The EFACTS (European Friedreich’s Ataxia Consortium for Translational Studies) Consortium will publish the newsletter EFACTS NEWS aimed at communicating the activities of the Network and progress in FRDA research to affected families, the general public, health care professionals and the scientific community. The newsletter will be published annually and the issues will appear on the EFACTS Website
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Wednesday, September 21, 2011
Mutation in Fe-S scaffold Isu bypasses frataxin deletion
Biochem. J. (2011) Immediate Publication, doi:10.1042/BJ20111637
Heeyong Yoon, Ramesh Golla, Emmanuel Lesuisse, Jayashree Pain, Jason Donald, Elise R. Lyver, Debkumar Pain and Andrew Dancis
University of Pennsylvania, Philadelphia, U.S.A.
Keywords: Frataxin, Friedreich’s ataxia, iron homeostasis, Fe-S cluster assembly, cysteine desulfurase (Nfs1), accessory protein (Isd11), scaffold protein (Isu), single amino acid substitution.
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Heeyong Yoon, Ramesh Golla, Emmanuel Lesuisse, Jayashree Pain, Jason Donald, Elise R. Lyver, Debkumar Pain and Andrew Dancis
University of Pennsylvania, Philadelphia, U.S.A.
Keywords: Frataxin, Friedreich’s ataxia, iron homeostasis, Fe-S cluster assembly, cysteine desulfurase (Nfs1), accessory protein (Isd11), scaffold protein (Isu), single amino acid substitution.
FULL TEXT PDF
Orphan Drugs, Big Pharma
Human Gene Therapy. September 2011, 22(9): 1035-1038. doi:10.1089/hum.2011.2515.
—Alex Philippidis, Senior News Editor
—Alex Philippidis, Senior News Editor
Sunday, September 18, 2011
Safety and Efficacy of Intravenous Immune Globulin in Treating Friedreich's Ataxia and Spinocerebellar Ataxia
Sponsor: University of South Florida
Collaborator: Baxter Healthcare Corporation
Information provided by (Responsible Party): Theresa Zesiewicz, University of South Florida
ClinicalTrials.gov Identifier: NCT01350440
This study is currently recruiting participants. (Last Updated on September 9, 2011)
Collaborator: Baxter Healthcare Corporation
Information provided by (Responsible Party): Theresa Zesiewicz, University of South Florida
ClinicalTrials.gov Identifier: NCT01350440
This study is currently recruiting participants. (Last Updated on September 9, 2011)
Neuroprotective and metabolic effects of resveratrol: Therapeutic implications for huntington's disease and other neurodegenerative disorders
doi:10.1016/j.expneurol.2011.08.014
Giulio Maria Pasinettilow asterisk, a, E-mail The Corresponding Author, Jun Wanga, Philippe Marambauda, Mario Ferruzzia, Paul Gregora, Lindsay Alexis Knablea and Lap Hoa
a Center of Excellence for Research in Complementary and Alternative Medicine in Alzheimer's Disease, Department of Neurology, Mount Sinai School of Medicine, New York, NY 1002
Keywords: Resveratrol, polyphenolic compound, aging, metabolic disorders, inflammation , cancer, currently being tested in numerous clinical trials, key metabolic sensor/effector proteins, potential neuroprotective effects, SRT501 , Huntington's disease (HD)., diabetes mellitus.
Giulio Maria Pasinettilow asterisk, a, E-mail The Corresponding Author, Jun Wanga, Philippe Marambauda, Mario Ferruzzia, Paul Gregora, Lindsay Alexis Knablea and Lap Hoa
a Center of Excellence for Research in Complementary and Alternative Medicine in Alzheimer's Disease, Department of Neurology, Mount Sinai School of Medicine, New York, NY 1002
Keywords: Resveratrol, polyphenolic compound, aging, metabolic disorders, inflammation , cancer, currently being tested in numerous clinical trials, key metabolic sensor/effector proteins, potential neuroprotective effects, SRT501 , Huntington's disease (HD)., diabetes mellitus.
Friday, September 16, 2011
Iron Efflux from Oligodendrocytes Is Differentially Regulated in Gray and White Matter
The Journal of Neuroscience, 14 September 2011, 31(37): 13301-13311; doi: 10.1523/JNEUROSCI.2838-11.2011
Katrin Schulz 1, Chris D. Vulpe 2, Leah Z. Harris 3, and Samuel David 1
1Center for Research in Neuroscience, The Research Institute of the McGill University Health Center, Montreal, Quebec H3G 1A4, Canada,
2Department of Nutritional Sciences and Toxicology, University of California, Berkeley, California 94720, and
3Department of Pediatrics, Vanderbilt University, Nashville, Tennessee 37232
Keywords: Accumulation of iron, neurodegenerative diseases, generate toxic free radicals, Iron homeostasis, ferroportin, ferroxidase, astrocytes, oligodendrocytes, hephaestin.
"Dysregulation of such efflux mechanisms leads to iron accumulation in the CNS."
Katrin Schulz 1, Chris D. Vulpe 2, Leah Z. Harris 3, and Samuel David 1
1Center for Research in Neuroscience, The Research Institute of the McGill University Health Center, Montreal, Quebec H3G 1A4, Canada,
2Department of Nutritional Sciences and Toxicology, University of California, Berkeley, California 94720, and
3Department of Pediatrics, Vanderbilt University, Nashville, Tennessee 37232
Keywords: Accumulation of iron, neurodegenerative diseases, generate toxic free radicals, Iron homeostasis, ferroportin, ferroxidase, astrocytes, oligodendrocytes, hephaestin.
"Dysregulation of such efflux mechanisms leads to iron accumulation in the CNS."
Wednesday, September 14, 2011
Evaluation of histone deacetylase inhibitors as therapeutics for neurodegenerative diseases.
Methods Mol Biol. 2011;793:495-508.
Soragni E, Xu C, Cooper A, Plasterer HL, Rusche JR, Gottesfeld JM.
Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA, USA.
Keywords: neurodegenerative diseases, aberrant gene expression, pimelic o-aminobenzamide histone deacetylase (HDAC) inhibitors, Friedreich's ataxia (FRDA), Huntington's disease (HD), cellular models.
Soragni E, Xu C, Cooper A, Plasterer HL, Rusche JR, Gottesfeld JM.
Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA, USA.
Keywords: neurodegenerative diseases, aberrant gene expression, pimelic o-aminobenzamide histone deacetylase (HDAC) inhibitors, Friedreich's ataxia (FRDA), Huntington's disease (HD), cellular models.
Superando la barrera hematoencefálica
Traduccion de EurekAlert!.org, 13 septiembre 2011, que se encuentra en Bitnavegantes
"Por primera vez, los investigadores descubrieron que, cuando los receptores de adenosina se activan en las células que forman la barrera hematoencefálica, se abre una puerta de entrada a través dicha barrera."
"Por primera vez, los investigadores descubrieron que, cuando los receptores de adenosina se activan en las células que forman la barrera hematoencefálica, se abre una puerta de entrada a través dicha barrera."
Breaching the blood-brain barrier
EurekAlert!, Public release date: 13-Sep-2011
"For the first time, the researchers discovered that when adenosine receptors are activated on cells that comprise the blood-brain barrier, a gateway into the blood-brain barrier can be established."
Adenosine Receptor Signaling Modulates Permeability of the Blood–Brain Barrier
The Journal of Neuroscience, 14 September 2011, 31(37): 13272-13280; doi: 10.1523/JNEUROSCI.3337-11.2011
Aaron J. Carman, Jeffrey H. Mills, Antje Krenz, Do-Geun Kim, and Margaret S. Bynoe
Department of Microbiology and Immunology, Cornell University, College of Veterinary Medicine, Ithaca, New York 14853
"For the first time, the researchers discovered that when adenosine receptors are activated on cells that comprise the blood-brain barrier, a gateway into the blood-brain barrier can be established."
Adenosine Receptor Signaling Modulates Permeability of the Blood–Brain Barrier
The Journal of Neuroscience, 14 September 2011, 31(37): 13272-13280; doi: 10.1523/JNEUROSCI.3337-11.2011
Aaron J. Carman, Jeffrey H. Mills, Antje Krenz, Do-Geun Kim, and Margaret S. Bynoe
Department of Microbiology and Immunology, Cornell University, College of Veterinary Medicine, Ithaca, New York 14853
Acute myocardial infarction after botulinum toxin injection.
QJM (2011) 104(7): 615-616
B.E. Stähli, L. Altwegg, T.F. Lüscher and R. Corti
Department of Cardiology, Cardiovascular Center, University Hospital Zürich, Zürich, Switzerland
Keywords: Friedreich ataxia, ventricular fibrillation, botulinum toxin A, neurogenic bladder dysfunction,thrombotic occlusion.
B.E. Stähli, L. Altwegg, T.F. Lüscher and R. Corti
Department of Cardiology, Cardiovascular Center, University Hospital Zürich, Zürich, Switzerland
Keywords: Friedreich ataxia, ventricular fibrillation, botulinum toxin A, neurogenic bladder dysfunction,thrombotic occlusion.
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