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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.


Rationale for the Development of 2-Aminobenzamide Histone Deacetylase Inhibitors as Therapeutics for Friedreich Ataxia

Numerous studies have pointed to histone deacetylase inhibitors as potential therapeutics for various neurodegenerative diseases, and clinical trials with several histone deacetylase inhibitors have been performed or are under way. However, histone deacetylase inhibitors tested to date either are highly cytotoxic or have very low specificities for different histone deacetylase enzymes.

Read More: Rationale for the Development of 2-Aminobenzamide Histone Deacetylase Inhibitors as Therapeutics for Friedreich Ataxia

Cardiomyopathy in Friedreich Ataxia: Clinical Findings and Research

Friedreich ataxia is the most common human ataxia and results from inadequate production of the frataxin protein, most often the result of a triplet expansion in the nuclear FXN gene. The gene cannot be transcribed to generate the messenger ribonucleic acid for frataxin. Frataxin is an iron-binding protein targeted to the mitochondrial matrix. In its absence, multiple iron-sulfur-dependent proteins in mitochondria and the cytosol lack proper assembly, destroying mitochondrial and nuclear function.

Read More: Cardiomyopathy in Friedreich Ataxia: Clinical Findings and Research

A functional MRI study of motor dysfunction in Friedreich's Ataxia

Friedreich's ataxia (FRDA) is the most common form of hereditary ataxia. In addition to proximal spinal cord and brain stem atrophy, mild to moderate atrophy of the cerebellum has been reported in advanced FRDA. The aim of this study was to examine dysfunction in motor-related areas involved in the execution of finger tapping tasks in individuals with FRDA, and to investigate functional re-organization of cortico-cerebellar, cortico-striatal and parieto-frontal loops as a result of the cerebellar pathology. Thirteen right-handed individuals with FRDA and fourteen right-handed controls participated.

Read More: A functional MRI study of motor dysfunction in Friedreich's Ataxia

DNA triplex structures in neurodegenerative disorder, Friedreich's ataxia

It is now established that a small fraction of genomic DNA does adopt the non-canonical B-DNA structure or 'unusual' DNA structure. The unusual DNA structures like DNA-hairpin, cruciform, Z-DNA, triplex and tetraplex are represented as hotspots of chromosomal breaks, homologous recombination and gross chromosomal rearrangements since they are prone to the structural alterations. Friedreich's ataxia (FRDA), the autosomal recessive degenerative disorder of nervous and muscles tissue, is caused by the massive expansion of (GAA) repeats that occur in the first intron of Frataxin gene X25 on chromosome 9q13-q21.1.

Read More: DNA triplex structures in neurodegenerative disorder, Friedreich's ataxia

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