ReviewMolecular brain2023
Pathophysiology of ion channels in amyotrophic lateral sclerosis.
Review in Molecular brain, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 19 citations in OpenAlex.
- Neural Control of Mastication: Ion-Channel Mechanisms in the Brainstem Central Pattern Generator.Brain sciences · 2026Review
- The Diagnostic Potential of Axon Excitability Is Consistent Across Hand Muscles in Amyotrophic Lateral Sclerosis.Muscle & nerve · 2026Article
- Vitamins as Modulators of Neurodegenerative Disease Pathways: Mechanisms and Therapeutic Perspectives.Nutrients · 2026Review
- Splicing the narrative: alternative TARDBP splicing and its relation to neurodegeneration in ALS and FTD.The Journal of clinical investigation · 2026Review
- Microglial HVCN1 Deficiency Improves Movement and Survival of SOD1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Calpain-2 Regulates Kinesin and Dynein Dysfunction in Neurotoxin-Induced Motoneuron Injury.Brain sciences · 2026Article
- Astrocytic KFrontiers in aging neuroscience · 2026Review
- Electrophysiological characterization of sourced human iPSC-derived motor neurons.Channels (Austin, Tex.) · 2025Article
- Nrf2/Keap1 Signaling Axis in the Brain: Master Regulator of Oxidative Stress in Neurodegenerative and Psychiatric Disorders.Molecular neurobiology · 2025Review
- Motor neuron axonal excitability changes in the clinical course of amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Genetic Variants inInternational journal of molecular sciences · 2025Article
- Neuromusculoskeletal Modeling and Force Prediction: Verification Through Experimental Neuromuscular Dynamics.Annals of biomedical engineering · 2025Article
- Artificial Intelligence-Assisted Comparative Analysis of the Overlapping Molecular Pathophysiology of Alzheimer's Disease, Amyotrophic Lateral Sclerosis, and Frontotemporal Dementia.International journal of molecular sciences · 2024Article
- Article
- Review
- New Insights into Oxidative Stress and Inflammatory Response in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Alternative Splicing and CaV-Associated Channelopathies.Wiley interdisciplinary reviews. RNAReview
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 at 1 institution in 2 countries.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) stands as the most prevalent and severe form of motor neuron disease, affecting an estimated 2 in 100,000 individuals worldwide. It is characterized by the progressive loss of cortical, brainstem, and spinal motor neurons, ultimately resulting in muscle weakness and death. Although the etiology of ALS remains poorly understood in most cases, the remodelling of ion channels and alteration in neuronal excitability represent a hallmark of the disease, manifesting not only during the symptomatic period but also in the early pre-symptomatic stages. In this review, we delve into these alterations observed in ALS patients and preclinical disease models, and explore their consequences on neuronal activities. Furthermore, we discuss the potential of ion channels as therapeutic targets in the context of ALS.
Indexed as
Identifiers
What Socratic 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 Socratic graph.