Evidence map›Paper›PMID 33004840›Full record

ArticleScientific reports2020

The neurophysiological architecture of semantic dementia: spectral dynamic causal modelling of a neurodegenerative proteinopathy.

Elia Benhamou, Charles R Marshall, Lucy L Russell, Chris J D Hardy, Rebecca L Bond, Harri Sivasathiaseelan, Caroline V Greaves, Karl J Friston, Jonathan D Rohrer, Jason D Warren and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Executive functions in primary progressive aphasia: A meta-analysis.Cortex; a journal devoted to the study of the nervous system and behavior · 2022
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Symptom-led staging for semantic and non-fluent/agrammatic variants of primary progressive aphasia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  9. Article
  10. Article
  11. Symptom-led staging for primary progressive aphasia.medRxiv : the preprint server for health sciences · 2023
    Article
  12. Temporopolar regions of the human brain.Brain : a journal of neurology · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Primary Progressive Aphasia: Toward a Pathophysiological Synthesis.Current neurology and neuroscience reports · 2021
    Review
  20. Review
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

11 authors at 4 institutions in 2 countries.

Elia BenhamouDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK. elia.benhamou.16@ucl.ac.uk.
Charles R MarshallDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Lucy L RussellDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Chris J D HardyDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Rebecca L BondDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Harri SivasathiaseelanDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Caroline V GreavesDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Karl J FristonWellcome Centre for Human Neuroimaging, UCL Institute of Neurology, University College London, London, UK.
Jonathan D RohrerDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Jason D WarrenDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, 8-11 Queen Square, London, WC1N 3AR, UK.
Adeel RaziWellcome Centre for Human Neuroimaging, UCL Institute of Neurology, University College London, London, UK.
University College London · GBNational Hospital for Neurology and Neurosurgery · GBUK Dementia Research Institute · GBWellcome Centre for Human Neuroimaging · GB

Funding

Department of HealthThe Dunhill Medical Trust PA23_HardyWellcome TrustWellcome Trust 088130/Z/09/Z
6 · The paper itself

Abstract

The selective destruction of large-scale brain networks by pathogenic protein spread is a ubiquitous theme in neurodegenerative disease. Characterising the circuit architecture of these diseases could illuminate both their pathophysiology and the computational architecture of the cognitive processes they target. However, this is challenging using standard neuroimaging techniques. Here we addressed this issue using a novel technique-spectral dynamic causal modelling-that estimates the effective connectivity between brain regions from resting-state fMRI data. We studied patients with semantic dementia-the paradigmatic disorder of the brain system mediating world knowledge-relative to healthy older individuals. We assessed how the effective connectivity of the semantic appraisal network targeted by this disease was modulated by pathogenic protein deposition and by two key phenotypic factors, semantic impairment and behavioural disinhibition. The presence of pathogenic protein in SD weakened the normal inhibitory self-coupling of network hubs in both antero-mesial temporal lobes, with development of an abnormal excitatory fronto-temporal projection in the left cerebral hemisphere. Semantic impairment and social disinhibition were linked to a similar but more extensive profile of abnormally attenuated inhibitory self-coupling within temporal lobe regions and excitatory projections between temporal and inferior frontal regions. Our findings demonstrate that population-level dynamic causal modelling can disclose a core pathophysiological feature of proteinopathic network architecture-attenuation of inhibitory connectivity-and the key elements of distributed neuronal processing that underwrite semantic memory.

Indexed as

AgedFemaleFrontotemporal DementiaFunctional NeuroimagingHumansMagnetic Resonance ImagingMaleModels, NeurologicalNerve Tissue ProteinsNeural PathwaysNeuropsychological TestsNerve Tissue Proteins

Identifiers

PMID33004840
PMCPMC7530731
OpenAlexW3090022549

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.