ArticleThe Journal of biological chemistry2011
Mitochondrial dysfunction and oxidative stress contribute to the pathogenesis of spinocerebellar ataxia type 12 (SCA12).
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 65 citations in OpenAlex.
- Abnormal Amyloidogenesis Identified in Plasma of Patients with Spinocerebellar Ataxia Type 12.Cerebellum (London, England) · 2026Article
- Cerebellar deep brain stimulation rescues Purkinje cell mitochondrial density in a genetic mouse model of cerebellar ataxia.Brain research bulletin · 2026Article
- Wings of Discovery: UsingCells · 2025Review
- Adaptation of the Protocol for the Isolation of Biotinylated Protein Complexes forInternational journal of molecular sciences · 2025Article
- Systemic Effects of Photoactivated 5,10,15,20-tetrakis(Biotech (Basel (Switzerland)) · 2024Article
- Influence of Redox and Dopamine Regulation in Cocaine-Induced Phenotypes UsingAntioxidants (Basel, Switzerland) · 2023Article
- Calycosin Alleviates Paraquat-Induced Neurodegeneration by Improving Mitochondrial Functions and Regulating Autophagy in aAntioxidants (Basel, Switzerland) · 2022Article
- Naturally Occurring Antioxidant Therapy in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2022Review
- New spinocerebellar ataxia subtype caused byBrain communications · 2022Article
- Selective Neuron Vulnerability in Common and Rare Diseases-Mitochondria in the Focus.Frontiers in molecular biosciences · 2021Review
- RNA toxicity in non-coding repeat expansion disorders.The EMBO journal · 2020Review
- An Efficient Screen for Cell-Intrinsic Factors Identifies the Chaperonin CCT and Multiple Conserved Mechanisms as Mediating Dendrite Morphogenesis.Frontiers in cellular neuroscience · 2020Article
- Tert-butylhydroquinone post-treatment attenuates neonatal hypoxic-ischemic brain damage in rats.Neurochemistry international · 2018Article
- Pre-B-cell colony-enhancing factor protects against apoptotic neuronal death and mitochondrial damage in ischemia.Scientific reports · 2016Article
- Skeletal muscle cellular metabolism in older HIV-infected men.Physiological reports · 2016Article
- Recurrent Sleep Fragmentation Induces Insulin and Neuroprotective Mechanisms in Middle-Aged Flies.Frontiers in aging neuroscience · 2016Article
- Nrf2/ARE Pathway Involved in Oxidative Stress Induced by Paraquat in Human Neural Progenitor Cells.Oxidative medicine and cellular longevity · 2016Article
- Neuropathology and Cellular Pathogenesis of Spinocerebellar Ataxia Type 12.Movement disorders : official journal of the Movement Disorder Society · 2015Article
- The autosomal dominant spinocerebellar ataxias: emerging mechanistic themes suggest pervasive Purkinje cell vulnerability.Journal of neurology, neurosurgery, and psychiatry · 2015Review
- Alternative kynurenic acid synthesis routes studied in the rat cerebellum.Frontiers in cellular neuroscience · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cerebellar ataxia type 12 (SCA12) has been attributed to the elevated expression of ppp2r2b. To better elucidate the pathomechanism of the neuronal disorder and to search for a pharmacological treatment, Drosophila models of SCA12 were generated by overexpression of a human ppp2r2b and its Drosophila homolog tws. Ectopic expression of ppp2r2b or tws caused various pathological features, including neurodegeneration, apoptosis, and shortened life span. More detailed analysis revealed that elevated ppp2r2b and tws induced fission of mitochondria accompanied by increases in cytosolic reactive oxygen species (ROS), cytochrome c, and caspase 3 activity. Transmission electron microscopy revealed that fragmented mitochondria with disrupted cristae were engulfed by autophagosomes in photoreceptor neurons of flies overexpressing tws. Additionally, transgenic flies were more susceptible to oxidative injury induced by paraquat. By contrast, ectopic Drosophila Sod2 expression and antioxidant treatment reduced ROS and caspase 3 activity and extended the life span of the SCA12 fly model. In summary, our study demonstrates that oxidative stress induced by mitochondrial dysfunction plays a causal role in SCA12, and reduction of ROS is a potential therapeutic intervention for this neuropathy.
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