Evidence map›Paper›PMID 36054198›Full record

ArticlePLoS computational biology2022

High-order functional redundancy in ageing explained via alterations in the connectome in a whole-brain model.

Marilyn Gatica, Fernando E Rosas, Pedro A M Mediano, Ibai Diez, Stephan P Swinnen, Patricio Orio, Rodrigo Cofré, Jesus M Cortes

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  3. Structural signatures of synergy and redundancy in human brain function.bioRxiv : the preprint server for biology · 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

8 authors at 8 institutions in 6 countries.

Marilyn GaticaCentro Interdisciplinario de Neurociencia de Valparaíso, Universidad de Valparaíso, Valparaíso, Chile.ORCID 0000-0001-5783-8283
Fernando E RosasCentre for Psychedelic Research, Department of Brain Science, Imperial College London, London, United Kingdom.ORCID 0000-0001-7790-6183
Pedro A M MedianoDepartment of Psychology, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0003-1789-5894
Ibai DiezDepartment of Radiology, Division of Nuclear Medicine and Molecular Imaging, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.ORCID 0000-0001-5769-0178
Stephan P SwinnenResearch Center for Movement Control and Neuroplasticity, Department of Movement Sciences, KU Leuven, Leuven, Belgium.ORCID 0000-0001-7173-435X
Patricio OrioCentro Interdisciplinario de Neurociencia de Valparaíso, Universidad de Valparaíso, Valparaíso, Chile.ORCID 0000-0003-0332-8098
Rodrigo CofréCIMFAV-Ingemat, Facultad de Ingeniería, Universidad de Valparaíso, Valparaíso, Chile.ORCID 0000-0002-7498-7122
Jesus M CortesNeuroimaging Lab, Biocruces-Bizkaia Health Research Institute, Barakaldo, Spain.
Harvard University · USIkerbasque · ESInstitut des Neurosciences Paris-Saclay · FRQueen Mary University of London · GBUniversity of Sussex · GBUniversity of the Basque Country · ESUniversity of Valparaíso · CLVIB-KU Leuven Center for Brain & Disease Research · BE

Funding

Wellcome TrustWellcome Trust 210920/Z/18/Z
6 · The paper itself

Abstract

The human brain generates a rich repertoire of spatio-temporal activity patterns, which support a wide variety of motor and cognitive functions. These patterns of activity change with age in a multi-factorial manner. One of these factors is the variations in the brain's connectomics that occurs along the lifespan. However, the precise relationship between high-order functional interactions and connnectomics, as well as their variations with age are largely unknown, in part due to the absence of mechanistic models that can efficiently map brain connnectomics to functional connectivity in aging. To investigate this issue, we have built a neurobiologically-realistic whole-brain computational model using both anatomical and functional MRI data from 161 participants ranging from 10 to 80 years old. We show that the differences in high-order functional interactions between age groups can be largely explained by variations in the connectome. Based on this finding, we propose a simple neurodegeneration model that is representative of normal physiological aging. As such, when applied to connectomes of young participant it reproduces the age-variations that occur in the high-order structure of the functional data. Overall, these results begin to disentangle the mechanisms by which structural changes in the connectome lead to functional differences in the ageing brain. Our model can also serve as a starting point for modeling more complex forms of pathological ageing or cognitive deficits.

Indexed as

ConnectomeAdolescentAdultAgedAged, 80 and overAgingBrainChildCognitionHumansMagnetic Resonance ImagingMiddle AgedNerve NetYoung Adult

Identifiers

PMID36054198
PMCPMC9477425
OpenAlexW4294295396

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.