ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Defects in mitochondrial axonal transport and membrane potential without increased reactive oxygen species production in a Drosophila model of Friedreich ataxia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 84 citations in OpenAlex.
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- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
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- Decoding Neurodegeneration: A Comprehensive Review of Molecular Mechanisms, Genetic Influences, and Therapeutic Innovations.International journal of molecular sciences · 2023Review
- Downregulation of oxidative stress-mediated glial innate immune response suppresses seizures in a fly epilepsy model.Cell reports · 2023Article
- Analysis of Mitochondrial Function in Cell Membranes as Indicator of Tissue Vulnerability to Drugs in Humans.Biomedicines · 2022Article
- Copper, Iron, and Manganese Toxicity in Neuropsychiatric Conditions.International journal of molecular sciences · 2021Review
- Review
- Molecular Defects in Friedreich's Ataxia: Convergence of Oxidative Stress and Cytoskeletal Abnormalities.Frontiers in molecular biosciences · 2020Review
- Truncated Tau Induces Mitochondrial Transport Failure Through the Impairment of TRAK2 Protein and Bioenergetics Decline in Neuronal Cells.Frontiers in cellular neuroscience · 2020Article
- Axonal transport and neurological disease.Nature reviews. Neurology · 2019Review
- Mitochondrial transport serves as a mitochondrial quality control strategy in axons: Implications for central nervous system disorders.CNS neuroscience & therapeutics · 2019Review
- The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.Frontiers in neuroscience · 2019Review
- Impact ofInternational journal of molecular sciences · 2018Review
- The role of oxidative stress in Friedreich's ataxia.FEBS letters · 2018Review
- Mitochondria at the neuronal presynapse in health and disease.Nature reviews. Neuroscience · 2018Review
- Review
- Mitofusin-Dependent ER Stress Triggers Glial Dysfunction and Nervous System Degeneration in aFrontiers in molecular neuroscience · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Friedreich ataxia, a neurodegenerative disorder resulting from frataxin deficiency, is thought to involve progressive cellular damage from oxidative stress. In Drosophila larvae with reduced frataxin expression (DfhIR), we evaluated possible mechanisms of cellular neuropathology by quantifying mitochondrial axonal transport, membrane potential (MMP), and reactive oxygen species (ROS) production in the DfhIR versus wild-type nervous system throughout development. Although dying-back neuropathy in DfhIR larvae did not occur until late third instar, reduced MMP was already apparent at second instar in the cell bodies, axons and neuromuscular junctions (NMJs) of segmental nerves. Defects in axonal transport of mitochondria appeared late in development in distal nerve of DfhIR larvae, with retrograde movement preferentially affected. As a result, by late third instar the neuromuscular junctions (NMJs) of DfhIR larvae accumulated a higher density of mitochondria, many of which were depolarized. Notably, increased ROS production was not detected in any neuronal region or developmental stage in DfhIR larvae. However, when challenged with antimycin A, neurons did respond with a larger increase in ROS. We propose that pathology in the frataxin-deficient nervous system involves decreased MMP and ATP production followed by failures of mitochondrial transport and NMJ function.
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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.