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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.


Rapamycin reduces oxidative stress in frataxin-deficient yeast cells

Friedreich ataxia (FRDA) is a common form of ataxia caused by decreased expression of the mitochondrial protein frataxin. Oxidative damage of mitochondria is thought to play a key role in the pathogenesis of the disease. Therefore, a possible therapeutic strategy should be directed to an antioxidant protection against mitochondrial damage.

Rapamycin reduces oxidative stress in frataxin-deficient yeast cells

Articulatory Kinematics in the Dysarthria Associated with Friedreich's Ataxia

Electromagnetic articulography (EMA) was used to investigate the tongue kinematics in the dysarthria associated with Friedreich's ataxia (FRDA). The subject group consisted of four individuals diagnosed with FRDA. Five nonneurologically impaired individuals, matched for age and gender, served as controls.

Articulatory Kinematics in the Dysarthria Associated with Friedreich's Ataxia

Evaluation of histone deacetylase inhibitors as therapeutics for neurodegenerative diseases

Various neurodegenerative diseases are associated with aberrant gene expression. We recently identified a novel class of pimelic o-aminobenzamide histone deacetylase (HDAC) inhibitors that show promise as therapeutics in the neurodegenerative diseases Friedreich's ataxia (FRDA) and Huntington's disease (HD). 

Evaluation of histone deacetylase inhibitors as therapeutics for neurodegenerative diseases

Overexpression of human and fly frataxins in Drosophila provokes deleterious effects at biochemical, physiological & developmental levels

Friedreich's ataxia (FA), the most frequent form of inherited ataxias in the Caucasian population, is caused by a reduced expression of frataxin, a highly conserved protein. Model organisms have contributed greatly in the efforts to decipher the function of frataxin; however, the precise function of this protein remains elusive. 

Overexpression of human and fly frataxins in Drosophila provokes deleterious effects at biochemical, physiological and developmental levels

Overexpression of human and fly frataxins in Drosophila provokes deleterious effects at biochemical, physiological and developmental levels

Friedreich's ataxia (FA), the most frequent form of inherited ataxias in the Caucasian population, is caused by a reduced expression of frataxin, a highly conserved protein. Model organisms have contributed greatly in the efforts to decipher the function of frataxin; however, the precise function of this protein remains elusive. 

Overexpression of human and fly frataxins in Drosophila provokes deleterious effects at biochemical, physiological and developmental levels

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