Evidence map›Paper›PMID 31619490›Full record

ReviewThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Phenotypic Suppression of ALS/FTD-Associated Neurodegeneration Highlights Mechanisms of Dysfunction.

Mathieu Bartoletti, Daryl A Bosco, Sandrine Da Cruz, Clotilde Lagier-Tourenne, Nicole Liachko, Sebastian Markmiller, Kristin M Webster, Kristi A Wharton

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. ALS-linked PFN1 variants exhibit loss and gain of functions in the context of formin-induced actin polymerization.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. Review
  7. 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

8 authors at 6 institutions in 1 country.

Mathieu BartolettiDepartment of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912.ORCID 0000-0003-3648-5524
Daryl A BoscoDepartment of Neurology, University of Massachusetts Medical School, Worcester, Massachusetts 01605.ORCID 0000-0002-3735-3729
Sandrine Da CruzLudwig Institute for Cancer Research, University of California at San Diego, La Jolla, California 92093.
Clotilde Lagier-TourenneDepartment of Neurology, Sean M. Healey and AMG Center for ALS, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129.
Nicole LiachkoDivision of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington, Seattle, Washington 98104.
Sebastian MarkmillerDepartment of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, California 92093.
Kristin M WebsterDepartment of Neuroscience, Brown University, Providence, Rhode Island, 02906, and.
Kristi A WhartonDepartment of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912, kristi_wharton@brown.edu.ORCID 0000-0001-9625-4336
Allen Institute for Brain Science · USUniversity of California San Diego · USBroad Institute · USBrown University · USUniversity of Massachusetts Chan Medical School · USUniversity of Puget Sound · US

Funding

Training Program in Basic Clinical GeneticsT32GM008666 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAMILTON, BRUCE A · 1998 to 2021
$8.6M
Multimodal analysis and therapeutic targeting of aberrant nucleocytoplasmic compartmentalization in FUS-related neurodegenerative diseaseR01NS108769 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Daryl Angela Bosco, Ankur Jain · 2019 to 2026
$5.2M
Using RNA signatures for therapy development in neurodegeneration due to C9orf72 expansionsR01NS087227 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LAGIER-TOURENNE, CLOTILDE · 2014 to 2018
$1.5M
Investigating calcineurin regulation of pathological TDP-43 phosphorylation in ALSI01BX004044 · VA · VA PUGET SOUND HEALTHCARE SYSTEM · PI LIACHKO, NICOLE FARON · 2019 to 2022
–
BLRD VA I01 BX004044Medical Research CouncilNIGMS NIH HHS T32 GM008666NINDS NIH HHS R01 NS087227NINDS NIH HHS R01 NS108769Wellcome Trust
6 · The paper itself

Abstract

A fundamental question regarding the etiology of amyotrophic lateral sclerosis (ALS) is whether the various gene mutations associated with the disease converge on a single molecular pathway or act through multiple pathways to trigger neurodegeneration. Notably, several of the genes and cellular processes implicated in ALS have also been linked to frontotemporal dementia (FTD), suggesting these two diseases share common origins with varied clinical presentations. Scientists are rapidly identifying ALS/FTD suppressors that act on conserved pathways from invertebrates to vertebrates to alleviate degeneration. The elucidation of such genetic modifiers provides insight into the molecular pathways underlying this rapidly progressing neurodegenerative disease, while also revealing new targets for therapeutic development.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease ProgressionFrontotemporal DementiaHumansMutationALSdisease modelsFTDgenetic modifiersRBPsstress granules

Identifiers

PMID31619490
PMCPMC6794934
OpenAlexW2980877881

What OpenQuestion holds

Textmetadata
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.