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Scientific News

FARA funds research progress

In this section, you will find the most recent FA research publications, many of which are funded by FARA, as well as information on upcoming conferences and symposiums. You can search for articles by date using the archive box in the right hand column. To locate FARA Funded or Supported Research, click the hyperlink in the right hand column. You may also search for specific content using key words or phrases in the search button at the top right of your screen. Please be sure to visit other key research sections of our website for information on FARA’s Grant Program and the Treatment Pipeline.


Altered lipid metabolism in a Drosophila model of Friedreich's ataxia

Friedreich’s ataxia (FRDA) is the most common form of autosomal recessive ataxia caused by a deficit in the mitochondrial protein frataxin. Although demyelination is a common symptom in FRDA patients, no multicellular model has yet been developed to study the involvement of glial cells in FRDA. Using the recently established RNAi-lines for targeted suppression of frataxin in Drosophila, we were able to study the effects of general versus glial specific frataxin downregulation. In particular we wanted to study the interplay between lowered frataxin content, lipid accumulation and peroxidation and the consequences of these effects on the sensitivity to oxidative stress and fly fitness.

Altered lipid metabolism in a Drosophila model of Friedreich's ataxia

Carbamylated erythropoietin increases frataxin independent from the erythropoietin receptor

Friedreich's ataxia (FRDA) is a neurodegenerative disorder caused by decreased expression of the mitochondrial protein frataxin. Recently we showed in a clinical pilot study in Friedreich's ataxia patients that recombinant human erythropoietin (rhuEPO) significantly increases frataxin-expression. In this in vitro study, we investigated the role of the erythropoietin receptor (EPO-R) in the frataxin increasing effect of rhuEPO and if nonerythropoietic carbamylated erythropoietin (CEPO), which cannot bind to the classical EPO-R increases frataxin expression.

Carbamylated erythropoietin increases frataxin independent from the erythropoietin receptor

Nitric oxide & frataxin: two players contributing to maintain cellular iron homeostasis

Nitric oxide (NO) is a signalling and physiologically active molecule in animals, plants and bacteria. The specificity of the molecular mechanism(s) involved in transducing the NO signal within and between cells and tissues is still poorly understood. NO has been shown to be an emerging and potent signal molecule in plant growth, development and stress physiology. The NO donor S-nitrosoglutathion (GSNO) was shown to be a biologically active compound in plants and a candidate for NO storage and/or mobilization between plant tissues and cells. NO has been implicated as a central component in maintaining iron bioavailavility in plants. 

Nitric oxide and frataxin: two players contributing to maintain cellular iron homeostasis

Dysarthria in Friedreich's Ataxia: A Perceptual Analysis

he University of Queensland, Brisbane, Qld., bBruce Lefroy Centre, Murdoch Childrens Research Institute, Royal Children’s Hospital, Melbourne, Vic., and cRoyal Children’s Hospital, Brisbane, Qld., Australia 

Dysarthria in Friedreich's Ataxia: A Perceptual Analysis

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