CARACTERIZACIÓN Y ANÁLISIS FUNCIONAL DE UNA FAMILIA

Full text: http://www.tesisenred.net/TESIS_UdL/AVAILABLE/TDX-0204105-125138//Tmrm01de04.pdf

CARACTERIZACIÓN Y ANÁLISIS FUNCIONAL DE UNA FAMILIADE GLUTAREDOXINAS MONOTIÓLICAS EN LA LEVADURA Saccharomyces cerevisiae

Teresa Rodríguez-Manzaneque Martínez Julio 2002

Cluster Fe-S-Frataxin

Evolution based on domain combinations: the case of glutaredoxins

Full text: http://www.biomedcentral.com/content/pdf/1471-2148-9-66.pdf


Evolution based on domain combinations: the case of glutaredoxin

BMC Evolutionary Biology 2009, 9:66 doi:10.1186/1471-2148-9-66
Rui Alves (ralves@cmb.udl.es)
Ester Vilapinyo (evilaprinyo@cmb.udl.es)
Albert Sorribas (albert.sorribas@cmb.udl.es)
Enrique Herrero (enric.herrero@cmb.udl.es

PGC-1/β induced expression partially compensates for respiratory chain defects in cells from patients with mitochondrial disorders

Human Molecular Genetics Advance Access originally published online on March 18, 2009
Human Molecular Genetics 2009 18(10):1805-1812; doi:10.1093/hmg/ddp093

PGC-1/β induced expression partially compensates for respiratory chain defects in cells from patients with mitochondrial disorders

Sarika Srivastava1,,, Francisca Diaz1,, Luisa Iommarini1,3, Karine Aure4, Anne Lombes4 and Carlos T. Moraes1,2,*
1 Department of Neurology 2 Department of Cell Biology and Anatomy, University of Miami School of Medicine, 1095 NW 14th Terrace, Miami, FL 33136, USA 3 Dipartimento di Scienze Neurologiche, Università di Bologna, Bologna, Italy 4 Inserm 582; UPMC-Paris6; AP/HP, Paris F-75013, France
* To whom correspondence should be addressed. Tel: +1 3052435858; Fax: +1 3052433914; Email: cmoraes@med.miami.edu

Present address: Harvard Medical School, Boston, MA 02115, USA.

Resveratrol Highlights

http://www.lmcfood.dk/fileadmin/lmc_files/food/Kristensen-5_Resveratrol-Cell-2006.pdf

Lagouge et al., Resveratrol Improves Mitochondrial Function and Protects against Metabolic Disease by Activating SIRT1 and PGC-1a,
Cell (2006), doi:10.1016/j.cell.2006.11.013

Resveratrol Improves Mitochondrial Function and Protects against Metabolic Disease by Activating SIRT1 and PGC-1a

Marie Lagouge,8,1 Carmen Argmann,8,1 Zachary Gerhart-Hines,2 Hamid Meziane,3 Carles Lerin,2
Frederic Daussin,4 Nadia Messadeq,3 Jill Milne,5 Philip Lambert,5 Peter Elliott,5 Bernard Geny,4 Markku Laakso,6
Pere Puigserver,2 and Johan Auwerx1,3,7,* 1 Institut de Ge´ ne´ tique et de Biologie Mole´ culaire et Cellulaire, CNRS / INSERM / ULP, 67404 Illkirch, France
2Department of Cell Biology, John Hopkins University School of Medicine, Baltimore, MD 21205, USA
3 Institut Clinique de la Souris, BP10142, 67404, Illkirch, France
4Department of Respiratory, Cardiocirculatory and Exercise Physiology, Hoˆ pitaux Universitaires, 67000 Strasbourg, France
5 Sirtris Pharmaceutical, Cambridge, MA 02139, USA
6Department of Medicine, University of Kuopio, 70211 Kuopio, Finland
7IGBMC-ICS, 67404 Illkirch, France
8These authors contributed equally to this work.

*Contact: auwerx@igbmc.u-strasbg.fr

--------------------------------------------------------------

http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ArtikelNr=85386&Ausgabe=230907&ProduktNr=224154&filename=85386.pdf

Neurosignals 2005;14:61–70
DOI: 10.1159/000085386
Received: December 6, 2004
Accepted after revision: March 1, 2005

Unique Properties of Polyphenol Stilbenes in the Brain: More than Direct Antioxidant Actions; Gene/Protein Regulatory Activity

Sylvain Doré
Johns Hopkins University, School of Medicine, Baltimore, Md. , USA

________________________________

http://www.ncbi.nlm.nih.gov/pubmed/18629638?dopt=Abstract

Neurochem Res. 2008 Dec;33(12):2444-71. Epub 2008 Jul 16.

Cellular stress response: a novel target for chemoprevention and nutritional neuroprotection in aging, neurodegenerative disorders and longevity.

Calabrese V, Cornelius C, Mancuso C, Pennisi G, Calafato S, Bellia F, Bates TE, Giuffrida Stella AM, Schapira T, Dinkova Kostova AT, Rizzarelli E.Section of Biochemistry and Molecular Biology, Department of Chemistry, Faculty of Medicine, University of Catania, Viale Andrea Doria 6, 95100, Catania, Italy. calabres@unict.it


_________________________________


http://www3.interscience.wiley.com/journal/121682622/abstract?CRETRY=1&SRETRY=0

Histone Deacetylase Inhibition Activity and Molecular Docking of (E )-Resveratrol: Its Therapeutic Potential in Spinal Muscular Atrophy

Didem Dayangaç-Erden 1,*, Gamze Bora 1 , Peruze Ayhan 2 , Çetin Kocaefe 1 , Sevim Dalkara 3 , Kemal Yelekçi 4 , Ayhan S. Demir 2 and Hayat Erdem-Yurter 1
1 Department of Medical Biology, Faculty of Medicine, Hacettepe University, Ankara, Turkey 2 Department of Chemistry, Middle East Technical University, Ankara, Turkey 3 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey 4 Department of Statistics and Computer Sciences, Faculty of Arts and Science, Kadir Has University, Istanbul, Turkey
Correspondence to *Dr Didem Dayangaç-Erden, didayan@hacettepe.edu.tr
Copyright Journal compilation © 2009 Blackwell Munksgaard
KEYWORDS
(E )-resveratrol • molecular docking • SMN2 • spinal muscular atrophy

________________________________



http://ntp.niehs.nih.gov/ntp/htdocs/Chem_Background/ExSumPDF/resveratrol.pdf

Functional genomic analysis of frataxin deficiency reveals tissue-specific alterations and identifies the PPAR{gamma} pathway as a therapeutic target

Hum Mol Genet. 2009 Apr 17. [Epub ahead of print]
Functional genomic analysis of frataxin deficiency reveals tissue-specific alterations and identifies the PPAR{gamma} pathway as a therapeutic target in Friedreich's ataxia.
Coppola G, Marmolino D, Lu D, Wang Q, Cnop M, Rai M, Acquaviva F, Cocozza S, Pandolfo M, Geschwind DH.
Program in Neurogenetics, Department of Neurology David Geffen School of Medicine, University of California at Los Angeles, CA 90095.

OPEN ACCESS:

http://hmg.oxfordjournals.org/cgi/content/full/18/13/2452

http://hmg.oxfordjournals.org/cgi/reprint/18/13/2452.pdf

Brain iron homeostasis and neurodegenerative disease

Citation:

Neurology, Vol. 72, Issue 16, 1436-1440, April 21, 2009
CLINICAL IMPLICATIONS OF NEUROSCIENCE RESEARCH

Brain iron homeostasis and neurodegenerative disease
Eduardo E. Benarroch

Article topics:
Physiology..Transferrin
Medicine..Genes
Medicine..Iron Metabolism
Cell Biology..Endothelial Cells
Physiology..Homeostasis
Medicine..Gene Expression
Medicine..Genetics
Medicine..Neurodegenerative Diseases
Medicine..Cardiovascular Genetics
Biochemistry..Ferritin
Medicine..Friedreich Ataxia
Biochemistry..Pantothenate Kinase
Cell Biology..Astrocytes
Biochemistry..Kinases
Medicine..Ataxia

http://www.neurology.org/cgi/content/citation/72/16/1436?rss=1

E. coli mismatch repair acts downstream of replication fork stalling to stabilize the expanded (GAA.TTC)(n) sequence.

Mutat Res.Author manuscript; available in PMC 2009 February 10.
Published in final edited form as:
Mutat Res. 2009 February 10; 661(1-2): 71–77.
Published online 2008 November 13. doi: 10.1016/j.mrfmmm.2008.11.003. PMCID: PMC2637364
NIHMSID: NIHMS83510

Copyright notice and Disclaimer
E. coli mismatch repair acts downstream of replication fork stalling to stabilize the expanded (GAA·TTC)n sequence
Rebecka L. Bourn,1 Paul M. Rindler,1 Laura M. Pollard,1 and Sanjay I. Bidichandani1,2
1Department of Biochemistry & Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
2Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
Address all correspondence and requests for reprints to: Sanjay I. Bidichandani, MBBS, PhD, 975 NE 10th St., BRC458, Oklahoma City, OK 73104, USA, Tel: (405) 271-1360, Fax: (405) 271-3910, Email: Sanjay-Bidichandani@ouhsc.edu
The publisher's final edited version of this article is available at Mutat Res.


Keywords: mismatch repair, triplet repeat instability, GAA triplet repeat, replication fork stalling

SCA-LSVD: A repeat-oriented locus-specific variation database for genotype to phenotype correlations in spinocerebellar ataxias.

http://www.ncbi.nlm.nih.gov/pubmed/19370769?dopt=Abstract

Hum Mutat. 2009 Mar 3. [Epub ahead of print]

SCA-LSVD: A repeat-oriented locus-specific variation database for genotype to phenotype correlations in spinocerebellar ataxias.

Faruq M, Scaria V, Singh I, Tyagi S, Srivastava AK, Mukerji M.Genomics and Molecular Medicine, Institute of Genomics and Integrative Biology-Council of Scientific and Industrial Research (IGIB-CSIR), Delhi, India.



The database is accessible online at http://miracle.igib.res.in/ataxia. Hum Mutat 30:1-6, 2009. (c) 2009 Wiley-Liss, Inc.PMID: 19370769 [PubMed - as supplied by publisher]

NOTE: Direct link to FXN information (http://miracle.igib.res.in/ataxia/home.php?select_db=FXN )

Infrared thermography as an access pathway for individuals with severe motor impairments

Infrared thermography as an access pathway for individuals with severe motor impairments
Negar Memarian , Anastasios N Venetsanopoulos and Tom Chau
Journal of NeuroEngineering and Rehabilitation 2009, 6:11doi:10.1186/1743-0003-6-11

http://www.jneuroengrehab.com/content/6/1/11

Published:
16 April 2009

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production http://www.jneuroengrehab.com/content/pdf/1743-0003-6-11.pdf

Enfermedades raras-ANALES DEL SISTEMA SANITARIO DE NAVARRA

http://www.cfnavarra.es/salud/anales/textos/suple31_2.htm

ANALES DEL SISTEMA SANITARIO DE NAVARRA
Enfermedades raras
Vol. 31, suplemento 2, 2008

The mitochondrial cocktail: Rationale for combined nutraceutical therapy in mitochondrial cytopathies

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T3R-4SX3NP0-D&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=44757feb1cd3228a6ef48eea38534a90

doi:10.1016/j.addr.2008.05.001


Copyright © 2008 Published by Elsevier B.V.
The mitochondrial cocktail: Rationale for combined nutraceutical therapy in mitochondrial cytopathies

References and further reading may be available for this article. To view references and further reading you must purchase this article.


M.A. Tarnopolsky, a,
aDepartment of Pediatrics and Medicine, McMaster University, 1200 Main St. W., HSC-2H26, Hamilton, Ontario, Canada L8N 3Z5

Received 23 April 2008; accepted 2 May 2008. Available online 4 July 2008.

Alpha lipoic acid and frataxin: A new indication for an old antioxidant?

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WFG-4W2W5M9-4&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=446442ddfc68762ae8d5723da8aee971 doi:10.1016/j.expneurol.2009.04.001
Copyright © 2009 Published by Elsevier Inc.

Discussion

Alpha lipoic acid and frataxin: A new indication for an old antioxidant?

References and further reading may be available for this article. To view references and further reading you must purchase this article.
James W. Russell, a, aDepartment of Neurology, University of Maryland School of Medicine & Maryland VA Medical Center, 22 South Greene Street, Box 175, Baltimore, MD 21201-1595, USA
Received 6 March 2009; revised 7 April 2009; accepted 7 April 2009. Available online 15 April 2009.

Low-dose idebenone treatment in Friedreich's ataxia with and without cardiac hypertrophy.

http://www.ncbi.nlm.nih.gov/pubmed/19363628?dopt=AbstractPlus&holding=f1000,f1000m,isrctn

J Neurol. 2009 Apr 12. [Epub ahead of print]

Low-dose idebenone treatment in Friedreich's ataxia with and without cardiac hypertrophy.

Rinaldi C, Tucci T, Maione S, Giunta A, De Michele G, Filla A.
Department of Neurological Sciences, University of "Federico II", Via Pansini, 5, 80131, Naples, Italy, rinaldi.ca@gmail.com.

Creating Ideal Neural Cells For Clinical Use

http://www.sciencedaily.com/releases/2009/04/090413141303.htm

Creating Ideal Neural Cells For Clinical Use
ScienceDaily (Apr. 13, 2009) — Investigators at the Burnham Institute for Medical Research (Burnham) have developed a protocol to rapidly differentiate human embryonic stem cells (hESCs) into neural progenitor cells that may be ideal for transplantation.

Human ES Cells Progress Slowly In Myelin's Direction

http://www.sciencedaily.com/releases/2009/04/090409103342.htm
Human ES Cells Progress Slowly In Myelin's Direction
ScienceDaily (Apr. 9, 2009) — Scientists from the University of Wisconsin report in the journal Development the successful generation from human embryonic stem cells of a type of cell that can make myelin, a finding that opens up new possibilities for both basic and clinical research.

Risk of Stroke and Thrombus Formation From Delay Incontinence of a PLAATO-Device in Friedreich Ataxia

1: Clin Cardiol. 2009 Apr 7. [Epub ahead of print]Risk of Stroke and Thrombus Formation From Delay Incontinence of a PLAATO-Device in Friedreich Ataxia.Stöllberger C, Finsterer J, Avanzini M, Mölzer G, Weidinger F.Second Medical Department, Krankenanstalt Rudofstiftung.We present the case of a 76-year-old female with suspected Friedreich ataxia, in whom leakage and thrombosis of a percutaneously implanted left atrial appendage occluder (PLAATO) was observed 2 years after implantation. Because of late developing leakages and thrombi, regular transesophageal echocardiographic examinations should be carried out in patients with occluded left atrial appendagaes. In view of these complications and the potential important hemodynamic role of the left atrial appendage, the benefit of its occlusion is questionable, and the indications of PLAATO should be strongly reconsidered. Copyright (c) 2009 Wiley Periodicals, Inc.PMID: 19353681 [PubMed - as supplied by publisher] Source: http://www.ncbi.nlm.nih.gov/pubmed/19353681

Team Regrows Neurons Controlling Movement in Rats

http://news.yahoo.com/s/hsn/20090406/hl_hsn/teamregrowsneuronscontrollingmovementinrats;_ylt=AsWK6hIycwjUHGBmTJZ0CTy3j7AB

Team Regrows Neurons Controlling Movement in Rats
By Jennifer ThomasHealthDay Reporter by Jennifer Thomashealthday Reporter – Mon Apr 6, 7:04 pm ET
MONDAY, April 6 (HealthDay News) --

Diagnosis and treatment of Friedreich ataxia: a European perspective.

http://www.ncbi.nlm.nih.gov/pubmed/19347027?dopt=Abstract

Nat Rev Neurol. 2009 Apr;5(4):222-34.
Related Articles

Diagnosis and treatment of Friedreich ataxia: a European perspective.

Schulz JB, Boesch S, Bürk K, Dürr A, Giunti P, Mariotti C, Pousset F, Schöls L, Vankan P, Pandolfo M.

Department of Neurology, University Hospital, RWTH Aachen, Aachen, Germany.

VIRxSYS Publishes New Study On RNA Therapy

http://www.medicalnewstoday.com/articles/145267.php

Article Date: 07 Apr 2009 - 0:00 PDT

VIRxSYS Publishes New Study On RNA Therapy

Axons Necessary For Voluntary Movement Regenerated

http://www.sciencedaily.com/releases/2009/04/090406192229.htm

Axons Necessary For Voluntary Movement Regenerated



Adapted from materials provided by University of California - San Diego, via EurekAlert!, a service of AAAS

All-you-can-eat: autophagy in neurodegeneration and neuroprotection

http://www.molecularneurodegeneration.com/content/4/1/16

full text: http://www.molecularneurodegeneration.com/content/pdf/1750-1326-4-16.pdf

All-you-can-eat: autophagy in neurodegeneration and neuroprotection
Philipp A Jaeger and Tony Wyss-Coray
Molecular Neurodegeneration 2009, 4:16doi:10.1186/1750-1326-4-16

Published: 6 April 2009

Novel insights into iron metabolism by integrating deletome and transcr iptome analysis in an iron deficiency model of the yeast Saccharomyces cerevis

http://www.biomedcentral.com/1471-2164/10/130/abstract

Full text: http://www.biomedcentral.com/content/pdf/1471-2164-10-130.pdf

Novel insights into iron metabolism by integrating deletome and transcr iptome analysis in an iron deficiency model of the yeast Saccharomyces cerevisiae
William J. Jo1,9, Jeung Hyoun Kim1,9, Eric Oh1,9, Daniel Jaramillo2, Patricia Holman1, Alex V. Loguinov1, Adam P. Arkin3,4, Corey Nislow5,6,8, Guri Giaever5, 7, 8 and Chris D. Vulpe 1,10 1 Department of Nutritional Sciences and Toxicology, University of California, Berkeley, California 94720 2 Stanford Genome Technology Center, Stanford University, Palo Alto, California 94304 3 Department of Bioengineering, University of California, Berkeley, California 94720 4 Physical Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720 5 University of Toronto, Department of Molecular Genetics, Toronto, Ontario M5S3E1, Canada 6 University of Toronto, Banting and Best Department of Medical Research, Toronto, Ontario M5S3E1, Canada 7University of Toronto, Department of Pharmaceutical Sciences, Toronto, Ontario M5S3E1, Canada 8 University of Toronto, Donnelley Centre for Cellular and Biomolecular Research, Toronto, Ontario M5S3E1, Canada 9 These authors contributed equally on this paper 10 Corresponding author: 119 Morgan Hall, University of California, Berkeley, California 94720, Phone: (510) 642-
1834, Fax: (510) 642-0535 Email addresses: WJJ williamjo@berkeley.edu; JHK jhkim19@berkeley.edu; EO eric_oh@berkeley.edu; DJ nddano@gmail.com; PH ttyholman@yahoo.com; AVL Avl53@aol.com; APA aparkin@lbl.gov; CN corey.nislow@utoronto.ca; GG guri.giaever@utoronto.ca; CDV vulpe@berkeley.edu

Chapter 14 Nucleotide-Dependent Iron-Sulfur Cluster Biogenesis of Endogenous and Imported Apoproteins in Isolated Intact Mitochondria

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7CV2-4W0SP7V-N&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=5402f229212062f111307c76b58a5ca2

doi:10.1016/S0076-6879(08)04414-5


Copyright © 2009 Elsevier Inc. All rights reserved.
Chapter 14 Nucleotide-Dependent Iron-Sulfur Cluster Biogenesis of Endogenous and Imported Apoproteins in Isolated Intact Mitochondria
Boominathan Amutha*, Donna M. Gordon‡, Andrew Dancis† and Debkumar Pain*

*Department of Pharmacology and Physiology, UMDNJ, New Jersey Medical School, Newark, New Jersey, USA

†Department of Medicine, Division of Hematology-Oncology, University of Pennsylvania, Philadelphia, Pennsylvania, USA

‡Department of Biological Sciences, Mississippi State University, Mississippi State, Mississippi, USA


Available online 5 April 2009.

Chapter 12 twelve Controlled Expression of Iron-Sulfur Cluster Assembly Components for Respiratory Chain Complexes in Mammalian Cells

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7CV2-4W0SP7V-K&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=31b0f067dc11fd11b523136280aa5dc4

doi:10.1016/S0076-6879(08)04412-1


Copyright © 2009 Elsevier Inc. All rights reserved.
Chapter 12 twelve Controlled Expression of Iron-Sulfur Cluster Assembly Components for Respiratory Chain Complexes in Mammalian Cells
Oliver Stehlinga, Alex D. Sheftela and Roland Lilla

aInstitut für Zytobiologie and Zytopathologie, Philipps-Universität, Marburg, Germany


Available online 5 April 2009.




Methods in Enzymology
Volume 456, 2009, Pages 209-231
Mitochondrial Function, Part A: Mitochondrial Electron Transport Complexes and Reactive Oxygen Species

Efficacy of EGb761 in Patients Suffering From Friedreich Ataxia

http://www.clinicaltrials.gov/ct2/show/NCT00824512?term=friedreich

Efficacy of EGb761 in Patients Suffering From Friedreich Ataxia

Rethinking The Genetic Theory Of Inheritance

http://www.sciencedaily.com/releases/2009/01/090118200632.htm

Rethinking The Genetic Theory Of Inheritance

An advance online publication of this study will be available on the Nature Genetics website on January 18, 2009.
Adapted from materials provided by Centre for Addiction and Mental Health, via EurekAlert!, a service of AAAS

Efficient gene delivery to the adult and fetal CNS using pseudotyped non-integrating lentiviral vectors

http://www.nature.com/gt/journal/vaop/ncurrent/abs/gt2008186a.html
Efficient gene delivery to the adult and fetal CNS using pseudotyped non-integrating lentiviral vectors
A Rahim1,2,3, A M S Wong4, S J Howe2, S M K Buckley3, A D Acosta-Saltos1, K E Elston4, N J Ward2, N J Philpott2, J D Cooper4, P N Anderson5, S N Waddington3, A J Thrasher2,6 and G Raivich1,5
1Perinatal Brain Protection and Repair Group, Department of Obstetrics and Gynaecology, University College London, London, UK
2Molecular Immunology Unit, Centre for Immunodeficiency, Institute of Child Health, University College London, London, UK
3Department of Haematology, Haemophilia Centre and Haemostasis Unit, Royal Free and University College Medical School, London, UK
4Pediatric Storage Disorders Laboratory, Department of Neuroscience, Institute of Psychiatry, Kings College London, London, UK
5Department of Anatomy and Developmental Biology, University College London, London, UK
6Great Ormond Street Hospital NHS Trust, London, UK
Correspondence: Dr AJ Thrasher, Molecular Immunology Unit, Centre for Immunodeficiency, Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK. E-mail: a.thrasher@ich.ucl.ac.uk
Received 12 June 2008; Revised 2 December 2008; Accepted 3 December 2008; Published online 22 January 2009.

Lateral-flow immunoassay for detecting drug-induced inhibition of mitochondrial DNA replication and mtDNA-encoded protein synthesis.

http://www.ncbi.nlm.nih.gov/pubmed/19152798?dopt=Abstract


Lateral-flow immunoassay for detecting drug-induced inhibition of mitochondrial DNA replication and mtDNA-encoded protein synthesis.

Nadanaciva S, Willis JH, Barker ML, Gharaibeh D, Capaldi RA, Marusich MF, Will Y.

MitoSciences Inc., 1850 Millrace Drive, Eugene, OR 97403, United States.

Impaired Nuclear Nrf2 Translocation Undermines the Oxidative Stress Response in Friedreich Ataxia

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004253



Impaired Nuclear Nrf2 Translocation Undermines the Oxidative Stress Response in Friedreich Ataxia
Vincent Paupe1,2, Emmanuel P. Dassa1,2, Sergio Goncalves1,2, Françoise Auchère3, Maria Lönn4, Arne Holmgren4, Pierre Rustin1,2*
1 Inserm, U676, Hôpital Robert Debré, Bât. Ecran, Paris, France, 2 Faculté de médecine Denis Diderot, IFR02, Université Paris 7, Laboratoire d'Ingénierie des Protéines et Contrôle Métabolique, Paris, France, 3 Département de Biologie des Génomes, Institut Jacques Monod (UMR 7592 CNRS - Universités Paris 6 & 7), Paris, France, 4 Medical Nobel Institute for Biochemistry, Department of Medical Biochemistry and Biophysics Karolinska Institutet, Stockholm, Sweden

Prevalence of hereditary ataxia and spastic paraplegia in southeast Norway: a population-based study.

http://www.ncbi.nlm.nih.gov/pubmed/19339254?dopt=Abstract

Brain. 2009 Mar 31. [Epub ahead of print]
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Prevalence of hereditary ataxia and spastic paraplegia in southeast Norway: a population-based study.

Erichsen AK, Koht J, Stray-Pedersen A, Abdelnoor M, Tallaksen CM.

1 Department of Neurology, Ullevål University Hospital, Oslo, Norway.

]

Rewrite The Textbooks: Transcription Is Bidirectional

http://www.sciencedaily.com/releases/2009/01/090125142123.htm

Rewrite The Textbooks: Transcription Is Bidirectional

Integration of functional bacterial artificial chromosomes into human cord blood-derived multipotent stem cells.

Gene Ther. 2009 Jan 29. [Epub ahead of print]

http://www.ncbi.nlm.nih.gov/pubmed/19177134?dopt=Abstract

Integration of functional bacterial artificial chromosomes into human cord blood-derived multipotent stem cells.

Zaibak F, Kozlovski J, Vadolas J, Sarsero JP, Williamson R, Howden SE.

[1] 1Department of Paediatrics, The University of Melbourne, Royal Children's Hospital, Parkville, Victoria, Australia [2] 2Murdoch Children Research Institute, Royal Children's Hospital, Parkville, Victoria, Australia.

Complex I and ATP Content Deficiency in Lymphocytes from Friedreich's Ataxia

http://cjns.metapress.com/app/home/contribution.asp?referrer=parent&backto=issue,7,28;journal,1,61;linkingpublicationresults,1:300307,1

The Canadian Journal of Neurological Sciences
Issue: Volume 36, Number 1 / January 2009
Pages: 26 - 31



Complex I and ATP Content Deficiency in Lymphocytes from Friedreich's Ataxia
Mohammad Mehdi Heidari A1, Massoud Houshmand A3, Saman Hosseinkhani A2, Shahriar Nafissi A4, Mehri Khatami A1
A1 Genetic Group, Tarbiat Modares University
A2 Biochemical Group Science School, Tarbiat Modares University
A3 Department of Medical Genetic, National Institute for Genetic Engineering and Biotechnology, Special Medical Center
A4 Department of Neurology, Medical Science, Tehran University, Tehran, Iran

Analysis of Diadochokinesis in Ataxic Dysarthria Using the Motor Speech Profile Program

Analysis of Diadochokinesis in Ataxic Dysarthria Using the Motor Speech Profile Program
Yu-Tsai Wanga, Ray D. Kentb, Joseph R. Duffyc, Jack E. Thomasc

aSchool of Dentistry, National Yang-Ming University, Taipei, Taiwan;
bWaisman Center, University of Wisconsin-Madison, Madison, Wisc., and
cMayo Clinic, Rochester, Minn., USA

Decreased contractility due to energy deprivation in a transgenic rat model of hypertrophic cardiomyopathy.

J Mol Med. 2009 Feb 3. [Epub ahead of print]
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Decreased contractility due to energy deprivation in a transgenic rat model of hypertrophic cardiomyopathy.

Luedde M, Flögel U, Knorr M, Grundt C, Hippe HJ, Brors B, Frank D, Haselmann U, Antony C, Voelkers M, Schrader J, Most P, Lemmer B, Katus HA, Frey N.

Department of Cardiology, University of Heidelberg, Heidelberg, Germany.

The therapeutic importance of understanding mechanisms of neuronal cell death in neurodegenerative disease

The therapeutic importance of understanding mechanisms of neuronal cell
death in neurodegenerative disease
Molecular Neurodegeneration
Todd E Golde (tgolde@mayo.edu)

full text: http://www.molecularneurodegeneration.com/content/pdf/1750-1326-4-8.pdf

Inborn errors of metabolism as rare diseases with a specific global situation

"Hay que evitar el uso de fármacos potencialmente tóxicos mitocondriales. Entre los antibióticos son eficaces las tetraciclinas, ciprofloxacina y aminoglicósidos. Entre los antivirales hay que tener presente que los antiretrovirales pueden producir deplección mitocondrial. Entre los antiepilépticos evitar a ser posible valproico, hidantoínas y fenobarbital. Entre los anestésicos evitar etomitadato y thipentona en el síndrome de Kearns-Sayre y recordar la gran sensibilidad de estos pacientes para el antracurio y el roncuronio."

http://www.cfnavarra.es/salud/anales/textos/Vol31/sup2/suple5a.html

Inborn errors of metabolism as rare diseases with a specific global situation

Identification of novel targets for PGC-1alpha and histone deacetylase inhibitors in neuroblastoma cells.

Biochem Biophys Res Commun. 2009 Feb 6;379(2):578-82. Epub 2008 Dec 30.

Identification of novel targets for PGC-1alpha and histone deacetylase inhibitors in neuroblastoma cells.
Cowell RM, Talati P, Blake KR, Meador-Woodruff JH, Russell JW.

Department of Psychiatry, University of Alabama, Birmingham, AL 35294, USA. rcowell@uab.edu

Friedreich's ataxia impact scale: A new measure striving to provide the flexibility required by today's studies

Friedreich's ataxia impact scale: A new measure striving to provide the flexibility required by today's studies
Stefan J. Cano, PhD 1 2, Afsane Riazi, PhD 1, Anthony H.V. Schapira, MD 3, J. Mark Cooper, PhD 3, Jeremy C. Hobart, PhD 1 2 *
1Neurological Outcome Measures Unit, Institute of Neurology, University College London, London, United Kingdom
2Department of Clinical Neuroscience, Peninsula College of Medicine and Dentistry, Plymouth, United Kingdom
3Department of Clinical Neuroscience, Royal Free and University College Medical School, London, United Kingdom



*Correspondence to Jeremy C. Hobart, Senior Lecturer and Honorary Consultant Neurologist, Peninsula College of Medicine and Dentistry, Room N16, ITTC Building, Tamar Science Park, Davy Road, Plymouth, PL6 8BX Devon, United Kingdom
Potential conflict of interest: None reported.

Funded by:
Royal Free Hospital
School of Education, Murdoch University, Perth, Western Australia
Royal Society of Medicine (Ellison-Cliffe Travelling Fellowship)
MS Society of Great Britain and Northern Ireland
NHS Technology Assessment Programme

HUMAN GENES PLACED IN STEM CELLS SHOWN TO FUNCTION PROPERLY

MEDIA RELEASE Embargo 10am Tuesday 10 February 2009

HUMAN GENES PLACED IN STEM CELLS
SHOWN TO FUNCTION PROPERLY

Human genes placed in stem cells have been shown to function properly, according to new research at the Murdoch Childrens Research Institute and Melbourne University.

This is the first report showing a full length human gene can be placed in a cord blood stem cell and work properly. This shows stem cells from patients with genetic diseases may be corrected in the lab, giving hope to those living with Cystic Fibrosis and Friedreich Ataxia.

The research found that when a normal copy of a gene was put into a cord blood stem cell, it worked properly when the stem cells form nerve, bone or lung cells in the laboratory. The paper will appear in the next issue of top journal Gene Therapy.

The researchers, led by Dr Faten Zaibak and Professor Bob Williamson, took a full length human gene that codes for a protein known as "frataxin". When this gene does not work properly, affected young people develop Friedreich Ataxia, a debilitating and life-threatening neurodegenerative disorder.

"This gene was introduced into a unique population of cord blood stem cells, which have been shown to form many different types of cells in the body. In some cases, the stem cells took up the gene and switched it on. The protein from the gene was found in the cells just as if it was made from a normal copy of the gene rather than one put there in the lab," Professor Williamson said.

"The stem cells continue to grow and retain the ability to form many cell types in the laboratory, including nerve and lung cells. This is the first report showing a full length human gene can be placed in a cord blood stem cell and work properly, with the stem cell remaining active and able to continue to multiply for months. However, it still remains to be shown that the cells will work if taken from the lab and used for treatment," Dr Zaibak said.

It is universally agreed that using cord blood stem cells is ethically acceptable, and free of the controversy surrounding embryonic stem cells.

"These results suggests that the cord blood stem cells capable of forming many different tissues can be collected from the patient at birth, corrected and then returned to the patient, bypassing any immune complications," Professor Williamson said.




The researchers, who are funded by the Australian Cystic Fibrosis Research Trust and the New Zealand Cystic Fibrosis Association, hope to carry out similar experiments with the cystic fibrosis gene. Currently, the cystic fibrosis gene is difficult to insert into the cell because of its large size.

The authors emphasised that treatment is still in the future, because it is essential to show that the cells can be introduced into a patient in a way that is proven to be safe and effective.

Reduction of Hydrophilic Ubiquinones by the Flavin in Mitochondrial NADH:Ubiquinone Oxidoreductase (Complex I) and Production of Reactive Oxygen Speci

Biochemistry. 2009 Feb 16. [Epub ahead of print]


Reduction of Hydrophilic Ubiquinones by the Flavin in Mitochondrial NADH:Ubiquinone Oxidoreductase (Complex I) and Production of Reactive Oxygen Species (dagger).

King MS, Sharpley MS, Hirst J.

Medical Research Council Dunn Human Nutrition Unit, Wellcome Trust/MRC Building, Hills Road, Cambridge CB2 0XY, U.K.

The wobbly child: an approach to inherited ataxias.

http://www.ncbi.nlm.nih.gov/pubmed/19073328?dopt=Abstract



The wobbly child: an approach to inherited ataxias.
Bernard G, Shevell M.
Department of Neurology/Neurosurgery, McGill University, Montreal Children's Hospital, McGill University Health Center, Montreal, Quebec, Canada.

StemCells, Inc. Comments On PLoS Medicine Article Concerning Cell Transplants In Russia

StemCells, Inc. Comments On PLoS Medicine Article Concerning Cell Transplants In Russia
Main Category: Stem Cell Research
Also Included In: Transplants / Organ Donations
Article Date: 23 Feb 2009 - 4:00 PST

Genomic and biochemical approaches in the discovery of mechanisms for selective neuronal vulnerability to oxidative stress

http://www.biomedcentral.com/content/pdf/1471-2202-10-12.pdf (FULL TEXT)

Genomic and biochemical approaches in the discovery of mechanisms for selective neuronal vulnerability to oxidative stress

Xinkun Wang , Asma Zaidi , Ranu Pal , Alexander S Garrett , Rogelio Braceras , Xue-wen Chen , Mary L Michaelis and Elias K Michaelis
BMC Neuroscience 2009, 10:12doi:10.1186/1471-2202-10-12
Published:19 February 2009

New Protein May Reverse Neurodegenerative Diseases

New Protein May Reverse Neurodegenerative Diseases
Main Category: Neurology / Neuroscience
Also Included In: Biology / Biochemistry; Genetics
Article Date: 25 Feb 2009 - 2:00 PST

University of Virginia Health System
PO Box 800795
Charlottesville
VA 22908-0795
United States
http://www.healthsystem.virginia.edu

Un nuevo 'software' permite estudiar los tractos de las fibras cerebrales

Un nuevo 'software' permite estudiar los tractos de las fibras cerebrales
Una nueva técnica de imagen basada en resonancia magnética de tensor de difusión permite observar las fibras cerebrales y el deterioro que en ellas causan las distintas patologías neurológicas, determinando las diferencias entre enfermedades y ofreciendo una ayuda al diagnóstico, el tratamiento e incluso la neurocirugía.
Beatriz Peñalba 06/03/2009

Functional Protein Delivery into Neurons Using Polymeric Nanoparticles

Originally published In Press as doi:10.1074/jbc.M805956200 on January 7, 2009
J. Biol. Chem., Vol. 284, Issue 11, 6972-6981, March 13, 2009

Functional Protein Delivery into Neurons Using Polymeric Nanoparticles*

Linda Hasadsri, Jörg Kreuter, Hiroaki Hattori¶, Tadao Iwasaki¶, and Julia M. George1
From the Department of Cell and Developmental Biology and College of Medicine (Medical Scholars Program), University of Illinois Urbana-Champaign, Urbana, Illinois 61801, the Institut für Pharmazeutische Technologie, Biozentrum, Johann Wolfgang Goethe Universität, Frankfurt D-60439, Germany, the ¶Department of Advanced Medical Technology and Development, BML, Inc., 1361-1 Matoba, Kawagoe, Saitama 350-1101, Japan, and the Department of Molecular and Integrative Physiology, University of Illinois Urbana-Champaign, Urbana, Illinois 61801

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1–S5.

1 To whom correspondence should be addressed: Dept. of Molecular and Integrative Physiology, 524 Burrill Hall, 407 S. Goodwin Ave, Urbana, IL 61801. Tel.: 217-244-4525; Fax: 217-333-1133; E-mail: j-george@illinois.edu.

Retinal ganglion cells neurodegeneration in mitochondrial inherited disorders

Biochim Biophys Acta. 2009 Mar 4. [Epub ahead of print]
Related Articles

Retinal ganglion cells neurodegeneration in mitochondrial inherited disorders.

Carelli V, Morgia CL, Valentino ML, Barboni P, Ross-Cisneros FN, Sadun AA.

Department of Neurological Sciences, University of Bologna, Italy.

OVEREXPRESSION OF MITOCHONDRIAL FERRITIN SENSITIZES CELLS TO OXIDATIVE STRESS VIA AN IRON-MEDIATED MECHANISM.

Antioxid Redox Signal. 2009 Mar 9. [Epub ahead of print]

OVEREXPRESSION OF MITOCHONDRIAL FERRITIN SENSITIZES CELLS TO OXIDATIVE STRESS VIA AN IRON-MEDIATED MECHANISM.
Lu Z, Nie G, Li Y, Soe-Lin S, Tao Y, Cao Y, Zhang Z, Liu N, Ponka P, Zhao B.
University of Minnesota, Medicine, 420 Delaware street, Medicine Cardiology Office, MMC508, minneapolis, Minnesota, United States, 55455, 6126263040, 6126264411; luxxx202@umn.edu.

Chromatin Remodeling in the Noncoding Repeat Expansion Diseases*

Originally published In Press as doi:10.1074/jbc.R800026200 on October 28, 2008
J. Biol. Chem., Vol. 284, Issue 12, 7413-7417, March 20, 2009

Chromatin Remodeling in the Noncoding Repeat Expansion Diseases*
Daman Kumari and Karen Usdin1
From the Section on Gene Structure and Disease, Laboratory of Molecular and Cellular Biology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892-0830


1 To whom correspondence should be addressed. E-mail: ku@helix.nih.gov.

An Iron-Sulfur Cluster Is Essential for the Binding of Broken DNA by AddAB-type Helicase-Nucleases*

An Iron-Sulfur Cluster Is Essential for the Binding of Broken DNA by AddAB-type Helicase-Nucleases*
Joseph T. P. Yeeles, Richard Cammack, and Mark S. Dillingham1
From the DNA-Protein Interactions Unit, Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom and the Molecular Biophysics Group, Pharmaceutical Science Research Division, King's College London, London SE1 9NH, United Kingdom
The on-line version of this article (available at http://www.jbc.org) contains supplemental text and Figs. S1–S6.

A combined voxel-based morphometry and (1)H-MRS study in patients with Friedreich's ataxia.

http://www.ncbi.nlm.nih.gov/pubmed/19280106?dopt=Abstract

A combined voxel-based morphometry and (1)H-MRS study in patients with Friedreich's ataxia.

França MC Jr, D'Abreu A, Yasuda CL, Bonadia LC, Santos da Silva M, Nucci A, Lopes-Cendes I, Cendes F.

Department of Neurology, University of Campinas (UNICAMP), Campinas, Sao Paulo, Brazil, mcfrancajr@uol.com.br.

Hydrogenosomes under microscopy

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WXF-4VVN4NH-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=88a208d4a6b5b9f8fd46ecf9b131966b

Hydrogenosomes under microscopy
Marlene Benchimol, a,
aUniversidade Santa Úrsula, Laboratório de Ultraestrutura Celular, Rio de Janeiro, Brazil

Evaluating the progression of Friedreich ataxia and its treatment

Evaluating the progression of Friedreich ataxia and its treatment

Martin B. Delatycki1, 2
(1) Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Flemington Road, Parkville, Victoria, 3052, Australia
(2) Dept. of Paediatrics, University of Melbourne, Parkville, Victoria, Australia

Clinical experience with high-dose idebenone in Friedreich ataxia

http://www.springerlink.com/content/w63656q2062g2818/

Clinical experience with high-dose idebenone in Friedreich ataxia

Jörg B. Schulz1 , Nicholas A. Di Prospero2 and Kenneth Fischbeck3
(1) Dept. of Neurology, University Medical Centre, RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany
(2) Johnson and Johnson Pharmaceutical Research and Development, Raritan, NJ, USA
(3) Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, MD, USA

Idebenone: An emerging therapy for Friedreich ataxia

Idebenone: An emerging therapy for Friedreich ataxia

Thomas Meier1 and Gunnar Buyse2
(1) Santhera Pharmaceuticals, Hammerstrasse 47, 4410 Liestal, Switzerland
(2) Child Neurology, University Hospitals Leuven, Leuven, Belgium

Multicellular models of Friedreich ataxia

Multicellular models of Friedreich ataxia

Hélène Puccio1
(1) IGBMC Inserm, U596, CNRS, Université Louis Pasteur, UMR7104, Collège de France, Chaire de génétique humaine, 1 rue Laurent Fries, BP10142, Illkirch, F-67400, France

Friedreich ataxia: The clinical picture

http://www.springerlink.com/content/jt7731372141671k/

Friedreich ataxia: The clinical picture

Massimo Pandolfo1
(1) Service de Neurologie, Université Libre de Bruxelles-Hôpital Erasme, Route de Lennik 808, B-1070 Bruxelles, Belgium

The pathogenesis of Friedreich ataxia and the structure and function of frataxin

http://www.springerlink.com/content/237n26h5wj083865/

The pathogenesis of Friedreich ataxia and the structure and function of frataxin

Massimo Pandolfo1 and Annalisa Pastore2
(1) Service de Neurologie, Hôpital Erasme – Université Libre de Bruxelles, Route de Lennik 808, B-1070 Brussels, Belgium
(2) The National Institute for Medical Research, The Ridgeway, London, NW7 1AA, UK

Stem cell-based cell therapy in neurological diseases: A review

Stem cell-based cell therapy in neurological diseases: A review

Seung U. Kim 1 2 *, Jean de Vellis 3
1Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, British Columbia, Canada
2Medical Research Institute, Chungang University School of Medicine, Seoul, Korea
3Mental Retardation Research Center, University of California Los Angeles School of Medicine, Los Angeles, California

Cognitive impairment in spinocerebellar degeneration.

Eur Neurol. 2009;61(5):257-68. Epub 2009 Mar 17.
Related Articles

Cognitive impairment in spinocerebellar degeneration.

Kawai Y, Suenaga M, Watanabe H, Sobue G.

Department of Neurology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Japan.

Computer Learning, Electrical Stimulation Offer Hope For Paralyzed

http://www.medicalnewstoday.com/articles/142964.php

Computer Learning, Electrical Stimulation Offer Hope For Paralyzed

Article Date: 20 Mar 2009 - 3:00 PDT

Bacterial frataxin CyaY is the gatekeeper of iron-sulfur cluster formation catalyzed by IscS.

Nat Struct Mol Biol. 2009 Mar 22. [Epub ahead of print]
Related Articles

Bacterial frataxin CyaY is the gatekeeper of iron-sulfur cluster formation catalyzed by IscS.

Adinolfi S, Iannuzzi C, Prischi F, Pastore C, Iametti S, Martin SR, Bonomi F, Pastore A.

National Institute for Medical Research, The Ridgeway, London, UK.

Frataxin is an essential mitochondrial protein whose reduced expression causes Friedreich's ataxia (FRDA), a lethal neurodegenerative disease. It is believed that frataxin is an iron chaperone that participates in iron metabolism. We have tested this hypothesis using the bacterial frataxin ortholog, CyaY, and different biochemical and biophysical techniques. We observe that CyaY participates in iron-sulfur (Fe-S) cluster assembly as an iron-dependent inhibitor of cluster formation, through binding to the desulfurase IscS. The interaction with IscS involves the iron binding surface of CyaY, which is conserved throughout the frataxin family. We propose that frataxins are iron sensors that act as regulators of Fe-S cluster formation to fine-tune the quantity of Fe-S cluster formed to the concentration of the available acceptors. Our observations provide new perspectives for understanding FRDA and a mechanistic model that rationalizes the available knowledge on frataxin.

PMID: 19305405 [PubMed - as supplied by publisher]

La Frataxina bacteriana CyaY es el supervisor de la formación del cluster hierro-azufre catalizada por IscS.

Nat Struct Mol Biol. 2009 Mar 22.

Bacterial frataxin CyaY is the gatekeeper of iron-sulfur cluster formation catalyzed by IscS.
Adinolfi S, Iannuzzi C, Prischi F, Pastore C, Iametti S, Martin SR, Bonomi F, Pastore A.
National Institute for Medical Research, The Ridgeway, London, UK.


La Frataxina bacteriana CyaY es el supervisor de la formación del cluster hierro-azufre catalizada por IscS.
La Frataxina es una proteína mitocondrial esencial cuya expresión reducida causa la ataxia de Friedreich (FRDA), una enfermedad neurodegenerativa letal. Se cree que la frataxina es una chaperona de hierro que participa en el metabolismo del hierro. Hemos probado esta hipótesis utilizando el ortólogo bacteriano de la frataxina, CyaY, y diferentes técnicas de bioquímica y biofísica. Observamos que CyaY participa en el ensamblaje del cluster hierro-azufre (Fe-S) como un inhibidor hierro-dependiente de la formación del cluster, a través de la unión a la desulfurasa IscS. La interacción con IscS implica la unión del hierro en la superficie de CyaY, que se conserva en toda la familia frataxina. Proponemos que las frataxinas son sensores del hierro que actúan como reguladores de la formación del cluster Fe-S para afinar la cantidad de cluster Fe-S que se forma según la concentración de los aceptores disponibles. Nuestras observaciones ofrecen nuevas perspectivas para entender el FRDA y un modelo mecanicista que racionaliza los conocimientos disponibles sobre la frataxina.

Gatekeeper: no tiene una traducción exacta al español, se puede traducir como guardián, supervisor, sensor….. en el contexto en que está lo mas adecuado es “supervisor” .

Pharmacotherapy for Friedreich Ataxia

Pharmacotherapy for Friedreich Ataxia
Authors: Tsou, Amy Y.1; Friedman, Lisa S.; Wilson, Robert B.2; Lynch, David R.
Source: CNS Drugs, Volume 23, Number 3, 2009 , pp. 213-223(11)

Temporal and spatial variability in speakers with Parkinson's Disease and Friedreich's Ataxia.

J Med Speech Lang Pathol. 2008 Dec;16(4):173-180.Related Articles

Temporal and spatial variability in speakers with Parkinson's Disease and Friedreich's Ataxia.

Anderson A, Lowit A, Howell P.
University College London Gower St., London WC1E 6BT.

Study Of Cat Diet Leads To Key Nervous System Repair Discovery - Restoration Of Myelin

Study Of Cat Diet Leads To Key Nervous System Repair Discovery - Restoration Of Myelin
Main Category: Neurology / NeuroscienceAlso Included In: Multiple SclerosisArticle Date: 31 Mar 2009 - 6:00 PDT

Development of iBAC-FRDA-Luciferase Fusion Vector for the Detection of Frataxin Expression

Human Gene TherapyBSGT 2009 Oral PresentationsTo cite this paper:Human Gene Therapy. April 2009, 20(4): 389-395. doi:10.1089/hum.2009.1032.
.../...
Or 6

Development of iBAC-FRDA-Luciferase Fusion Vector for the Detection of Frataxin Expression
Lufino MMP (presenting)1, Alegre-Abarrategui J1, Lim F2, Wade-Martins R11Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3QX2Departamento de Biologı´a Molecular, Centro de Biologı´a Molecular ‘‘Severo Ochoa’’ (CSIC-UAM), Universidad Auto´noma de Madrid, Madrid, Spain