Structural Insights into Aberrant Topological Patterns of Large-Scale Cortical Networks in Alzheimer's Disease
Open accessAbstract
Recent research on Alzheimer's disease (AD) has shown that cognitive and memory decline in this disease is accompanied by disrupted changes in the coordination of large-scale brain functional networks. However, alterations in coordinated patterns of structural brain networks in AD are still poorly understood. Here, we used cortical thickness measurement from magnetic resonance imaging to investigate large-scale structural brain networks in 92 AD patients and 97 normal controls. Brain networks were constructed by thresholding cortical thickness correlation matrices of 54 regions and analyzed using graph theoretical approaches. Compared with controls, AD patients showed decreased cortical thickness intercorrelations between the bilateral parietal regions and increased intercorrelations in several selective regions involving the lateral temporal and parietal cortex as well as the cingulate and medial frontal cortex regions. Specially, AD patients showed abnormal small-world architecture in the structural cortical networks (increased clustering and shortest paths linking individual regions), implying a less optimal topological organization in AD. Moreover, AD patients were associated with reduced nodal centrality predominantly in the temporal and parietal heteromodal association cortex regions and increased nodal centrality in the occipital cortex regions. Finally, the brain networks of AD were about equally as robust to random failures as those of controls, but more vulnerable against targeted attacks, presumably because of the effects of pathological topological organization. Our findings suggest that the coordinated patterns of cortical morphology are widely altered in AD patients, thus providing structural evidence for disrupted integrity in large-scale brain networks that underlie cognition. This work has implications for our understanding of how functional deficits in patients are associated with their underlying structural (morphological) basis.
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Large-world connectivity of distal networks including projections of the cingulate with frontal and temporal cortex predominates in AD, accompanied by degraded rich hubs.
“Indeed, “large world” connectivity of distal networks including projections of the cingulate with frontal and temporal cortex [42] predominates in AD, accompanied by degraded “rich hubs,” localized networks of high connectivity [43].”
From Effects of APOE2 and APOE4 on brain microstructure in older adults: modification by age, sex, and cognitive status (2024) · cites this paper as [42]
The Interregional correlations of cortical thickness section reports increased correlations in AD between the cingulate and frontal and temporal regions. The Altered small-world configurations section reports longer network paths and a shift toward a more regular configuration, but does not establish that “large-world” connectivity predominates or that the correlations are anatomical projections. The separate “rich hubs” clause is cited to [43], not this paper. (LLM, conf=0.85)
Experimental — accuracy not yet measuredWhite matter microstructural damage in Alzheimer's disease is associated with disrupted structural connectivity and impaired network functions.
“This damage is associated with disrupted structural connectivity and impaired network functions. 19 , 20 , 21”
From Apolipoprotein ε4 exacerbates white matter impairment in a mouse model of Aβ amyloidosis by decreasing actively myelinating oligodendrocytes (2025) · cites this paper as [21]
The Introduction (page unavailable) describes white-matter damage as a proposed cause of structural disconnection in Alzheimer’s disease. The Discussion reports disrupted cortical structural networks, but these were measured through cortical thickness, not white-matter microstructure; the section on structural and functional brain networks presents a link to functional impairment as speculation rather than a demonstrated association. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMicrostructural damage in the white matter of Alzheimer's disease patients has been reported in the corpus callosum, fornix, and cingulum.
“Microstructural damage in the white matter of AD patients has been reported in the corpus callosum, fornix, and cingulum. 19 , 20 , 21”
From Apolipoprotein ε4 exacerbates white matter impairment in a mouse model of Aβ amyloidosis by decreasing actively myelinating oligodendrocytes (2025) · cites this paper as [21]
The Introduction reports evidence suggesting AD-related abnormalities in white-matter structural integrity in the corpus callosum and cingulum. It names the superior longitudinal fasciculus, not the fornix, as the third example. The paper does not report microstructural measurements of all three tracts. (LLM, conf=0.88)
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“Indeed, “large world” connectivity of distal networks including projections of the cingulate with frontal and temporal cortex [42] predominates in AD, accompanied by degraded “rich hubs,” localized networks of high connectivity [43].”
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“Compared with healthy individuals, AD patients have a significant decrease in the structural association between the entorhinal cortex and the medial prefrontal cortex, the posterior cingulate cortex, the inferior orbitofrontal gyrus, the right superior parietal lobule, and the left superior occipital gyrus [24, 25],…”
BackgroundDrenthen, G. S., Backes, W. H., Freeze, W. M., Jacobs, H. I. L., Verheggen, I. C. M., van Boxtel, M. P. J., Hoff, E. I., Verhey, F. R., & Jansen, J. F. A. (2022) · Journal of Alzheimer’s Disease · doi:10.3233/jad-220175 · Cited by 10 · see citing works
Al‐Amin, M. M., Kim, B., Karahan, H., Tate, M. D., Walsh, S. P., Puntambekar, S. S., Bissel, S. J., Lamb, B. T., Wang, N., & Kim, J. (2025) · Alzheimer's & Dementia · doi:10.1002/alz.70791 · Cited by 6 · see citing works
- Authors
- He, Y., Chen, Z., & Evans, A.
- Affiliations
- Montreal Neurological Institute and Hospital (CA)
- Corresponding author
- Evans, Alan
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-04-30
- Volume
- 28
- Issue
- 18
- Pages
- 4756-4766
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6670444
- OpenAlex
- W1983537704
- Cited by
- 965
- References
- 92
- Citations by year
- 2026: 13 · 2025: 32 · 2024: 43 · 2023: 37 · 2022: 52 · 2021: 72 · 2020: 47 · 2019: 72 · 2018: 68 · 2017: 64 · 2016: 70 · 2015: 89 · 2014: 57 · 2013: 87 · 2012: 62
- FWCI
- 17.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, other-oa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Killam Trusts
- U.S. Public Health Service (P01MHO52176-11)
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Functional Brain Connectivity Studies
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Physical Sciences › Physics and Astronomy › Statistical and Nonlinear Physics › Complex Network Analysis Techniques
- Keywords
- Alzheimer's disease, structural brain networks, cortical thickness, network topology, node centrality, network robustness, parietal cortex, temporal cortex, cingulate cortex, medial frontal cortex, occipital cortex
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain Mapping, Cerebral Cortex, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Nerve Net, Stereotaxic Techniques, Neural Networks, Computer
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