Evidence map›Paper›PMID 25755633›Full record

ArticleFrontiers in cellular neuroscience2015

Truncated tau deregulates synaptic markers in rat model for human tauopathy.

Santosh Jadhav, Stanislav Katina, Andrej Kovac, Zuzana Kazmerova, Michal Novak, Norbert Zilka

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  3. Article
  4. Phosphorylated Tau in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2022
    Review
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  15. Article
  16. Tau-targeting therapies for Alzheimer disease.Nature reviews. Neurology · 2018
    Review
  17. 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 at 4 institutions in 2 countries.

Santosh JadhavInstitute of Neuroimmunology, Slovak Academy of Sciences Bratislava, Slovak Republic.
Stanislav KatinaAxon Neuroscience GmbH Bratislava, Slovak Republic ; Institute of Mathematics and Statistics, Masaryk University Brno, Czech Republic.
Andrej KovacAxon Neuroscience GmbH Bratislava, Slovak Republic.
Zuzana KazmerovaInstitute of Neuroimmunology, Slovak Academy of Sciences Bratislava, Slovak Republic.
Michal NovakInstitute of Neuroimmunology, Slovak Academy of Sciences Bratislava, Slovak Republic ; Axon Neuroscience GmbH Bratislava, Slovak Republic.
Norbert ZilkaInstitute of Neuroimmunology, Slovak Academy of Sciences Bratislava, Slovak Republic ; Axon Neuroscience GmbH Bratislava, Slovak Republic.
Institute of Neuroimmunology of the Slovak Academy of Sciences · SKSlovak Academy of Sciences · SKAXON Neuroscience (Slovakia) · SKMasaryk University · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic failure and neurofibrillary degeneration are two major neuropathological substrates of cognitive dysfunction in Alzheimer's disease (AD). Only a few studies have demonstrated a direct relationship between these two AD hallmarks. To investigate tau mediated synaptic injury we used rat model of tauopathy that develops extensive neurofibrillary pathology in the cortex. Using fractionation of cortical synapses, we identified an increase in endogenous rat tau isoforms in presynaptic compartment, and their mis-sorting to the postsynaptic density (PSD). Truncated transgenic tau was distributed in both compartments exhibiting specific phospho-pattern that was characteristic for each synaptic compartment. In the presynaptic compartment, truncated tau was associated with impairment of dynamic stability of microtubules which could be responsible for reduction of synaptic vesicles. In the PSD, truncated tau lowered the levels of neurofilaments. Truncated tau also significantly decreased the synaptic levels of Aβ40 but not Aβ42. These data show that truncated tau differentially deregulates synaptic proteome in pre- and postsynaptic compartments. Importantly, we show that alteration of Aβ can arise downstream of truncated tau pathology.

Indexed as

Alzheimer’s diseasephosphorylationsynaptic damagetau mislocalizationtruncated tau

Identifiers

PMID25755633
PMCPMC4337338
OpenAlexW2077048957

What OpenQuestion holds

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LicenceCC BY
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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.