نتایج جستجو برای: friedreich ataxia

تعداد نتایج: 17893  

Journal: :Journal of neuroimaging : official journal of the American Society of Neuroimaging 2014
Karl Egger Christian Clemm von Hohenberg Michael F Schocke Charles R G Guttmann Demian Wassermann Marlene C Wigand Wolfgang Nachbauer Christian Kremser Brigitte Sturm Barbara Scheiber-Mojdehkar Marek Kubicki Martha E Shenton Sylvia Boesch

BACKGROUND AND PURPOSE Erythropoietin (EPO) has received growing attention because of its neuroregenerative properties. Preclinical and clinical evidence supports its therapeutic potential in brain conditions like stroke, multiple sclerosis, and schizophrenia. Also, in Friedreich ataxia, clinical improvement after EPO therapy was shown. The aim of this study was to assess possible therapy-assoc...

Journal: :Neuroscience 2010
G Rance L A Corben E Du Bourg A King M B Delatycki

Friedreich ataxia (FRDA) is a neurodegenerative disease affecting motor and sensory systems. This study aimed to investigate the presence and perceptual consequences of auditory neuropathy (AN) in affected individuals and examine the use of personal-FM systems to ameliorate the resulting communication difficulties. Ten individuals with FRDA underwent a battery of auditory function tests and the...

2004
Cécile Bouton Laurence Reutenauer Ariane Hertzog Pawel Golik Vincent Procaccio Manisha Patel Jean-Claude Drapier Michel Koenig

1 Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS/INSERM/Université Louis Pasteur, 67404 Illkirch cedex, CU de Strasbourg, France. 2 Institut de Chimie des Substances Naturelles (ICSN), CNRS, avenue de la Terrasse, 91190 Gif-sur-Yvette, France. 3 Center for Molecular and Mitochondrial Medicine and Genetics (MAMMAG), University of California Irvine, Irvine, CA 92697,...

Journal: :Arquivos de neuro-psiquiatria 1999
I V Schwartz L B Jardim A C Puga S Cocozza S Leistner L C Lima

Friedreich ataxia (FRDA), the most common autosomal recessive ataxia, is caused in 94% of cases by homozygous expansions of an unstable GAA repeat localised in intron 1 of the X25 gene. We have investigated this mutation in five Brazilian patients: four with typical FRDA findings and one patient with atypical manifestations, who was considered to have some other form of cerebellar ataxia with r...

Journal: :Human molecular genetics 2005
Pilar González-Cabo Rafael P Vázquez-Manrique M Adelaida García-Gimeno Pascual Sanz Francesc Palau

Frataxin deficiency is the main cause of Friedreich ataxia, an autosomal recessive neurodegenerative disorder. Frataxin function in mitochondria has not been fully explained yet. In this work, we show that Saccharomyces cerevisiae frataxin orthologue Yfh1p interacts physically with succinate dehydrogenase complex subunits Sdh1p and Sdh2p of the yeast mitochondrial electron transport chain and a...

2017
Monica Benini Silvia Fortuni Ivano Condò Giulia Alfedi Florence Malisan Nicola Toschi Dario Serio Damiano Sergio Massaro Gaetano Arcuri Roberto Testi Alessandra Rufini

Friedreich ataxia (FRDA) is a severe genetic neurodegenerative disease caused by reduced expression of the mitochondrial protein frataxin. To date, there is no therapy to treat this condition. The amount of residual frataxin critically affects the severity of the disease; thus, attempts to restore physiological frataxin levels are considered therapeutically relevant. Frataxin levels are control...

2000
SANDRA LEISTNER LUCIANE C. LIMA

Friedreich ataxia (FRDA), the most common autosomal recessive ataxia, is caused in 94% of cases by homozygous expansions of an unstable GAA repeat localised in intron 1 of the X25 gene. We have investigated this mutation in five Brazilian patients: four with typical FRDA findings and one patient with atypical manifestations, who was considered to have some other form of cerebellar ataxia with r...

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