First causal treatment option for Friedreich's Ataxia via Erythropoietin (EPO)

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Abstract
An Austrian university offers the first treatment option for Friedreich´s Ataxia (FRDA), an inherited neurodegenerative disease. It causally targets FRDA
using Erythropoietin (EPO) to increase the level of Frataxin, decreased levels of which are reportedly responsible for the development of FRDA. So far
no other effective treatment is available which is at an advanced development stage. Industrial partners for further developing & commercialising
EPO for the treatment of FRDA are sought.

Date de creation: 23 July 2010

Insulin signaling meets mitochondria in metabolism.

Trends Endocrinol Metab (2010), Published by Elsevier Ltd. DOI: 10.1016/j.tem.2010.06.005

Zhiyong Cheng, Yolanda Tseng and Morris F White
Howard Hughes Medical Institute, Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, Boston MA, USA.

"chronic exposure to high ROS levels could alter mitochondrial function and thereby cause insulin resistance"

Klinik und Genetik der rezessiven Ataxien -[Clinical details and genetics of recessive ataxias.]

Nervenarzt. 2010 Jul 18. DOI: 10.1007/s00115-010-3079-4

Kühlke C, Kreuz F, Bürk K.

Institut für Humangenetik, Universität zu Lübeck.
[Article in German]

Iron-Sulfur (Fe-S) Cluster Assembly THE SufBCD COMPLEX IS A NEW TYPE OF Fe-S SCAFFOLD WITH A FLAVIN REDOX COFACTOR*

J. Biol. Chem. 2010 285: 23331-23341. First Published on May 11, 2010, doi:10.1074/jbc.M110.127449

Silke Wollers, Gunhild Layer, Ricardo Garcia-Serres, Luca Signor, Martin Clemancey, * Jean-Marc Latour, Marc Fontecave, and Sandrine Ollagnier de Choudens

ArmaGen® Re-engineers Erythropoietin For Brain Penetration

Medical News Today, Article Date: 17 Jul 2010

"EPO drug development for the brain is limited, because EPO does not cross the blood-brain barrier (BBB)"

"EPO-driven neuroprotection in human brain disorders is now possible with systemic administration of the HIRMAb-EPO fusion protein at doses that have minimal effects on erythropoiesis."

ArmaGen® Web

Oxidative stress, thiol redox signaling methods in epigenetics.

Methods Enzymol. 2010; 474: 213-44, doi:10.1016/S0076-6879(10)74013-1

Sundar IK, Caito S, Yao H, Rahman I

Keywords: Epigenetics, gene expression, posttranslational modifications, histones, histone acetylation, deacetylation, methylation, histone acetyltransferases (HATs), histone deacetylases (HDACs), reative oxygen species (ROS), signaling pathways, SIRT1.

Heterochromatin dysregulation in human diseases

J Appl Physiol 109: 232-242, 2010.
doi:10.1152/japplphysiol.00053.2010 

Matthias Hahn,^* Silvia Dambacher,^* and Gunnar Schotta
Munich Center for Integrated Protein Science (CiPS^M) and Adolf-Butenandt-Institute, Ludwig-Maximilians-University, Munich, Germany 

Keywords: epigenetics, heterochromatin, epigenetic therapy, FSHD, Friedreich's ataxia (FRDA), cancer

The Intermembrane Space of Mitochondria

Antioxidants & Redox Signaling.  doi:10.1089/ars.2009.3063.

Johannes M. Herrmann and Jan Riemer

Department of Cell Biology, University of Kaiserslautern, Kaiserslautern, Germany.

Review: Friedreich Ataxia and Erythropoietin

The Open Drug Discovery Journal, Volume 2, ISSN: 1877-3818
Review: Friedreich Ataxia and Erythropoietin, pp.18-24 (7)
Authors: Sylvia Boesch, Brigitte Sturm, Wolfgang Nachbauer, Sascha Hering, Hannes Steinkellner, Rainer Schneider, Werner Poewe, Barbara Scheiber-Mojdehkar
doi: 10.2174/1877381801002020018
FULL TEXT PDF

Iron-Overload Cardiomyopathy: Pathophysiology, Diagnosis, and Treatment

Journal of Cardiac Failure, Article in Press, Corrected Proof. Available online 3 July 2010.

Colm J. Murphy MD, FRCPC and Gavin Y. Oudit MD, PhD, FRCPC
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada

Keywords: Cardiomyopathy; hemochromatosis; oxidative stress; anemia; cardiac MRI; echocardiography; primary (hereditary) hemochromatosis; secondary iron overload (hemosiderosis); iron toxicosis (iron poisoning); myocardial ischemia-reperfusion injury; cardiomyopathy associated with Friedreich ataxia; vascular dysfunction.