Evidence map›Paper›PMID 32389059›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry

The Accumulation of Tau in Postsynaptic Structures: A Common Feature in Multiple Neurodegenerative Diseases?

Peter J Teravskis, Karen H Ashe, Dezhi Liao

Abstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Review
  2. Article
  3. Tau Protein Alterations Induced by Hypobaric Hypoxia Exposure.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Tau Toxicity in Neurodegeneration.Molecular neurobiology · 2022
    Review
  11. Article
  12. Review
  13. Observational
  14. Review
  15. Article
  16. Article
  17. Mechanical injuries of neurons induce tau mislocalization to dendritic spines and tau-dependent synaptic dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

3 authors.

Peter J TeravskisDepartment of Neuroscience, University of Minnesota, Minneapolis, MN, USA.ORCID 0000-0002-3204-8389
Karen H AsheDepartment of Neurology, University of Minnesota, Minneapolis, MN, USA.
Dezhi LiaoDepartment of Neuroscience, University of Minnesota, Minneapolis, MN, USA.ORCID 0000-0003-0342-4493

Funding

Caspase-2 Probe CompoundsR01AG062199 · NIA · UNIVERSITY OF MINNESOTA · PI ASHE, KAREN H, WALTERS, MICHAEL A. · 2019 to 2023
$3.9M
Role of Tau Cleavage and Phosphorylation in TauopathyRF1AG060766 · NIA · UNIVERSITY OF MINNESOTA · PI ASHE, KAREN H · 2018 to 2018
$3.0M
Tau-dependent cognitive deficits in alpha-synucleinopathiesR01NS108686 · NINDS · UNIVERSITY OF MINNESOTA · PI ARAQUE, ALFONSO, LEE, MICHAEL K · 2018 to 2022
$2.8M
Role of Tau Cleavage in TauopathyR01NS079374 · NINDS · UNIVERSITY OF MINNESOTA · PI ASHE, KAREN H · 2013 to 2016
$1.5M
Full human gene-replacement mouse models of ADRDsR61NS115089 · NINDS · UNIVERSITY OF MINNESOTA · PI EBNER, TIMOTHY J, KOOB, MICHAEL D · 2019 to 2019
$1.5M
Microbial Synthesis of Therapeutic Bile AcidsR41NS113732 · NINDS · METSELEX, INC. · PI LIAO, DEZHI, LOW, WALTER C · 2020 to 2020
$450k
Tau mislocalization in alpha-synuclein-induced synaptic dysfunctionR21NS084007 · NINDS · UNIVERSITY OF MINNESOTA · PI LIAO, DEZHI · 2014 to 2015
$418k
In Vitro Tauopathy Model for Traumatic Brain InjuryR21NS096437 · NINDS · UNIVERSITY OF MINNESOTA · PI LIAO, DEZHI · 2016 to 2017
$402k
NIA NIH HHS R01 AG062199NIA NIH HHS RF1 AG060766NINDS NIH HHS R01 NS079374NINDS NIH HHS R01 NS108686NINDS NIH HHS R21 NS084007NINDS NIH HHS R21 NS096437NINDS NIH HHS R41 NS113732NINDS NIH HHS R61 NS115089
6 · The paper itself

Abstract

Increasingly, research suggests that neurodegenerative diseases and dementias are caused not by unique, solitary cellular mechanisms, but by multiple contributory mechanisms manifesting as heterogeneous clinical presentations. However, diverse neurodegenerative diseases also share common pathological hallmarks and cellular mechanisms. One such mechanism involves the redistribution of the microtubule associated protein tau from the axon into the somatodendritic compartment of neurons, followed by the mislocalization of tau into dendritic spines, resulting in postsynaptic functional deficits. Here we review various signaling pathways that trigger the redistribution of tau to the cell body and dendritic tree, and its mislocalization to dendritic spines. The convergence of multiple pathways in different disease models onto this final common pathway suggests that it may be an attractive pathway to target for developing new treatments for neurodegenerative diseases.

Indexed as

Amyloid beta-PeptidesAnimalsDendritic SpinesHumansNeurodegenerative DiseasesNeuronsSynapsestau ProteinsAmyloid beta-PeptidesMAPT protein, humantau ProteinsAlzheimer’s diseaseAMPA receptorsdendritic spinesFTDP-17Huntington’s diseaseMAPTneuronal polarityParkinson’s diseasesynaptic plasticitytau

Identifiers

PMID32389059
PMCPMC8447404

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.