ReviewJournal of biomedicine & biotechnology2011
Genetic rodent models of amyotrophic lateral sclerosis.
Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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
31 citing papers in PubMed, 62 citations in OpenAlex.
- PPAR-Delta Agonist Therapies Did Not Rescue Hallmark Disease Phenotypes in Two Sets of Preclinical Trials in ALS TDP-43 and C9orf72 Model Mice.International journal of molecular sciences · 2026Article
- The Evolution of Technology-Driven In Vitro Models for Neurodegenerative Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Gangliosides as Therapeutic Targets for Neurodegenerative Diseases.Journal of lipids · 2024Review
- Prostaglandins in the Inflamed Central Nervous System: Potential Therapeutic Targets.Current drug targets · 2024Review
- Involvement of Lipids in the Pathogenesis of Amyotrophic Lateral Sclerosis.Life (Basel, Switzerland) · 2023Review
- Ceramide and Sphingosine-1-Phosphate in Neurodegenerative Disorders and Their Potential Involvement in Therapy.International journal of molecular sciences · 2022Review
- cGAS and DDX41-STING mediated intrinsic immunity spreads intercellularly to promote neuroinflammation in SOD1 ALS model.iScience · 2022Article
- Sex-dependent effects of amyloid precursor-like protein 2 in the SOD1-G37R transgenic mouse model of MND.Cellular and molecular life sciences : CMLS · 2021Article
- Copper-ATSM as a Treatment for ALS: Support from Mutant SOD1 Models and Beyond.Life (Basel, Switzerland) · 2020Review
- Exploring Sphingolipid Implications in Neurodegeneration.Frontiers in neurology · 2020Review
- Senataxin mutations elicit motor neuron degeneration phenotypes and yield TDP-43 mislocalization in ALS4 mice and human patients.Acta neuropathologica · 2018Article
- CRISPR/Cas9 Technology as an Emerging Tool for Targeting Amyotrophic Lateral Sclerosis (ALS).International journal of molecular sciences · 2018Review
- Etiogenic factors present in the cerebrospinal fluid from amyotrophic lateral sclerosis patients induce predominantly pro-inflammatory responses in microglia.Journal of neuroinflammation · 2017Article
- Host genetic background influences diverse neurological responses to viral infection in mice.Scientific reports · 2017Article
- Article
- Astroglia acquires a toxic neuroinflammatory role in response to the cerebrospinal fluid from amyotrophic lateral sclerosis patients.Journal of neuroinflammation · 2016Article
- CRISPR/Cas9: a powerful genetic engineering tool for establishing large animal models of neurodegenerative diseases.Molecular neurodegeneration · 2015Review
- Intramuscular Injections Along the Motor End Plates: A Minimally Invasive Approach to Shuttle Tracers Directly into Motor Neurons.Journal of visualized experiments : JoVE · 2015Article
- Significant expansion of the REST/NRSF cistrome in human versus mouse embryonic stem cells: potential implications for neural development.Nucleic acids research · 2015Article
- Autophagy-linked FYVE protein (Alfy) promotes autophagic removal of misfolded proteins involved in amyotrophic lateral sclerosis (ALS).In vitro cellular & developmental biology. Animal · 2015Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the selective death of motor neurons in the motor cortex, brainstem, and spinal cord. A large number of rodent models are available that show motor neuron death and a progressive motor phenotype that is more or less reminiscent of what occurs in patients. These rodent models contain genes with spontaneous or induced mutations or (over) express different (mutant) genes. Some of these models have been of great value to delineate potential pathogenic mechanisms that cause and/or modulate selective motor neuron degeneration. In addition, these genetic rodent models play a crucial role in testing and selecting potential therapeutics that can be used to treat ALS and/or other motor neuron disorders. In this paper, we give a systematic overview of the most important genetic rodent models that show motor neuron degeneration and/or develop a motor phenotype. In addition, we discuss the value and limitations of the different models and conclude that it remains a challenge to find more and better rodent models based on mutations in new genes causing ALS.
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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.