Evidence map›Paper›PMID 36741054›Full record

ArticleFrontiers in neuroscience2022

Comparing therapeutic modulators of the SOD1 G93A Amyotrophic Lateral Sclerosis mouse pathophysiology.

Albert J B Lee, Tyler E Kittel, Renaid B Kim, Thao-Nguyen Bach, Tian Zhang, Cassie S Mitchell

Abstract read
In one paragraph

Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Combination Pharmacology for ALS: A Mechanistic Rationale.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
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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

6 authors.

Albert J B LeeLaboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States.
Tyler E KittelLaboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States.
Renaid B KimLaboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States.
Thao-Nguyen BachLaboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States.
Tian ZhangLaboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States.
Cassie S MitchellLaboratory for Pathology Dynamics, Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA, United States.

Funding

Regulatory and Human Study Operations (RHSO) Core CU19AG065169 · NIA · UNIVERSITY OF ARIZONA · PI BARNES, CAROL A. · 2021 to 2025
$59.8M
Training in Computational Neural EngineeringT32EB025816 · NIBIB · GEORGIA INSTITUTE OF TECHNOLOGY · PI Michael Robert Borich, Christopher John Rozell · 2019 to 2026
$1.9M
A New Approach to ALSK01NS069616 · NINDS · GEORGIA INSTITUTE OF TECHNOLOGY · PI MITCHELL, CASSIE S · 2011 to 2015
$641k
Identification of Amyotrophic Lateral Sclerosis Clinical PredictorsR21NS081426 · NINDS · GEORGIA INSTITUTE OF TECHNOLOGY · PI MITCHELL, CASSIE S · 2013 to 2014
$389k
NIA NIH HHS U19 AG065169NIBIB NIH HHS T32 EB025816NINDS NIH HHS K01 NS069616NINDS NIH HHS R21 NS081426
6 · The paper itself

Abstract

Introduction: Amyotrophic Lateral Sclerosis (ALS) is a paralyzing, multifactorial neurodegenerative disease with limited therapeutics and no known cure. The study goal was to determine which pathophysiological treatment targets appear most beneficial. Methods: A big data approach was used to analyze high copy SOD1 G93A experimental data. The secondary data set comprised 227 published studies and 4,296 data points. Treatments were classified by pathophysiological target: apoptosis, axonal transport, cellular chemistry, energetics, neuron excitability, inflammation, oxidative stress, proteomics, or systemic function. Outcome assessment modalities included onset delay, health status (rotarod performance, body weight, grip strength), and survival duration. Pairwise statistical analysis (two-tailed Results: Inflammation treatments were best at delaying onset ( Discussion: In summary, the most effective pathophysiological treatments change as function of assessment modality and disease progression. Shifting pathophysiological treatment category efficacy with disease progression supports the homeostatic instability theory of ALS disease progression.

Indexed as

Amyotrophic Lateral Sclerosis (ALS)motoneuron diseasemouse modelneuromuscularpharmacologySOD1SOD1 G93A mouse

Identifiers

PMID36741054
PMCPMC9893287

What OpenQuestion holds

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Registered trials

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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.