ArticleAntioxidants (Basel, Switzerland)2023
Defects in Glutathione System in an Animal Model of Amyotrophic Lateral Sclerosis.
Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 7 citations in OpenAlex.
- From animal models to metabolic interventions: Lessons from the Wobbler mouse.Neural regeneration research · 2026Article
- Baicalein Attenuates High Glucose and Sodium Palmitate-Induced Ferroptosis in Cardiomyocytes via the Nrf2/SLC7A11/GPX4 Signaling Pathway.International journal of molecular sciences · 2026Article
- The Glutamate-Glutathione axis in neuropsychiatric disorders and cancer: From shared mechanisms to non-invasive biomarkers.Redox biology · 2026Review
- Interaction between Poly(ADP-ribose) polymerase-1 and α-synuclein pathology in Parkinson's disease.Frontiers in neuroscience · 2026Review
- Integrated Network Toxicology and Metabolomics Reveal the Ovarian Toxicity Mechanisms of Chronic Carbofuran Exposure in Female Mice.International journal of molecular sciences · 2025Article
- Caffeine mitigates ROS accumulation and attenuates motor neuron degeneration in the wobbler mouse model of amyotrophic lateral sclerosis.Cell communication and signaling : CCS · 2025Article
- Article
- Cerebellum in Alzheimer's disease and other neurodegenerative diseases: an emerging research frontier.MedComm · 2024Review
- Elevated NLRP3 Inflammasome Activation Is Associated with Motor Neuron Degeneration in ALS.Cells · 2024Article
- Oxidative Stress-Induced Neurodegeneration and Antioxidative Strategies: Current Stage and Future Perspectives.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a progredient neurodegenerative disease characterized by a degeneration of the first and second motor neurons. Elevated levels of reactive oxygen species (ROS) and decreased levels of glutathione, which are important defense mechanisms against ROS, have been reported in the central nervous system (CNS) of ALS patients and animal models. The aim of this study was to determine the cause of decreased glutathione levels in the CNS of the ALS model wobbler mouse. We analyzed changes in glutathione metabolism in the spinal cord, hippocampus, cerebellum, liver, and blood samples of the ALS model, wobbler mouse, using qPCR, Western Blot, HPLC, and fluorometric assays. Here, we show for the first time a decreased expression of enzymes involved in glutathione synthesis in the cervical spinal cord of wobbler mice. We provide evidence for a deficient glutathione metabolism, which is not restricted to the nervous system, but can be seen in various tissues of the wobbler mouse. This deficient system is most likely the reason for an inefficient antioxidative system and, thus, for elevated ROS levels.
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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 Socratic graph.