Evidence map›Paper›PMID 29282133›Full record

ReviewMolecular neurodegeneration2017

Is amyotrophic lateral sclerosis/frontotemporal dementia an autophagy disease?

Zhiqiang Deng, Patricia Sheehan, Shi Chen, Zhenyu Yue

Abstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Nutrients · 2021
    Article
  17. Article
  18. Review
  19. Mitophagy in Human Diseases.International journal of molecular sciences · 2021
    Review
  20. C9ORF72: What It Is, What It Does, and Why It Matters.Frontiers in cellular neuroscience · 2021
    Review
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

4 authors.

Zhiqiang DengBrain center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, 430071, China.
Patricia SheehanDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, 10029, USA.
Shi ChenBrain center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, 430071, China. shichen@whu.edu.cn.
Zhenyu YueDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, 10029, USA. zhenyu.yue@mssm.edu.

Funding

Neuronal Autophagy: a Cell-Autonomous Protection MechanismR01NS060123 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Zhenyu Yue · 2008 to 2026
$9.2M
Mouse CoreP50NS094733 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2015 to 2020
$7.1M
NINDS NIH HHS P50 NS094733NINDS NIH HHS R01 NS060123NINDS NIH HHS R01NS060123
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative disorders that share genetic risk factors and pathological hallmarks. Intriguingly, these shared factors result in a high rate of comorbidity of these diseases in patients. Intracellular protein aggregates are a common pathological hallmark of both diseases. Emerging evidence suggests that impaired RNA processing and disrupted protein homeostasis are two major pathogenic pathways for these diseases. Indeed, recent evidence from genetic and cellular studies of the etiology and pathogenesis of ALS-FTD has suggested that defects in autophagy may underlie various aspects of these diseases. In this review, we discuss the link between genetic mutations, autophagy dysfunction, and the pathogenesis of ALS-FTD. Although dysfunction in a variety of cellular pathways can lead to these diseases, we provide evidence that ALS-FTD is, in many cases, an autophagy disease.

Indexed as

AutophagyAmyotrophic Lateral SclerosisAnimalsCell Cycle ProteinsDNA-Binding ProteinsFrontotemporal DementiaHumansMembrane Transport ProteinsMutationProtein Serine-Threonine KinasesSequestosome-1 ProteinTranscription Factor TFIIIACell Cycle ProteinsDNA-Binding ProteinsMembrane Transport ProteinsOPTN protein, humanProtein Serine-Threonine KinasesSequestosome-1 ProteinSQSTM1 protein, humanTBK1 protein, humanTranscription Factor TFIIIAAmyotrophic lateral sclerosisAutophagyAutophagy-related genesDisease-associated genesFrontotemporal dementia

Identifiers

PMID29282133
PMCPMC5746010

What OpenQuestion holds

Textmetadata
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.