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Cited by 142Functional Brain Connectivity StudiesDementia and Cognitive Impairment ResearchComplex Network Analysis Techniques

Disrupted Network Topology in Patients with Stable and Progressive Mild Cognitive Impairment and Alzheimer's Disease

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Pereira, Joana B., Mijalkov, Mite, Kakaei, Ehsan, Mecocci, Patricia, Vellas, Bruno, Tsolaki, Magda, Kłoszewska, Iwona, Soininen, Hilka +6 more·2016·Cerebral Cortex
DOI 10.1093/cercor/bhw128PMC PMC4961019
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Abstract

Recent findings suggest that Alzheimer's disease (AD) is a disconnection syndrome characterized by abnormalities in large-scale networks. However, the alterations that occur in network topology during the prodromal stages of AD, particularly in patients with stable mild cognitive impairment (MCI) and those that show a slow or faster progression to dementia, are still poorly understood. In this study, we used graph theory to assess the organization of structural MRI networks in stable MCI (sMCI) subjects, late MCI converters (lMCIc), early MCI converters (eMCIc), and AD patients from 2 large multicenter cohorts: ADNI and AddNeuroMed. Our findings showed an abnormal global network organization in all patient groups, as reflected by an increased path length, reduced transitivity, and increased modularity compared with controls. In addition, lMCIc, eMCIc, and AD patients showed a decreased path length and mean clustering compared with the sMCI group. At the local level, there were nodal clustering decreases mostly in AD patients, while the nodal closeness centrality detected abnormalities across all patient groups, showing overlapping changes in the hippocampi and amygdala and nonoverlapping changes in parietal, entorhinal, and orbitofrontal regions. These findings suggest that the prodromal and clinical stages of AD are associated with an abnormal network topology.

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  • Microstructural 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 [20]

    The Discussion (page unavailable) says that white-matter integrity loss or disruption of white-matter fibers has previously been observed in MCI and AD patients. It does not locate that damage in the corpus callosum, fornix, and cingulum; the cited paper’s reference-list entry about cingulum imaging does not establish the full three-tract claim. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • White 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 [20]

    The Discussion reports abnormal network organization in AD patients and interprets increased path length as less efficient communication between brain regions. But the Methods describe networks built from cortical thickness and subcortical volume, not measures of white-matter microstructural damage. The paper therefore supports disrupted network organization, but does not establish the claimed association with that damage or directly measure impaired network function. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Increased characteristic path length has also been observed in patients with AD using gray matter structural connectomes and EEG-based networks.

    “Increased characteristic path length has also been observed in patients with AD using gray matter structural connectomes (Kim et al., 2016; Pereira et al., 2016) and electroencephalography (EEG)-based networks (Stam et al., 2007).”

    From Functional and structural connectome properties in the 5XFAD transgenic mouse model of Alzheimer’s disease (2018) · cites this paper as Pereira et al., 2016

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Authors
Pereira, J. B., Mijalkov, M., Kakaei, E., Mecocci, P., Vellas, B., Tsolaki, M., Kłoszewska, I., Soininen, H., Spenger, C., Lovestone, S., Simmons, A., Wahlund, L.-O., Volpe, G., & Westman, E.
Affiliations
  • Karolinska Institutet (SE)
  • Inserm (FR)
  • Aristotle University of Thessaloniki (GR)
  • Medical University of Lodz (PL)
  • University of Eastern Finland (FI)
  • Karolinska University Hospital (SE)
  • Bilkent University (TR)
Corresponding author
Pereira, Joana B.
ORCID
Venue
Cerebral Cortex
Publisher
Oxford University Press (OUP)
Published
2016-05-13
Volume
26
Issue
8
Pages
3476-3493
ISSN
  • 1047-3211 (ISSN-L)
  • 1460-2199
DOI
10.1093/cercor/bhw128
PMC
PMC4961019
OpenAlex
W2374330807
Cited by
142
References
15
Citations by year
2026: 7 · 2025: 9 · 2024: 14 · 2023: 16 · 2022: 15 · 2021: 21 · 2020: 20 · 2019: 15 · 2018: 15 · 2017: 10
FWCI
8.48
Type
journal article
Language
en
Open access
Licence
other-oa
Locations
  • Cerebral Cortex (publishedVersion, other-oa)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Bilkent University Institutional Repository (Bilkent University) (submittedVersion, other-oa)
  • UEF eRepo (University of Eastern Finland) (submittedVersion, cc-by)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • U.S. Department of Defense (U01 AG024904, W81XWH, W81XWH-12-2-, W81XWH-12, AG024904)
  • Alzheimer's Association (U01 AG024904, W81XWH-12-2-0012)
  • Bristol-Myers Squibb (U01 AG024904, AG024904, W81XWH-12-2-0012)
  • Eli Lilly and Company (FP6-2004-LIFESCIHEALTH-5, U01 AG024904, AG024904, W81XWH-12-2-0012)
  • Pfizer (AG024904, W81XWH-12-2-0012, U01 AG024904)
  • Biogen (W81XWH-12-2-0012, U01 AG024904, AG024904)
  • F. Hoffmann-La Roche (W81XWH-12-2-0012, AG024904, U01 AG024904)
  • Medpace (U01 AG024904)
  • Meso Scale Diagnostics (U01 AG024904, AG024904, W81XWH-12-2-0012)
  • Synarc (U01 AG024904)
  • Alzheimer's Disease Neuroimaging Initiative (W81XWH-12-2–0012, U01AG024904, AG024904, W81XWH-12-2-)
  • BioClinica (U01 AG024904, W81XWH-12-2-0012, AG024904)
  • Novartis Pharmaceuticals Corporation (W81XWH-12-2-0012, U01 AG024904, AG024904)
  • Northern California Institute for Research and Education (U01 AG024904, W81XWH-12-2-0012)
  • European Commission (U01 AG024904, FP7-PEOPLE-2012-IEF, W81XWH-12-2-0012, FP6-2004-LIFESCIHEALTH-5, 328758)
  • Stiftelsen för Strategisk Forskning
  • Eisai (W81XWH-12-2-0012, U01 AG024904, AG024904)
  • Hjärnfonden
  • Karolinska Institutet
  • Servier (AG024904, W81XWH-12-2-0012, U01 AG024904)
  • IXICO (AG024904, W81XWH-12-2-0012, U01 AG024904)
  • National Institutes of Health (5u01ag024904-10, W81XWH, W81XWH-12-2-0012, U01-AG024904, AG024904)
  • Genentech (W81XWH-12-2-0012, AG024904, U01 AG024904)
  • University of California, Los Angeles
  • University of California, San Diego
  • Canadian Institutes of Health Research (U01 AG024904, W81XWH-12-2-0012)
  • National Institute on Aging (U01-AG-024904)
  • FP7 People: Marie-Curie Actions (FP7-PEOPLE-2012-IEF)
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, mild cognitive impairment, network topology, structural connectome, graph theory, path length, clustering coefficient, modularity, node centrality, hippocampus, amygdala, entorhinal cortex, orbitofrontal cortex, parietal cortex, disconnection syndrome, prodromal Alzheimer's disease
MeSH terms
Aged, Alzheimer Disease, Brain, Brain Mapping, Female, Humans, Magnetic Resonance Imaging, Male, Neural Pathways, Cohort Studies, Disease Progression, Cognitive Dysfunction

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