SynthesisMolecular neurobiology2025
The Current Potential Pathogenesis of Amyotrophic Lateral Sclerosis.
Synthesis in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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.
Who cites it
8 citing papers in PubMed.
- Protein Biomarkers in Risk and Prognosis of Amyotrophic Lateral Sclerosis.European journal of neurology · 2026Article
- JP1 peptide modulates oxidative stress and autophagy via Keap1-Nrf2-ARE in ALS model mice.BMC medicine · 2026Article
- The Microbiota-Gut-Brain Axis and Nutritional Interventions in Amyotrophic Lateral Sclerosis: Pathophysiological Mechanisms, Neuroinflammation, and Non-Motor Manifestations-Scoping Review.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- The Dual Role of Exosome-Mediated Central-Peripheral Immune Dialogue in Amyotrophic Lateral Sclerosis-Associated Neuroinflammation.Journal of inflammation research · 2026Review
- Increased serum fibroblast growth factor 2 levels, altered peripheral blood inflammatory indicators and their ratios in amyotrophic lateral sclerosis: a clinical exploratory study.Frontiers in neurology · 2026Article
- Multi-omics-based decoding of circulating biomarkers in amyotrophic lateral sclerosis and risks in environmental toxins.BMC pharmacology & toxicology · 2025Article
- Emerging biomarkers in amyotrophic lateral sclerosis: from pathogenesis to clinical applications.Frontiers in molecular biosciences · 2025Review
- Acupuncture for neurodegenerative diseases: mechanisms, efficacy, and future research directions.American journal of translational research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease mainly characterized by the accumulation of ubiquitinated proteins in the affected motor neurons. At present, the accurate pathogenesis of ALS remains unclear and there are still no effective treatment measures for ALS. The potential pathogenesis of ALS mainly includes the misfolding of some pathogenic proteins, the genetic variation, mitochondrial dysfunction, autophagy disorders, neuroinflammation, the misregulation of RNA, the altered axonal transport, and gut microbial dysbiosis. Exploring the pathogenesis of ALS is a critical step in searching for the effective therapeutic approaches. The current studies suggested that the genetic variation, gut microbial dysbiosis, the activation of glial cells, and the transportation disorder of extracellular vesicles may play some important roles in the pathogenesis of ALS. This review conducts a systematic review of these current potential promising topics closely related to the pathogenesis of ALS; it aims to provide some new evidences and clues for searching the novel treatment measures of ALS.
Indexed as
Identifiers
38829511What OpenQuestion holds
Registered trials
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.