUS:85108650206
SN - 1663-4365
VL - 13
JO - Frontiers in Aging Neuroscience
JF - Frontiers in Aging Neuroscience
M1 - 639795
ER -