Evidence map›Paper›PMID 38712321›Full record

ArticleBrain communications2024

Synaptic alterations associated with disrupted sensory encoding in a mouse model of tauopathy.

Soraya Meftah, Annalisa Cavallini, Tracey K Murray, Lukasz Jankowski, Suchira Bose, Michael C Ashby, Jonathan T Brown, Jonathan Witton

Abstract read
In one paragraph

Article in Brain communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Twenty years of therapeutic development in tauopathy mouse models: a scoping review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Review
  4. Article
  5. Desert Island Papers.Brain and neuroscience advances
    Article
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.

Soraya MeftahFaculty of Health and Life Sciences, Department of Clinical and Biomedical Science, University of Exeter, Exeter, EX1 2LU, UK.ORCID https://orcid.org/0000-0002-3408-5626
Annalisa CavalliniErl Wood Manor, Eli Lilly Pharmaceuticals, Windlesham, Surrey, GU20 6PH, UK.
Tracey K MurrayErl Wood Manor, Eli Lilly Pharmaceuticals, Windlesham, Surrey, GU20 6PH, UK.
Lukasz JankowskiErl Wood Manor, Eli Lilly Pharmaceuticals, Windlesham, Surrey, GU20 6PH, UK.
Suchira BoseErl Wood Manor, Eli Lilly Pharmaceuticals, Windlesham, Surrey, GU20 6PH, UK.
Michael C AshbySchool of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, BS8 1TD, UK.
Jonathan T BrownFaculty of Health and Life Sciences, Department of Clinical and Biomedical Science, University of Exeter, Exeter, EX1 2LU, UK.
Jonathan WittonFaculty of Health and Life Sciences, Department of Clinical and Biomedical Science, University of Exeter, Exeter, EX1 2LU, UK.

Funding

Wellcome Trust
6 · The paper itself

Abstract

Synapse loss is currently the best biological correlate of cognitive decline in Alzheimer's disease and other tauopathies. Synapses seem to be highly vulnerable to tau-mediated disruption in neurodegenerative tauopathies. However, it is unclear how and when this leads to alterations in function related to the progression of tauopathy and neurodegeneration. We used the well-characterized rTg4510 mouse model of tauopathy at 5-6 months and 7-8 months of age, respectively, to study the functional impact of cortical synapse loss. The earlier age was used as a model of prodromal tauopathy, with the later age corresponding to more advanced tau pathology and presumed progression of neurodegeneration. Analysis of synaptic protein expression in the somatosensory cortex showed significant reductions in synaptic proteins and NMDA and AMPA receptor subunit expression in rTg4510 mice. Surprisingly,

Indexed as

glutamatergicneurodegenerationsomatosensorysynapsestauopathy

Identifiers

PMID38712321
PMCPMC11073755

What OpenQuestion holds

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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.