ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2019
Phosphodiesterase Inhibitors Revert Axonal Dystrophy in Friedreich's Ataxia Mouse Model.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Review
- Alpha-lipoic acid supplementation improves pathological alterations in cellular models of Friedreich ataxia.Orphanet journal of rare diseases · 2025Article
- A new FRDA mouse model [Frontiers in neuroscience · 2023Article
- BRUCE silencing leads to axonal dystrophy by repressing autophagosome-lysosome fusion in Alzheimer's disease.Translational psychiatry · 2021Article
- Oxidative stress modulates rearrangement of endoplasmic reticulum-mitochondria contacts and calcium dysregulation in a Friedreich's ataxia model.Redox biology · 2020Article
- Extra-mitochondrial mouse frataxin and its implications for mouse models of Friedreich's ataxia.Scientific reports · 2020Article
- Cofilin dysregulation alters actin turnover in frataxin-deficient neurons.Scientific reports · 2020Article
- Molecular Mechanisms and Therapeutics for the GAA·TTC Expansion Disease Friedreich Ataxia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Friedreich's ataxia (FRDA) is a neurodegenerative disorder caused by an unstable GAA repeat expansion within intron 1 of the FXN gene and characterized by peripheral neuropathy. A major feature of FRDA is frataxin deficiency with the loss of large sensory neurons of the dorsal root ganglia (DRG), namely proprioceptive neurons, undergoing dying-back neurodegeneration with progression to posterior columns of the spinal cord and cerebellar ataxia. We used isolated DRGs from a YG8R FRDA mouse model and C57BL/6J control mice for a proteomic study and a primary culture of sensory neurons from DRG to test novel pharmacological strategies. We found a decreased expression of electron transport chain (ETC) proteins, the oxidative phosphorylation (OXPHOS) system and antioxidant enzymes, confirming a clear impairment in mitochondrial function and an oxidative stress-prone phenotype. The proteomic profile also showed a decreased expression in Ca
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Registered trials
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