Friedreich's ataxia is a neurodegenerative disorder associated with a GAA trinucleotide repeat expansion in intron 1 of the frataxin (FXN) gene. It is the most common autosomal recessive cerebellar ataxia, with a mean age of onset at 16 years. Nearly 95-98% of patients are homozygous for a 90-1300 GAA repeat expansion with only 2-5% demonstrating compound heterozygosity. Compound heterozygous individuals have a repeat expansion in one allele and a point mutation/deletion/insertion in the other. Compound heterozygosity and point mutations are very rare causes of Friedreich's ataxia and nonsense mutations are a further rarity among point mutations. We report a rare compound heterozygous Friedrich's ataxia patient who was found to have one expanded GAA FXN allele and a nonsense point mutation in the other. We summarize the four previously published cases of nonsense mutations and compare the phenotype to that of our patient. We compared clinical information from our patient with other nonsense FXN mutations reported in the literature. This nonsense mutation, to our knowledge, has only been described once previously; interestingly the individual was also of Cuban ancestry. A comparison with previously published cases of nonsense mutations demonstrates some common clinical characteristics.
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http://dx.doi.org/10.1155/2018/8587203 | DOI Listing |
Neurol Ther
December 2024
Patient-Reported Outcomes and Health Economics Research, Deutsches Zentrum für Neurodegenerative Erkrankungen/German Center for Neurodegenerative Diseases (DZNE), Site Rostock/Greifswald, Ellernholzstrasse 1-2, 17489, Greifswald, Germany.
Introduction: Friedreich Ataxia (FA) is a multisystem neurodegenerative disease. Affected individuals rely on mobility assistive technologies (MAT) (e.g.
View Article and Find Full Text PDFOrphanet J Rare Dis
December 2024
Discovery Research Division, Indian Council of Medical Research (ICMR) Headquarters, V. Ramalingaswami Bhawan, Ansari Nagar, P.O. Box 4911, New Delhi, 110029, India.
Background: Friedreich's ataxia (FA) is a rare genetic disorder caused by silencing of the frataxin gene (FXN), which leads to multiorgan damage. Nrf2 is a regulator of FXN, which is a modulator of oxidative stress in animals and humans. Omaveloxolone (Omav) is an Nrf2 activator and has been reported to have antioxidative potential in various disease conditions.
View Article and Find Full Text PDFNanomaterials (Basel)
December 2024
Center for Genomics and Precision Medicine, Institute of Bioscience and Technology, Texas A&M Health Science Center, Houston, TX 77030, USA.
Harsh acid oxidation of activated charcoal transforms an insoluble carbon-rich source into water-soluble, disc structures of graphene decorated with multiple oxygen-containing functionalities. We term these pleiotropic nano-enzymes as "pleozymes". A broad redox potential spans many crucial redox reactions including the oxidation of hydrogen sulfide (HS) to polysulfides and thiosulfate, dismutation of the superoxide radical (O*), and oxidation of NADH to NAD.
View Article and Find Full Text PDFFront Cell Dev Biol
December 2024
Department of Biological Sciences, University of Notre Dame, Notre Dame, IN, United States.
Background And Objectives: Friedreich's Ataxia (FRDA) is a genetic disease that affects a variety of different tissues. The disease is caused by a mutation in the gene ( which is important for the synthesis of iron-sulfur clusters. The primary pathologies of FRDA are loss of motor control and cardiomyopathy.
View Article and Find Full Text PDFNAR Mol Med
October 2024
Department of Biology, Tufts University, 200 Boston Ave., Medford, MA 02155, USA.
H-DNA is an intramolecular DNA triplex formed by homopurine/homopyrimidine mirror repeats. Since its discovery, the field has advanced from characterizing the structure to discovering its existence and role . H-DNA interacts with cellular machinery in unique ways, stalling DNA and RNA polymerases and causing genome instability.
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