Evidence map›Paper›PMID 40897992›Full record

ReviewCNS drugs2025

Genetic and Mechanistic Insights Inform Amyotrophic Lateral Sclerosis Treatment and Symptomatic Management: Current and Emerging Therapeutics and Clinical Trial Design Considerations.

Savannah E Quigley, Kellen H Quigg, Stephen A Goutman

Abstract readReview
In one paragraph

Review in CNS drugs, 2025. 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. Article
  2. Article
  3. Article
  4. 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

3 authors.

Savannah E QuigleyDepartment of Neurology, University of Michigan, 1500 E Medical Center Dr, Ann Arbor, MI, 48109-5223, USA.
Kellen H QuiggDepartment of Neurology, University of Michigan, 1500 E Medical Center Dr, Ann Arbor, MI, 48109-5223, USA.ORCID 0000-0003-4365-2298
Stephen A GoutmanDepartment of Neurology, University of Michigan, 1500 E Medical Center Dr, Ann Arbor, MI, 48109-5223, USA. sgoutman@med.umich.edu.ORCID 0000-0001-8780-6637

Funding

Developing novel strategies for personalized treatment and prevention of ALS: Leveraging the global exposome, genome, epigenome, metabolome, and inflammasome with data science in a case/control cohortR01NS127188 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BATTERMAN, STUART A, FELDMAN, EVA LUCILLE · 2021 to 2024
$3.4M
Creating a foundation for personalized age- and sex-based immune-targeted therapies from an ALS longitudinal cohort by identifying peripheral and central immune signaturesR01NS120926 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GOUTMAN, STEPHEN, MURDOCK, BENJAMIN JOSEPH · 2021 to 2025
$3.0M
ACL HHS R01TS000344ATSDR CDC HHS R01 TS000327Centers for Disease Control and Prevention/Agency for Toxic Substances and Disease Registry R01TS000327NIH HHS R01NS120926NIH HHS R01NS127188NINDS NIH HHS R01 NS120926NINDS NIH HHS R01 NS127188
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder affecting both upper and lower motor neurons. ALS is classically characterized by painless progressive weakness, causing impaired function of limbs, speech, swallowing, and respiratory function. The disease is fatal within 2-4 years, often the result of respiratory failure. The pathologic hallmark for a majority of ALS cases is aberrant cytoplasmic accumulations of the nuclear protein TAR-DNA binding protein (TDP-43). A total of 10-15% of ALS can be attributed to a single gene mutation, known as genetic or "familial" ALS, while the remainder of cases are termed nongenetic or "sporadic" although heritability has been measured in up to 37% in this population. Complex interactions between genetics, environment, and physiologic susceptibility are thought to contribute to disease. Management is primarily supportive in nature, though there are several approved treatments worldwide. This review details the mechanisms and evidence of approved disease-modifying treatments, relevant measures to track disease burden and progression used in clinical trials, and approaches to pharmacologic management of common symptoms in ALS. As there is not currently a cure for ALS, research into the complex pathophysiologic and genetic alterations contributing to disease is of great interest. This review further discusses the current understanding of genetic etiologies and altered physiology leading to disease, such as neuroinflammation, integrated stress response, aberrant proteostasis and mitochondrial dysfunction, among others. The translation of preclinical discoveries into current investigational therapeutics, novel therapeutic categories such as antisense oligonucleotides and stem cell transplantation, as well as future horizons harnessing the power of artificial intelligence in drug development and clinical trials are discussed.

Indexed as

Amyotrophic Lateral SclerosisAnimalsClinical Trials as TopicDNA-Binding ProteinsHumansDNA-Binding Proteins

Identifiers

PMID40897992
PMCPMC12423166

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.