Evidence map›Paper›PMID 28861336›Full record

ArticleNeuroImage. Clinical2017

A whole-brain computational modeling approach to explain the alterations in resting-state functional connectivity during progression of Alzheimer's disease.

Murat Demirtaş, Carles Falcon, Alan Tucholka, Juan Domingo Gispert, José Luis Molinuevo, Gustavo Deco

Open access · goldAbstract read
In one paragraph

Article in NeuroImage. Clinical, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 94 citations in OpenAlex.

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  4. Cortical synchrony is reduced in Alzheimer's disease and relates to arousal state.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 4 countries.

Murat DemirtaşCenter for Brain and Cognition, Computational Neuroscience Group, Department of Information and Communication Technologies, Universitat Pompeu Fabra, Barcelona 08018, Spain.
Carles FalconBarcelonaβeta Brain Research Center, Pasqual Maragall Foundation, Barcelona, Spain.
Alan TucholkaBarcelonaβeta Brain Research Center, Pasqual Maragall Foundation, Barcelona, Spain.
Juan Domingo GispertBarcelonaβeta Brain Research Center, Pasqual Maragall Foundation, Barcelona, Spain.
José Luis MolinuevoBarcelonaβeta Brain Research Center, Pasqual Maragall Foundation, Barcelona, Spain.
Gustavo DecoCenter for Brain and Cognition, Computational Neuroscience Group, Department of Information and Communication Technologies, Universitat Pompeu Fabra, Barcelona 08018, Spain.
Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESPasqual Maragall Foundation · ESInstitució Catalana de Recerca i Estudis Avançats · ESUniversitat Pompeu Fabra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common dementia with dramatic consequences. The research in structural and functional neuroimaging showed altered brain connectivity in AD. In this study, we investigated the whole-brain resting state functional connectivity (FC) of the subjects with preclinical Alzheimer's disease (PAD), mild cognitive impairment due to AD (MCI) and mild dementia due to Alzheimer's disease (AD), the impact of APOE4 carriership, as well as in relation to variations in core AD CSF biomarkers. The synchronization in the whole-brain was monotonously decreasing during the course of the disease progression. Furthermore, in AD patients we found widespread significant decreases in functional connectivity (FC) strengths particularly in the brain regions with high global connectivity. We employed a whole-brain computational modeling approach to study the mechanisms underlying these alterations. To characterize the causal interactions between brain regions, we estimated the effective connectivity (EC) in the model. We found that the significant EC differences in AD were primarily located in left temporal lobe. Then, we systematically manipulated the underlying dynamics of the model to investigate simulated changes in FC based on the healthy control subjects. Furthermore, we found distinct patterns involving CSF biomarkers of amyloid-beta (Aβ1 - 42) total tau (t-tau) and phosphorylated tau (p-tau). CSF Aβ1 - 42 was associated to the contrast between healthy control subjects and clinical groups. Nevertheless, tau CSF biomarkers were associated to the variability in whole-brain synchronization and sensory integration regions. These associations were robust across clinical groups, unlike the associations that were found for CSF Aβ1 - 42. APOE4 carriership showed no significant correlations with the connectivity measures.

Indexed as

Models, TheoreticalProdromal SymptomsAgedAlzheimer DiseaseAmyloid beta-PeptidesBrainCognitive DysfunctionConnectomeFemaleHumansMagnetic Resonance ImagingMaleMiddle Agedtau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer's diseaseBiomarkersComputational modelingDynamic functional connectivityResting state fMRI

Identifiers

PMID28861336
PMCPMC5568172
OpenAlexW2525626228

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.