Evidence map›Paper›PMID 24027553›Full record

ReviewFrontiers in neurology2013

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease.

Adrianne S Chesser, Susanne M Pritchard, Gail V W Johnson

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 217 citations in OpenAlex.

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57 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Adrianne S ChesserNeuroscience Graduate Program, Department of Anesthesiology, University of Rochester , Rochester, NY , USA.
Susanne M Pritchard
Gail V W Johnson
University of Rochester · US

Funding

Autophagy, p62 and the Nrf2 Intersect to Protect Against Tau ToxicityR21NS076789 · NINDS · UNIVERSITY OF ROCHESTER · PI JOHNSON, GAIL V. W. · 2012 to 2013
$418k
Mitochondrial dynamics underlie gene-environment interactions in Parkinson'sF30ES020081 · NIEHS · UNIVERSITY OF ROCHESTER · PI CHESSER, ADRIANNE · 2011 to 2014
$189k
NIEHS NIH HHS F30 ES020081NINDS NIH HHS R21 NS076789
6 · The paper itself

Abstract

One of the defining pathological features of Alzheimer disease (AD) is the intraneuronal accumulation of tau. The tau that forms these accumulations is altered both posttranslationally and conformationally, and there is now significant evidence that soluble forms of these modified tau species are the toxic entities rather than the insoluble neurofibrillary tangles. However there is still noteworthy debate concerning which specific pathological forms of tau are the contributors to neuronal dysfunction and death in AD. Given that increases in aberrant forms of tau play a role in the neurodegeneration process in AD, there is growing interest in understanding the degradative pathways that remove tau from the cell, and the selectivity of these different pathways for various forms of tau. Indeed, one can speculate that deficits in a pathway that selectively removes certain pathological forms of tau could play a pivotal role in AD. In this review we will discuss the different proteolytic and degradative machineries that may be involved in removing tau from the cell. How deficits in these different degradative pathways may contribute to abnormal accumulation of tau in AD will also be considered. In addition, the issue of the selective targeting of specific tau species to a given degradative pathway for clearance from the cell will be addressed.

Indexed as

autophagydegradationproteasomeproteolysistau

Identifiers

PMID24027553
PMCPMC3759803
OpenAlexW2074059686

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.