ArticleOxidative medicine and cellular longevity2021
Increased ROS-Dependent Fission of Mitochondria Causes Abnormal Morphology of the Cell Powerhouses in a Murine Model of Amyotrophic Lateral Sclerosis.
Article in Oxidative medicine and cellular longevity, 2021. 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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10 citing papers in PubMed, 18 citations in OpenAlex.
- From animal models to metabolic interventions: Lessons from the Wobbler mouse.Neural regeneration research · 2026Article
- Targeting mitochondrial quality control: Ginsenoside Rg1 as a therapeutic candidate for neuromuscular diseases.Journal of ginseng research · 2026Review
- 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
- Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Corresponding Therapeutic Strategies.Biomedicines · 2025Review
- Elevated NLRP3 Inflammasome Activation Is Associated with Motor Neuron Degeneration in ALS.Cells · 2024Article
- Defects in Glutathione System in an Animal Model of Amyotrophic Lateral Sclerosis.Antioxidants (Basel, Switzerland) · 2023Article
- Mitochondrial dynamics in neurological diseases: a narrative review.Annals of translational medicine · 2023Review
- Dysregulated expression and distribution of Kif5α in neurites of wobbler motor neurons.Neural regeneration research · 2023Article
- ROS scavengers decrease γH2ax spots in motor neuronal nuclei of ALS model miceFrontiers in cellular neuroscience · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease in humans and remains to have a fatal prognosis. Recent studies in animal models and human ALS patients indicate that increased reactive oxygen species (ROS) play an important role in the pathogenesis. Considering previous studies revealing the influence of ROS on mitochondrial physiology, our attention was focused on mitochondria in the murine ALS model, wobbler mouse. The aim of this study was to investigate morphological differences between wild-type and wobbler mitochondria with aid of superresolution structured illumination fluorescence microscopy, TEM, and TEM tomography. To get an insight into mitochondrial dynamics, expression studies of corresponding proteins were performed. Here, we found significantly smaller and degenerated mitochondria in wobbler motor neurons at a stable stage of the disease. Our data suggest a ROS-regulated, Ox-CaMKII-dependent Drp1 activation leading to disrupted fission-fusion balance, resulting in fragmented mitochondria. These changes are associated with numerous impairments, resulting in an overall self-reinforcing decline of motor neurons. In summary, our study provides common pathomechanisms with other ALS models and human ALS cases confirming mitochondria and related dysfunctions as a therapeutic target for the treatment of ALS.
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