Evidence map›Paper›PMID 29495325›Full record

ReviewInternational journal of molecular sciences2018

Tau Spreading Mechanisms; Implications for Dysfunctional Tauopathies.

Almudena Fuster-Matanzo, Félix Hernández, Jesús Ávila

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Trial
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  14. Article
  15. Possible Mechanisms of Tau Spread and Toxicity in Alzheimer's Disease.Frontiers in cell and developmental biology · 2021
    Review
  16. Mitochondrial Defects in Fibroblasts of PathogenicFrontiers in cell and developmental biology · 2021
    Article
  17. Article
  18. Brain sciences · 2020
    Review
  19. Article
  20. 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.

Almudena Fuster-MatanzoCentro de Biología Molecular "Severo Ochoa" CSIC-UAM, Universidad Autónoma de Madrid, C/Nicolás Cabrera 1, 28049 Madrid, Spain. a.fuster@ms-c.es.
Félix HernándezCentro de Biología Molecular "Severo Ochoa" CSIC-UAM, Universidad Autónoma de Madrid, C/Nicolás Cabrera 1, 28049 Madrid, Spain. fhernandez@cbm.csic.es.
Jesús ÁvilaCentro de Biología Molecular "Severo Ochoa" CSIC-UAM, Universidad Autónoma de Madrid, C/Nicolás Cabrera 1, 28049 Madrid, Spain. javila@cbm.csic.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tauopathies comprise a group of progressive age-associated neurodegenerative diseases where tau protein deposits are found as the predominant pathological signature (primary tauopathies) or in combination with the presence of other toxic aggregates (secondary tauopathies). In recent years, emerging evidence suggests that abnormal tau accumulation is mediated through spreading of seeds of the protein from cell to cell, favouring the hypothesis of a prion-like transmission of tau to explain the propagation of the pathology. This would also support the concept that the pathology initiates in a very small part of the brain before becoming symptomatic and spreads across the brain over time. To date, many key questions still remain unclear, such as the nature of the tau species involved in the spreading, the precise seeding/template and uptaking mechanisms or the selectivity explaining why certain neurons are affected and some others are not. A better understanding of the tau spreading machinery will contribute to the development of new therapeutic approaches focused on halting the abnormal propagation, offering also new perspectives for early diagnosis and preventive therapies. In this review, we will cover the most recent advances in tau spreading mechanisms as well as the implications of these findings for dysfunctional tauopathies.

Indexed as

AnimalsGene Expression RegulationHumansProtein AggregatesProtein Aggregation, PathologicalProtein TransportTauopathiestau ProteinsProtein Aggregatestau Proteinsprion-like transmissionspreadingtautauopathies

Identifiers

PMID29495325
PMCPMC5877506

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.