Evidence map›Paper›PMID 28917666›Full record

ArticleNeurobiology of aging2017

Hippocampal neurophysiology is modified by a disease-associated C-terminal fragment of tau protein.

Francesco Tamagnini, Darren A Walsh, Jon T Brown, Marie K Bondulich, Diane P Hanger, Andrew D Randall

Abstract read
In one paragraph

Article in Neurobiology of aging, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Proteomic analysis links truncated tau to lysosome motility, autophagy, and endo-lysosomal dysfunction.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
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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.

Francesco TamagniniInstitute of Clinical and Biomedical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK. Electronic address: F.tamagnini@reading.ac.uk.
Darren A WalshInstitute of Clinical and Biomedical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK.
Jon T BrownInstitute of Clinical and Biomedical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK.
Marie K BondulichKing's College London, Institute of Psychiatry, Psychology & Neuroscience, Maurice Wohl Clinical Neuroscience Institute, London, UK.
Diane P HangerKing's College London, Institute of Psychiatry, Psychology & Neuroscience, Maurice Wohl Clinical Neuroscience Institute, London, UK.
Andrew D RandallInstitute of Clinical and Biomedical Sciences, University of Exeter Medical School, University of Exeter, Exeter, UK.

Funding

Medical Research Council G1100623Wellcome Trust
6 · The paper itself

Abstract

The accumulation of cleaved tau fragments in the brain is associated with several tauopathies. For this reason, we recently developed a transgenic mouse that selectively accumulates a C-Terminal 35 kDa human tau fragment (Tau35). These animals develop progressive motor and spatial memory impairment, paralleled by increased hippocampal glycogen synthase kinase 3β activity. In this neurophysiological study, we focused on the CA1 subfield of the hippocampus, a brain area involved in memory encoding. The accumulation of Tau35 results in a significant increase of short-term facilitation of the synaptic response in the theta frequency range (10 Hz), without affecting basal synaptic transmission and long-term synaptic plasticity. Tau35 expression also alters the intrinsic excitability of CA1 pyramidal neurons. Thus, Tau35 presence is associated with increased and decreased excitability at hyperpolarized and depolarized potentials, respectively. These observations are paralleled by a hyperpolarization of the voltage-sensitivity of noninactivating K

Indexed as

Alzheimer DiseaseAnimalsCA1 Region, HippocampalCognitionDementiaGlycogen Synthase Kinase 3 betaMemory DisordersMice, TransgenicMotor ActivityNeuronal PlasticityPsychomotor DisordersSpatial MemorySupranuclear Palsy, ProgressiveSynaptic Transmissiontau ProteinsGlycogen Synthase Kinase 3 betatau ProteinsAlzheimer's diseaseDementiaHippocampusMembrane electrical propertiesNeuronal excitabilityProgressive supranuclear palsySynaptic plasticityTauopathy

Identifiers

PMID28917666
PMCPMC5654728

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Registered trials

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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.