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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.


Metal Ion Binding in Wild-Type and Mutated Frataxin: A Stability Study

This work studies the stability of wild-type frataxin and some of its variants found in cancer tissues upon Co2+ binding. Although the physiologically involved metal ion in the frataxin enzymatic activity is Fe2+, Co2+ is most often used in experiments because Fe2+ is extremely unstable owing to the fast oxidation reaction Fe2+ → Fe3+. Protein stability is monitored following the conformational changes induced by Co2+ binding as measured by circular dichroism, fluorescence spectroscopy, and melting temperature measurements. The stability ranking among the wild-type frataxin and its variants obtained in this way is confirmed by a detailed comparative analysis of the XAS spectra of the metal-protein complex at the Co K-edge. In particular, a fit to the EXAFS region of the spectrum allows to positively identify the frataxin acidic ridge as the most likely location of the metal-binding sites. Furthermore, the surprising feature emerging from a detailed analysis of the XANES region of the spectrum can be explained by the fact that the longer 81-210 frataxin fragment has a smaller propensity for Co2+ binding than the shorter 90-210 one. This fact is explained by the peculiar role of the N-terminal disordered tail in modulating the protein ability to interact with the metal.

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Hereditary Ataxia Overview

The purpose of this overview on hereditary ataxia is to increase the awareness of clinicians regarding the causes of hereditary ataxia, related genetic counseling issues, and management.

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FARA General Research Grants - Letter of Intent Deadline - August 15, 2022

The deadline for Letters of Intent (LOIs) within the FARA grant program is approaching on August 15. Submissions for General Research Grants, Postdoctoral Awards, and Postdoctoral Fellowships are being accepted. FARA supports research through funding competitive grants across the spectrum from basic research through drug development and clinical research programs in Friedreich's Ataxia (FA).

In 2020/2021, about 50% of LOIs received were invited to submit a full application. All investigators interested in FA-related research are invited to submit an LOI through our submission portal. The proposed research must fall within FARA's Grant Program Priorities and more information on how to apply for a FARA grant can be found here.

Please note the grant funding start dates for each cycle and select your submission cycle accordingly.

View Grant types, Deadlines, and Budget Limits
 

Neuroinflammation in Friedreich's Ataxia

Although the overt manifestations of FRDA in the nervous system are mainly observed in the neurons, alterations in non-neuronal cells may also contribute to the pathogenesis of the disease, as recently suggested for other neurodegenerative disorders. In FRDA, the involvement of glial cells can be ascribed to direct effects caused by frataxin loss, eliciting different aberrant mechanisms. Iron accumulation, mitochondria dysfunction, and reactive species overproduction, mechanisms identified as etiopathogenic in neurons in FRDA, can similarly affect glial cells, leading them to assume phenotypes that can concur to and exacerbate neuron loss. Recent findings obtained in FRDA patients and cellular and animal models of the disease have suggested that neuroinflammation can accompany and contribute to the neuropathology. In this review article, the authors discuss evidence about the involvement of neuroinflammatory-related mechanisms in models of FRDA and provide clues for the modulation of glial-related mechanisms as a possible strategy to improve disease features.

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Advantages and Limitations of Gene Therapy and Gene Editing for Friedreich's Ataxia

In this review, the authors provide an overview on the current and emerging prospects of gene therapy for FRDA, with specific focus on advantages of CRISPR/Cas9-mediated gene editing of FXN as a viable option to restore endogenous frataxin expression. They also assess the potential of ex vivo gene editing in hematopoietic stem and progenitor cells as a potential autologous transplantation therapeutic option and discuss its advantages in tackling FRDA-specific safety aspects for clinical translation.

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