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         Friedreich Ataxia:     more books (31)
  1. Friedreich Ataxia - A Bibliography and Dictionary for Physicians, Patients, and Genome Researchers by Philip M. Parker, 2007-07-16
  2. The Official Parent's Sourcebook on Friedreich's Ataxia: A Revised and Updated Directory for the Internet Age by Icon Health Publications, 2002-11-18
  3. The Hereditary Ataxias and Related Disorders (Clinical Neurology and Neurosurgery Monographs, Volume 6) by A. E. Harding, 1984-12
  4. Sweet FA: The Autobiography of Alun Peredur Jones Who Suffers from Friedreich's Ataxia, an Inherited Disease by Alun Peredur Jones, 1989-01
  5. Friedreich ataxia: An entry from Thomson Gale's <i>Gale Encyclopedia of Neurological Disorders</i> by Dawn, MS, CGC Cardeiro, 2005
  6. Temporal and spatial variability in speakers with Parkinson's disease and Friedreich's ataxia.: An article from: Journal of Medical Speech - Language Pathology by Andrew Anderson, Anja Lowit, et all 2008-12-01
  7. Gale Encyclopedia of Medicine: Friedreich's ataxia by Rosalyn Carson-DeWitt MD, 2002-01-01
  8. Role of Frataxin in Mitochondrial Iron and Haem Metabolism: Development of Potential Iron Chelators for the Treatment of Friedreich's Ataxia by Erika Becker, Des R. Richardson, 2009-08-18
  9. Co[Q.sub.10] and vitamin E slow progression of some aspects of Friedreich's ataxia while reversing others.(ABSTRACTS OF INTEREST): An article from: Original Internist by Steve Austin, 2005-09-01
  10. Science & Medicine Magazine May/June 2000 (Vol. 7 No. 3, Friedreich's Ataxia, Autoimmune Diabetes, Shiga Toxigenic E. Coli) by various, 2000
  11. Sweet F.A.: The Autobiography of Alun Peredur Jones Who Suffers from Friedreich's Ataxia, an Inherited Disease by Alun Peredur Jones, 1989-10-31
  12. Friedreich's Ataxia: An entry from Gale's <i>Gale Encyclopedia of Medicine, 3rd ed.</i> by Rosalyn, MD Carson-DeWitt, 2006
  13. Friedreich's ataxia: An entry from Thomson Gale's <i>Gale Encyclopedia of Children's Health: Infancy through Adolescence</i> by Judith Sims, Rosalyn, M.D. Carson-DeWitt, 2006
  14. Finding a drug target for Friedreich's Ataxia: An overview of FRDA, current research and a new finding by Nadine Chapman-Rothe, 2010-02-26

81. Friedreich's Ataxia
Maharishi Vedic Vibration Consultation application form for friedreich's ataxia. 7)(required) How disabling is your case friedreich's ataxia or its symptoms?
http://vedicvibration.com/apply/neurological/ataxia.html
Please note! You must have JavaScript enabled to use our on line application His Holiness
Maharishi
Mahesh Yogi showSessionButtonsInner(0) Neurological Main Category Index Alphabetic Index Friedreich's ataxia
Your answers will enable us to develop your personalized consultation. Issues (required) Check one or more characteristics or information relevant to your current case of Friedreich's ataxia and its symptoms.
Weakness of the lower extremities General weakness Abnormal gait Confined to a wheelchair Poor circulation Tremors Slurred speech Heart problems None (required) Check one or more primary areas to be addressed. Head Heart Left Upper extremities Hip Thigh Lower leg Ankle Foot Toes All Right Upper extremities Hip Thigh Lower leg Ankle Foot Toes All Left Lower extremities Shoulder Upper arm Lower arm Wrist Hand Thumb and fingers All Right Lower extremities Shoulder Upper arm Lower arm Wrist Hand Thumb and fingers All (required) Check one or more Sensations that are predominant in your case of Friedreich's ataxia.
Shakiness Itching Numbness Heaviness Weakness Rawness Pain Stiffness, rigidity and/or tightness

82. Friedreich-ataxia (FA)
friedreichataxia (FA) Informatie van VSN; friedreich's ataxia ParentsGroup Informatie en lotgenotencontact, engelstalig. Info op maat?
http://www.erfocentrum.nl/zena/fried.php
erfelijkheid.nl winkel mail ons nieuwsbrief ... sitemap ZIEKTEN EN AANDOENINGEN ERFELIJKHEID LITERATUUR (PARA)MEDICI
Beginpagina
... Ziekten en aandoeningen Friedreich-ataxia (FA)
Friedreich-ataxia (FA) Korte beschrijving
FA is een aangeboren ziekte waarbij geleidelijk het weefsel van de kleine hersenen, het ruggemerg en de gevoelszenuwen wordt afgebroken. Als gevolg van deze afbraak treedt functieverlies van het zenuwstelsel op. De klachten beginnen voor het 20e levensjaar. Er ontstaan in ernst toenemende coördinatiestoornissen, stoornissen in het gevoel, spraakstoornissen en doofheid. Bij 10% bestaat diabetes mellitus (suikerziekte). Bovendien ontwikkelt zich een afwijking van de hartspier, waardoor een stoornis in de functie van het hart kan ontstaan. Dit is de meest voorkomende oorzaak van overlijden. De gemiddelde levensverwachting is op dit moment boven de 30 jaar. Diagnose
Naast het hebben van bovengenoemde kenmerken, wordt de diagnose bevestigd door neurologisch en genetisch onderzoek. Behandeling
Een aangeboren aandoening is niet te genezen. De behandeling richt zich voor zover mogelijk op vermindering en verlichting van de klachten. Voorkomen
Deze aandoening komt bij 1-2 per 100.000 mensen voor.

83. Health Library: All Topics: F: Friedreich's Ataxia - Healthfinder®
Facts About friedreich's ataxia Basic consumer health information about friedreich'sataxia, an inherited, progressive disorder of the nervous system
http://www.healthfinder.gov/Scripts/SearchContext.asp?topic=332

84. Friedreich's Ataxia | Building Better Health
You are here Home Health A to Z friedreich's ataxiaHealth Topics AZ friedreich's ataxia. Robinson, Richard.
http://www.buildingbetterhealth.com/topic/topic100586846

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Friedreich's Ataxia
Robinson, Richard
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Definition Description Causes and symptoms Diagnosis ... Resources Definition Friedreich's ataxia (FA) is an inherited, progressive nervous system disorder causing loss of balance and coordination. Description Ataxia is a condition marked by impaired coordination. Friedreich's ataxia is the most common inherited ataxia, affecting between 3,000-5,000 people in the United States. FA is an autosomal recessive disease, which means that two defective gene copies must be inherited to develop symptoms, one from each parent. A person with only one defective gene copy will not show signs of FA, but may pass along the gene to offspring. Couples with one child affected by FA have a 25% chance in each pregnancy of conceiving another affected child. Causes and symptoms Causes The gene for FA codes for a protein called frataxin. Normal frataxin is found in the cellular energy structures known as mitochondria, where it is thought to be involved in regulating the transport of iron. In FA, the frataxin gene on chromosome 9 is expanded with nonsense information known as a "triple repeat." This extra DNA interferes with normal production of frataxin, thereby impairing iron transport. Normally, there are 10-21 repeats of the frataxin gene. In FA, this sequence may be repeated between 200-900 times. The types of symptoms and severity of FA seems to be associated with the number of repetitions. Patients with more copies have more severe symptomatology. Researchers are still wrestling with how frataxin and the repeats on chromosome 9 are involved in causing FA. One theory suggests that FA develops in part because defects in iron transport prevent efficient use of cellular energy supplies.

85. Friedreich's Ataxia | Vhihealthe
.......friedreich's ataxia. friedreich's ataxia (FA) is an inherited, progressive nervoussystem disorder causing loss of balance and coordination.
http://www2.vhihealthe.com/topic/topic100586846
You are here: Home Health A to Z
Friedreich's Ataxia
Robinson, Richard Below:
Definition

Description

Causes and symptoms

Diagnosis
...
Resources

Definition
Friedreich's ataxia (FA) is an inherited, progressive nervous system disorder causing loss of balance and coordination. Description
Ataxia is a condition marked by impaired coordination. Friedreich's ataxia is the most common inherited ataxia, affecting between 3,000-5,000 people in the United States. FA is an autosomal recessive disease, which means that two defective gene copies must be inherited to develop symptoms, one from each parent. A person with only one defective gene copy will not show signs of FA, but may pass along the gene to offspring. Couples with one child affected by FA have a 25% chance in each pregnancy of conceiving another affected child. Causes and symptoms Causes The gene for FA codes for a protein called frataxin. Normal frataxin is found in the cellular energy structures known as mitochondria, where it is thought to be involved in regulating the transport of iron. In FA, the frataxin gene on chromosome 9 is expanded with nonsense information known as a "triple repeat." This extra DNA interferes with normal production of frataxin, thereby impairing iron transport. Normally, there are 10-21 repeats of the frataxin gene. In FA, this sequence may be repeated between 200-900 times. The types of symptoms and severity of FA seems to be associated with the number of repetitions. Patients with more copies have more severe symptomatology. Researchers are still wrestling with how frataxin and the repeats on chromosome 9 are involved in causing FA. One theory suggests that FA develops in part because defects in iron transport prevent efficient use of cellular energy supplies.

86. Friedreich's Ataxia
MAIN SEARCH INDEX friedreich's ataxia. friedreich's ataxia (FA) is an inherited,progressive nervous system disorder causing loss of balance and coordination.
http://www.hendrickhealth.org/healthy/000563.htm
MAIN SEARCH INDEX
Friedreich's ataxia
Definition
Friedreich's ataxia (FA) is an inherited, progressive nervous system disorder causing loss of balance and coordination.
Description
Ataxia is a condition marked by impaired coordination. Friedreich's ataxia is the most common inherited ataxia, affecting between 3,000-5,000 people in the United States. FA is an autosomal recessive disease, which means that two defective gene copies must be inherited to develop symptoms, one from each parent. A person with only one defective gene copy will not show signs of FA, but may pass along the gene to offspring. Couples with one child affected by FA have a 25% chance in each pregnancy of conceiving another affected child.
Causes and symptoms
Causes The gene for FA codes for a protein called frataxin. Normal frataxin is found in the cellular energy structures known as mitochondria, where it is thought to be involved in regulating the transport of iron. In FA, the frataxin gene on chromosome 9 is expanded with nonsense information known as a "triple repeat." This extra DNA interferes with normal production of frataxin, thereby impairing iron transport. Normally, there are 10-21 repeats of the frataxin gene. In FA, this sequence may be repeated between 200-900 times. The types of symptoms and severity of FA seems to be associated with the number of repetitions. Patients with more copies have more severe symptomatology. Researchers are still wrestling with how frataxin and the repeats on chromosome 9 are involved in causing FA. One theory suggests that FA develops in part because defects in iron transport prevent efficient use of cellular energy supplies.

87. Friedreich's Ataxia
Fact Sheet 17 friedreich's ataxia. Partial loss of the sense of touch or sensitivityto pain and temperature may also occur in friedreich's ataxia.
http://www.accessarkansas.org/ascc/fact17.html
Fact Sheet 17: Friedreich's Ataxia
Reader: Family
Alternate Names:
Familial Ataxia, Friedreich's Disease, Friedreich's Tabes, Hereditary Ataxia, Spinocerebellar Ataxia and Spinal Ataxia.
Description:
Friedreich's Ataxia is a progressive, hereditary disease that affects the neuromuscular system, usually beginning in children or teenagers. The average age of onset is 13, with a range from 5 to 25 years of age. Symptoms of Friedreich's Ataxia are caused by the gradual deterioration of nerve cells on the back portion of the spinal nerves, spinal cord and brain. This deterioration affects speech and movement (motor coordination) producing numbness or weakness of the arms and legs, curvature of the spine, and lower limb paralysis. The patient gets progressively worse as time passes and many patients are severely disabled by their mid-twenties. However, unexplained sudden remissions of five to ten years in duration have been reported.
Symptoms:
Causes:
Friedreich's Ataxia is caused by an inherited genetic trait. Human traits are the product of the interaction of two genes, one received from the father and one from the mother. The disease does not appear unless a person inherits the same defective gene from each parent. During 1988 scientists located a genetic marker for Friedreich's Ataxia and they hope to identify the defect and understand how it causes this disease. New treatments may then be developed to alter progression of the disease.
Treatment:
There is no specific medical or surgical treatment that is effective in altering the course of Friedreich's Ataxia. Medical problems associated with the symptoms may require appropriate treatment. Continuous medical supervision is recommended to avoid potential complications involving the heart, lungs, spine, bones and muscles. Prevention of pneumonia is a challenge in the care of people in the advanced stages of Friedreich's Ataxia. Patients may be more susceptible to infection and require medication, insulin for controlling diabetes, or corrective devices and drugs for vision and hearing problems.

88. Friedreich's Ataxia And I
friedreich'S ataxia AND I. I friedreich's ataxia doesn't affect the partsof the brain responsible for thinking and feeling. Reasoning
http://ohbother.co.uk/ataxia.htm
FRIEDREICH'S ATAXIA AND I I was diagnosed with Friedreich’s Ataxia (FA) when I was eight years of age.
First are some facts and figures about FA. For more about my own experience with FA scroll down.
How is it caused?
FA is a rare inherited genetic disorder. As it is recessive, which means that two copies of the faulty gene must be inherited from both parents for someone to develop FA, it can lie dormant in many generations before cropping up. For instance, although each and every generation of my mother’s and father’s families must have carried the defective gene, I am the first family member to actually develop FA. This is because a carrier has to meet another carrier (as my own patents did) before their child is a risk of inheriting two defective genes and therefore developing FA. The problem lies within the genetic code on chromosome 9 and the number of GAA repeats present (these letters form part of the genetic code).
These three bits of code tell the cells how to make proteins in the body. The number of GAA repeats normally ranges from 10 to 40, but if the number is exceeds 100 (as it does with those who have FA) it causes the cells to produce a lack of a protein called Frataxin.
How does a lack of Frataxin cause the symptoms of FA?

89. Friedreich's Ataxia | AHealthyAdvantage
You are here Home Health A to Z friedreich'sataxia. friedreich's ataxia. Robinson, Richard.
http://www.ahealthyadvantage.com/topic/topic100586846
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You are here: Home Health A to Z Friedreich's Ataxia
Friedreich's Ataxia
Robinson, Richard
Below:
Definition

Description

Causes and symptoms

Diagnosis
...
Resources

Definition Friedreich's ataxia (FA) is an inherited, progressive nervous system disorder causing loss of balance and coordination. Description Ataxia is a condition marked by impaired coordination. Friedreich's ataxia is the most common inherited ataxia, affecting between 3,000-5,000 people in the United States. FA is an autosomal recessive disease, which means that two defective gene copies must be inherited to develop symptoms, one from each parent. A person with only one defective gene copy will not show signs of FA, but may pass along the gene to offspring. Couples with one child affected by FA have a 25% chance in each pregnancy of conceiving another affected child. Causes and symptoms Causes The gene for FA codes for a protein called frataxin. Normal frataxin is found in the cellular energy structures known as mitochondria, where it is thought to be involved in regulating the transport of iron. In FA, the frataxin gene on chromosome 9 is expanded with nonsense information known as a "triple repeat." This extra DNA interferes with normal production of frataxin, thereby impairing iron transport. Normally, there are 10-21 repeats of the frataxin gene. In FA, this sequence may be repeated between 200-900 times. The types of symptoms and severity of FA seems to be associated with the number of repetitions. Patients with more copies have more severe symptomatology. Researchers are still wrestling with how frataxin and the repeats on chromosome 9 are involved in causing FA. One theory suggests that FA develops in part because defects in iron transport prevent efficient use of cellular energy supplies.

90. Friedreich's Ataxia Society Ireland
friedreich's ataxia Society Ireland, Mr and Mrs T Creedon San Martino, Mart Lane,Dublin 18, Ireland Tel. +353 (0) 1 2894788 http//www.fasi.ie Email fasi
http://www.ataxie.nl/organisaties/naam_organisatie/friedreichs_ataxia_society_ir
Werkgever gezocht voor: kwaliteitsanalist / ICT testspecialist / webmaster / beleidsmedewerker
De informatie op deze pagina's wordt u aangeboden door de patiëntenvereniging ADCA-Vereniging Nederland Home : Cerebellaire atrofie/ataxie ]
Bunnik, 17 mei 2003: Landelijke contactdag ADCA-Vereniging Nederland. Thema: Wetenschappelijk onderzoek.
  • Friedreich's Ataxia Society Ireland,
    Mr and Mrs T Creedon
    San Martino, Mart Lane, Dublin 18, Ireland
    Tel.: +353 (0) 1 2894788
    http://www.fasi.ie

    E-mail: fasi@tinet.ie
    Eire; English; Friedreich.
Home Inhoud Zoeken ADCA-Vereniging Nederland
Adres: ADCA-Vereniging Nederland, Fazantenkamp 839, NL-3607 EC Maarssen.
Tel.: 0346-563913 (+31 346-563913). Fax: 0346-580417 (+31 346 580417). E-mail: info@ataxie.nl Telefonisch spreekuur op dinsdag en donderdag tussen 14:00 en 16:00 uur. Kamer van Koophandel (Chamber of Commerce) ( kvk.nl ) Utrecht, Nederland, nr. 40482798. Postbank (National Girobank), nr. 6932464, AVN - Maarssen - Nederland. Redactie en beheer: Marco Meinders

91. The DRM WebWatcher: Ataxia
by ataxia (incoordination). friedreich's ataxia and Marie's ataxiaare the most common types of hereditary ataxia. There are also
http://www.disabilityresources.org/ATAXIA.html
Home Subjects States Librarians ... Contact Us
The DRM WebWatcher (Subjects) Ataxia Updated 12/2001 A B C D ... About/Hints/Link
Hereditary ataxia is a group of progressive, degenerative neurological disorders characterized by ataxia (incoordination). Friedreich's ataxia and Marie's ataxia are the most common types of hereditary ataxia. There are also sporadic ataxias, which occur spontaneously in individuals with no known family history of ataxia. Here are some useful resources.
The A-T Children's Project
This excellent web site focuses on ataxia telangiectasia, a progressive, degenerative disorder which is characterized by "telangiectases" (tiny red "spider" veins in the corners of the eyes or on the surface of ears and cheeks exposed to sunlight) as well as ataxia. It includes information about the disorder, including general information, diagnosis, photos, research, etc.; information about the organization; and information for researcher scientists and physicians.
Facts About Friedreich's Ataxia
A fact sheet from the Muscular Dystrophy Association.

92. NIH Press Release - Study May Reveal Clues To Friedreich's Ataxia - 06/12/1997
Study May Reveal Clues to friedreich's ataxia. For years friedreich’sataxia strikes about one in every 50,000 persons. Loss of
http://www.nih.gov/news/pr/jun97/ninds-12.htm
NATIONAL INSTITUTES OF HEALTH
National Institute of Neurological

Disorders and Stroke
EMBARGOED FOR RELEASE
Thursday, Jun. 12, 1997
4:00 PM Eastern Time
Marcia Vital
Study May Reveal Clues to Friedreich's Ataxia For years neurologists witnessed the slow decline of their Friedreich’s ataxia patients, helpless to prevent damage to the spinal cord, heart and pancreas. The cause of the damage always eluded researchers until now. A new study in the June 13, 1997, issue of Science may offer an explanation for this neurodegenerative disease and eventually lead to the development of treatments. The study, sponsored by the National Institute of Neurological Disorders and Stroke and by the National Institute of Diabetes and Digestive and Kidney Diseases, examines a yeast protein similar to the human protein coded by the Friedreich’s ataxia gene. The study traces the path of the yeast protein to the mitochondria, the energy-producing power plants of cells, and demonstrates the protein’s role in controlling the levels of iron, an essential element in cell metabolism. The absence of this protein in a cell leads to a toxic buildup of iron in the mitochondria. This "iron overload" reacts with oxygen, producing free radicals, toxic and highly reactive substances that kill the mitochondria and compromise cell metabolism. Eventually, cells shut down and die from oxidative damage to the lipids, proteins and nucleic acids, the essential structures of cells. "I’m cautiously optimistic about the finding," says Massimo Pandolfo, M.D., a co-author of the study. "Further research may give us clues to understanding the pathogenesis of this disease and lead to treatments."

93. Friedreich's Ataxia Group
friedreich's ataxia Group Address Rooms 10 10A, Winchester HouseKennington Park, Cranmer Road London SW9 1HW. Aims Funding of
http://www.charitiesdirect.com/charity6/ch001866.htm
Key Statistics Total Income Admin costs as % of
Total Expenditure Admin costs as % of
Total Income Fundraising costs as
% of Total Exp Fundraising costs as
% of Voluntary Inc Total Funds Total Investments Friedreich's Ataxia Group Address:
Kennington Park, Cranmer Road
London
Aims: Funding of research and providing welfare for all sufferers of Friedreich's and Cerebellar Ataxias Tel: Fax: CC registration: Internet: www.ataxia.org.uk Constitution: Trust. GAYE no:
click on www.charitiesdirect.com for more information

94. Neuropsychological Test Performance Of Patients With Friedreich's Ataxia
Neuropsychological Test Performance of Patients With friedreich's ataxia. ToneWollmann 1 , Jose Barroso 1 , Fernando I. Monton 2 and Antonieta Nieto 1.
http://www.szp.swets.nl/szp/journals/jc245677.htm
Journal of Clinical and Experimental Neuropsychology
2002, Vol.24, No.5, pp. 677-686
Neuropsychological Test Performance of Patients With Friedreich's Ataxia Tone Wollmann , Jose Barroso , Fernando I. Monton and Antonieta Nieto Universidad de La Laguna, Unidad de Neuropsicología, Facultad de Psicología, España Hospital de Nuestra Señora de Candelaria, Sección de Neurología, España Although recognized as one of the most common hereditary diseases of the nervous system, the neuropsychological deficits in Friedreich's ataxia (FA) have rarely been studied. A protocol was constructed to assess the major cognitive areas in patients with FA and pair-matched normal controls. Motor difficulties, dysarthria and fatigability were taken into account. Neuropsychological assessment showed decreased motor and mental reaction times, reduced verbal span, deficits in letter fluency, impaired acquisition and consolidation of verbal information, proactive interference effect, and alterations in complex visuoperceptual and visuoconstructive abilities, in comparison with the control group. Magnetic resonance images showing cerebellar atrophy in the majority of patients suggest that cerebellar degeneration and the interruption of afferent and efferent cerebellar connections could be related to the cognitive deficits shown by our patients.

95. The Changing Nature Of Epilepsy, Part 2:...
Translate this page des sciences neurologiques. Article, Zinc and taurine in friedreich'sAtaxia. Identification, No 4 (Supplement) 11 1984 Pages 623-25.
http://www.cidg.com/~marienf/k/i/n/m015472.htm
# Article : A0026089 Cote/Call Number Auteur/Author
  • Hickey, Melinda Titre/Title Exceptional Parent Article The changing nature of epilepsy, Part 2: Educating the child, family, and community : a never-ending dilemma Identification Aug., no 8 29 1999 Pages: 71-74 Descripteurs/Descriptors
  • Demande par
    courrier
    Client (nom, adresse...):
    Type de demande: PEB Photocp (frais) Commentaires:
  • 96. ETenet - Library
    friedreich's ataxia. Definition. friedreich's ataxia is caused by an abnormalityin one of the genes, called X25, located in the ninth chromosome pair.
    http://www.etenet.com/Apps/Library/Corporate.asp?ID=6

    97. Index

    http://www.ataxia.org.uk/

    98. FRIEDREICHS ATAXIA

    http://www.fasi.ie/

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