Evidence map›Paper›PMID 36012668›Full record

ArticleInternational journal of molecular sciences2022

4-Phenylbutyric Acid (4-PBA) Derivatives Prevent SOD1 Amyloid Aggregation In Vitro with No Effect on Disease Progression in SOD1-ALS Mice.

Leenor Alfahel, Shirel Argueti-Ostrovsky, Shir Barel, Mahmood Ali Saleh, Joy Kahn, Salome Azoulay-Ginsburg, Ayelet Rothstein, Simon Ebbinghaus, Arie Gruzman, Adrian Israelson

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Molecular Research on Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2022
    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

10 authors at 3 institutions in 2 countries.

Leenor AlfahelDepartment of Physiology and Cell Biology and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 8410501, Israel.
Shirel Argueti-OstrovskyDepartment of Physiology and Cell Biology and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 8410501, Israel.
Shir BarelDepartment of Physiology and Cell Biology and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 8410501, Israel.
Mahmood Ali SalehDepartment of Physiology and Cell Biology and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 8410501, Israel.
Joy KahnDepartment of Physiology and Cell Biology and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 8410501, Israel.
Salome Azoulay-GinsburgDepartment of Chemistry, Faculty of Exact Sciences, Campus Ramat-Gan, Bar-Ilan University, Ramat-Gan 5290002, Israel.ORCID 0000-0002-9140-5331
Ayelet RothsteinDepartment of Chemistry, Faculty of Exact Sciences, Campus Ramat-Gan, Bar-Ilan University, Ramat-Gan 5290002, Israel.
Simon EbbinghausInstitute of Physical and Theoretical Chemistry, TU Braunschweig, Rebenring 56, 38106 Braunschweig, Germany.
Arie GruzmanDepartment of Chemistry, Faculty of Exact Sciences, Campus Ramat-Gan, Bar-Ilan University, Ramat-Gan 5290002, Israel.
Adrian IsraelsonDepartment of Physiology and Cell Biology and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 8410501, Israel.ORCID 0000-0002-8289-7653
Ben-Gurion University of the Negev · ILBar-Ilan University · ILTechnische Universität Braunschweig · DE

Funding

German-Israeli Foundation for Scientific Research and Development I-5-201.6-2016Israel Science Foundation # 284/19
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the degeneration of motor neurons. Mutations in the superoxide dismutase (SOD1) gene, causing protein misfolding and aggregation, were suggested as the pathogenic mechanisms involved in familial ALS cases. In the present study, we investigated the potential therapeutic effect of C4 and C5, two derivatives of the chemical chaperone 4-phenylbutyric acid (4-PBA). By combining in vivo and in vitro techniques, we show that, although C4 and C5 successfully inhibited amyloid aggregation of recombinant mutant SOD1 in a dose-dependent manner, they failed to suppress the accumulation of misfolded SOD1. Moreover, C4 or C5 daily injections to SOD1

Indexed as

Amyotrophic Lateral SclerosisNeurodegenerative DiseasesAmyloidAmyloidogenic ProteinsAnimalsButylaminesDisease Models, AnimalDisease ProgressionMiceMice, TransgenicMolecular ChaperonesPhenylbutyratesSpinal CordSuperoxide DismutaseSuperoxide Dismutase-14-phenylbutylamine4-phenylbutyric acidAmyloidAmyloidogenic ProteinsButylaminesMolecular ChaperonesPhenylbutyratesSuperoxide DismutaseSuperoxide Dismutase-1aggregationamyotrophic lateral sclerosis (ALS)chemical chaperonesmisfolded proteinsmutant SOD1

Identifiers

PMID36012668
PMCPMC9409193
OpenAlexW4293256950

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.