نتایج جستجو برای: friedreich ataxia frda

تعداد نتایج: 17926  

Journal: :Human molecular genetics 2004
Hervé Seznec Delphine Simon Laurent Monassier Paola Criqui-Filipe Anne Gansmuller Pierre Rustin Michel Koenig Hélène Puccio

Friedreich ataxia (FRDA), a progressive neurodegenerative disorder associated with cardiomyopathy, is caused by severely reduced frataxin, a mitochondrial protein involved in Fe-S cluster assembly. We have recently generated mouse models that reproduce important progressive pathological and biochemical features of the human disease. Our frataxin-deficient mouse models initially demonstrate time...

Journal: :Human molecular genetics 2002
Patrizia Cavadini Heather A O'Neill Oldrich Benada Grazia Isaya

Friedreich ataxia (FRDA) is an autosomal recessive degenerative disease caused by a deficiency of frataxin, a conserved mitochondrial protein of unknown function. Mitochondrial iron accumulation, loss of iron-sulfur cluster-containing enzymes and increased oxidative damage occur in yeast and mouse frataxin-depleted mutants as well as tissues and cell lines from FRDA patients, suggesting that fr...

Journal: :Annals of neurology 2011
Giovanni Coppola Ryan Burnett Susan Perlman Revital Versano Fuying Gao Heather Plasterer Myriam Rai Francesco Saccá Alessandro Filla David R Lynch James R Rusche Joel M Gottesfeld Massimo Pandolfo Daniel H Geschwind

OBJECTIVE Gene expression studies in peripheral tissues from patients with neurodegenerative disorders can provide insights into disease pathogenesis, and identify potential biomarkers, an important goal of translational research in neurodegeneration. Friedreich Ataxia (FRDA) is a chronic neurodegenerative disease caused by reduced transcription of frataxin, a ubiquitously expressed protein. We...

Journal: :Archives of neurology 2010
David R Lynch Susan L Perlman Thomas Meier

OBJECTIVE To assess the efficacy of idebenone on neurological function in patients with Friedreich ataxia. DESIGN Randomized, double-blind, placebo-controlled intervention trial. SETTING Children's Hospital of Philadelphia and the University of California at Los Angeles. PARTICIPANTS Seventy ambulatory pediatric patients (age, 8-18 years) with a baseline International Cooperative Ataxia R...

Journal: :Archives of neurology 1999
M Pandolfo

Friedreich ataxia, the most common type of inherited ataxia, is itself caused in most cases by a large expansion of an intronic GAA repeat, resulting in decreased expression of the target frataxin gene. The autosomal recessive inheritance of the disease gives this triplet repeat mutation some unique features of natural history and evolution. Frataxin is a mitochondrial protein that has homologu...

2012
Alain Martelli Marek Napierala Hélène Puccio

In 1996, a link was identified between Friedreich's ataxia (FRDA), the most common inherited ataxia in men, and alterations in the gene encoding frataxin (FXN). Initial studies revealed that the disease is caused by a unique, most frequently biallelic, expansion of the GAA sequence in intron 1 of FXN. Since the identification of this link, there has been tremendous progress in understanding fra...

2015
Yogesh K. Chutake Whitney N. Costello Christina C. Lam Aniruddha C. Parikh Tamara T. Hughes Michael G. Michalopulos Mark A. Pook Sanjay I. Bidichandani Annalisa Pastore

BACKGROUND Friedreich ataxia is caused by an expanded GAA triplet-repeat sequence in intron 1 of the FXN gene that results in epigenetic silencing of the FXN promoter. This silencing mechanism is seen in patient-derived lymphoblastoid cells but it remains unknown if it is a widespread phenomenon affecting multiple cell types and tissues. METHODOLOGY / PRINCIPAL FINDINGS The humanized mouse mo...

Journal: :Pediatric Neurology Briefs 1997

Journal: :Movement disorders : official journal of the Movement Disorder Society 2016
Francesco Saccà Giorgia Puorro Angela Marsili Antonella Antenora Chiara Pane Carlo Casali Christian Marcotulli Giovanni Defazio Daniele Liuzzi Chiara Tatillo Donata Maria Cambriglia Giuseppe Schiano di Cola Luigi Giuliani Vincenzo Guardasole Andrea Salzano Antonio Ruvolo Anna De Rosa Antonio Cittadini Giuseppe De Michele Alessandro Filla

BACKGROUND Friedreich ataxia is an autosomal recessive disease with no available therapy. Clinical trials with erythropoietin in Friedreich ataxia patients have yielded conflicting results, and the long-term effect of the drug remains unknown. METHODS We designed a double-blind, placebo-controlled, multicenter trial to test the efficacy of epoetin alfa on 56 patients with Friedreich ataxia. T...

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