http://health.groups.yahoo.com/group/FA_babelFAmily/message/2142 (FRA)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2146 (ITA) 

http://www.revamoto.com/news/news.htm

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2143 (FRA)

Traduzione: Dott.ssa Stefania Grasso

-----Messaggio Originale -----

Da: "Fanegex"

A: <afaf@...>

Inviato: giovedì, 28 agosto 2008 20:28

Oggetto: [afaf] BOL D'OR

Buongiorno,

mi concedo una breve comparsa per darvi qualche informazione sull’associazione REVAMOTO, Ricercare, Sperare e Vincere l’Atassia in motocicletta.

Dopo 6 mesi di attività, e in sinergia con l’incomparabile lavoro svolto dall’AFAF, i motociclisti continuano a mobilitarsi contro l’AF. Tra qualche giorno verseremo un secondo assegno di 5000 euro a Pierre Rustin dell’INSERM.

Per coloro che già conoscono o vorrebbero scoprire questo mondo del motociclismo, ricordo che il prossimo BOL D’OR (13 e 14 settembre 2008) indosserà i colori della lotta contro questa malattia...

Infatti le 2 moto campioni mondiali di resistenza porteranno sulle loro carene, per le 24 ore di durata della corsa, gli adesivi “Ricercare, Sperare e Vincere l’Atassia”.

Prova mitica e sorella gemella della 24 ore di Le Mans, il BOL D’OR si svolge a Magny Cours, vicino a Nevers, e renderà pubblico il suo sostegno a tutti i malati di AF attraverso i colori della SUZUKI, squadra campione del mondo.

La squadra, che si chiama S.E.R.T., è il team più noto e più titolato del campionato mondiale di resistenza. Quindi tutti i malati di AF e coloro che lottano contro l’AF avranno delle buone ragioni di essere fieri…

Sono molto emozionato all’idea altamente simbolica di vedere che la lotta contro l’AF unisce campioni di questo calibro, e vi invito a sostenere la squadra del SERT colmo di speranza per tutti i nostri cari o bambini con AF. Mi auguro che una delle nostre due moto del SERT sia ancora una volta incoronata vincitrice al termine di quest’ultima prova del campionato mondiale 2008 di resistenza.

Sosteniamo le due moto GSXR del SERT, perchè correranno per noi affrontando ogni rischio per arrivare vincitrici ancora una volta quest’anno!!!!

Grazie per la vostra attenzione.

Cordialmente e motociclisticamente vostro,

Stéphane TOTH Revamoto.

http://www.revamoto.com/

P.S. Grazie anche a Sylvie Bonnot, la mamma di Colin e Ninon (entrambi AF), che organizza un weekend motociclistico il 7 settembre in Franche Comté per sostenere la lotta contro l’AF. Non meno di sette side car, una trike, un quad e una ventina di moto verranno ad illuminare questo weekend…

http://www3.interscience.wiley.com/journal/121392032/abstract

^*Correspondence to Sylvia Boesch, Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria

The first two authors contributed equally to this work.

Funded by:
RoFAR-Foundation, Switzerland

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2142 (FRA)

Traduzione: Dott.ssa Stefania Grasso

http://www.revamoto.com/news/news.htm

Lettera del Prof. Pierre Rustin ricercatore presso l’INSERM (03/06/2008)

REVAMOTO: E’ veramente giunta l’ora! In questo inizio secolo stiamo vivendo un momento molto particolare nella lotta contro l’Atassia di Friedreich. In effetti, dopo la scoperta nel 1997 del gene responsabile di questa malattia (gene che contiene l’informazione necessaria alla produzione di un piccolo costituente delle cellule detto fratassina) e, in seguito, delle conseguenze delle anomalie di questo gene (più frequentemente un’espansione anomala che provoca una sorta di avvolgimento del gene disturbandone la lettura), il mondo della ricerca si trova di fronte ad una sfida ancora più grande: trovare una soluzione per lottare contro questa malattia!

In realtà ci sono numerosi gruppi di ricerca che attraverso il mondo focalizzano la loro attività su questo obiettivo. A tutt’oggi sono stati proposti cinque approcci terapeutici che mirano a vari aspetti di ciò che riteniamo di sapere su questa malattia;

-         permettere una migliore lettura del gene tramite molecole in grado di intervenire  sulla sua espressione (negli USA);

-         aumentare la produzione della fratassina utilizzando il gene così com’è (in Austria);

-         catturare il ferro che è probabilmente in eccesso in alcuni compartimenti cellulari - i mitocondri, in cui la tappa finale della combustione degli alimenti produce l’energia per tutta la cellula e per tutto l’organismo (in Francia);

-         catturare mediante un farmaco (l’idebenone o Mnesis) i composti dannosi dell’ossigeno (i famosi radicali liberi) che sono senza dubbio in parte responsabili  della malattia (in Francia);

-         aumentare le difese dell’organismo contro i radicali liberi (sperimentazione col Pioglitazone) (in Francia).

Sì, avete letto bene: tre di questi cinque approcci sono messi a punto in Francia dai nostri gruppi di ricerca! Quanto basta per smentire i discorsi sulla cosiddetta non competitività dei nostri gruppi in Francia. Tuttavia, per la ricerca non è tutto così semplice nel nostro paese, perchè mancano i mezzi; i costi della ricerca aumentano di giorno in giorno, il prezzo dei macchinari spesso ammonta a cifre esorbitanti, gli studenti che vengono formati nei nostri laboratori si rifugiano all’estero per sfuggire al precariato, soprattutto quando si tratta di quelli migliori. Di fronte a ciò soltanto dei discorsi, delle promesse, comitati di esperti, riorganizzazioni a non più finire per non affrontare il problema: il motivo della guerra, il denaro!

E’ in questo contesto che l’idea di REVAMOTO assume significato: un segnale forte per dare sviluppo alla ricerca. Per i nostri ricercatori un segnale per perseverare e amplificare ancora i nostri sforzi. Per coloro che prendono decisioni in alto loco, un segnale affinché finalmente capiscano il semplice messaggio dei malati, dei loro famigliari e di tutti coloro che sono solidali coi ricercatori: il futuro del paese, la lotta contro i flagelli e le malattie, passano attraverso lo sviluppo della ricerca, da quella più basica a quella più applicata.

In questa lotta contro la malattia è utile ogni centesimo, ogni euro raccolto, per ciò che rappresenta. Questo denaro sarà devoluto interamente alla ricerca scientifica condotta dall’Ospedale Robert Debré per la lotta contro l’Atassia di Friedreich.

Come non ringraziarvi!

Il gruppo di ricerca dell’Ospedale Robert Debrè che si occupa di Atassia di Friedreich.

Paul Benit, Emmanuel Dassa, Sergio Goncalves, Isabelle Husson, Sandrine Loublier, Vincent Paupe e Pierre Rustin

http://www3.interscience.wiley.com/journal/121392069/abstract

^*Correspondence to Alison La Pean, Neurogenetics Branch, NINDS, 35 Convent Drive, Building 35, Room 2A-114, Bethesda, MD 20892-3705

Funded by:
National Institute of Neurological Disorders and Stroke

http://www.revamoto.com/news/news.htm

Lettre du Professeur Pierre RUSTIN, chercheur à l'INSERM    (03/06/2008)

REVAMOTO: C’est vraiment l’heure! En ce début de siècle, nous vivons un moment très particulier dans la lutte contre l’Ataxie de Friedreich. En effet, après la découverte du gène responsable de cette maladie en 1997 (gène qui contient l’information nécessaire à la production d’un petit constituant des cellules, appelé la frataxine), puis celle des conséquences des anomalies dans ce gène (le plus souvent une expansion anormale qui provoque une sorte d’enroulement du gène et en perturbe la lecture), le monde de la recherche est en face d’un défi encore plus grand: trouver une solution pour lutter contre la maladie !
 
De fait, ce sont de nombreuses équipes de recherches qui à travers le monde focalisent leurs activités sur cet objectif. A ce jour, cinq approches ont été proposées qui visent des étapes différentes dans ce que nous pensons savoir de la maladie: permettre une meilleure lecture du gène par des molécules susceptibles de dérouler le gène (aux USA); augmenter la fabrication de la frataxine en utilisant le gène tel qu’il est (en Autriche); piéger le fer qui est peut être en excès dans certains compartiments des cellules (les mitochondries, compartiments où l’étape finale de la combustion des aliments produit l’énergie pour toute la cellule et tout l’organisme) (en France) ; piéger avec un médicament (l’idébénone ou Mnesis) les composés dangereux de l’oxygène (les fameux radicaux libres) qui sont sans doute responsables d’une partie de la maladie (en France); augmenter les défenses de l’organisme contre les radicaux libres (essai de la Pioglitazone) (en France). Oui vous avez bien lu: trois des cinq approches sont développées en France par nos équipes de recherche! De quoi démentir les discours sur la prétendue non compétitivité de nos équipes en France. Et pourtant tout n’est pas simple pour la recherche dans notre pays car les moyens manquent: la recherche coûte cher au jour le jour, les machines coûtent souvent des prix  exorbitants, les étudiants formés dans nos laboratoires se réfugient à l’étranger pour fuir la précarité et ce d’autant plus facilement qu’ils sont excellents…
Face à cela, seulement des discours, des promesses, des comités d’expertise, des réorganisations à n’en plus finir pour ne pas traiter le problème: le nerf de la guerre, l’argent !
 
C’est dans ce contexte que l’idée de REVAMOTO prend tout son sens : un signal fort pour développer la recherche. Pour nous chercheurs, un signal pour persévérer et amplifier encore nos efforts; Pour ceux qui décident en haut lieu, un signal pour qu’ils entendent enfin le message simple des malades, de leur familles et de tous ceux qui sont solidaires des chercheurs: L’avenir du pays, la lutte contre les fléaux et les maladies, passent par le développement de la recherche, de la plus fondamentale à la plus appliquée.
 
Dans ce combat contre la maladie, tout centime, tout euro collecté, de par ce qu’il représente est utile. Il va intégralement à la recherche scientifique menée à l’Hôpital Robert Debré pour lutter contre l’ataxie de Friedreich.
 
Comment ne pas vous remercier !
 
L’équipe de Recherche de l’Hôpital Robert Debré travaillant sur l’Ataxie de Friedreich.
 
Paule Bénit, Emmanuel Dassa, Sergio Goncalves, Isabelle Husson, Sandrine Loublier, Vincent Paupe et Pierre Rustin
 

http://www.the-signal.com/news/article/3657/

Helping the less fortunate

Full Speed to Port!

Gary Horton
Posted: Aug. 26, 2008  3:33 p.m.
Updated: Aug. 27, 2008 4:30 a.m.

My sister, Cathy Horton Bagnall, recently passed away after a long, stoic battle with Machado-Joseph Disease. Cathy, once active and vibrant, had been reduced by this inherited illness to a life defined by paralysis, wheelchairs and hospital beds.

The weeks before and after her passing have been deeply reflective for us. One night at dinner with Carrie before Cathy died, the thought crossed my mind, "The things present on our respective tables express the disparity our contrasting genetic fortunes have wrought." At our home, our table was graced with the good things of life. Green salads with bright tasty vegetables. Grilled savory chicken. Two pleasant glasses of wine. Hard work and good health have brought us - fortunate lives.

At sister Cathy's home, her scene, while once like ours years ago, had decayed to something starkly different. Her table had become a bed stand, and her life's fortune reduced to a hospital bed. The things on her table were Morphine drops, Adavan, Pedialyte and small cups with straws and spoons. Cathy couldn't eat solids anymore. Fluids were fed to her with a thickening agent so she could take them without choking. Hers was a life where hard work had built a once rewarding life, but an illness completely outside her control had stripped it all away.

Cathy was in the final stages of Joseph's Disease. It's a progressive genetic neurological ataxia, passed from parent to child. Each offspring faces a 50-50 chance of inheriting the mutant gene and disease. Symptoms appear in the late 20s, leading to profound disability, and then to death by mid-life. Cathy lost on the spin of this awful genetic lottery through no fault of her own. Sister Adria and I both got a lucky pass. We don't have it, and we can't pass it on.

Cathy had lived productively and vibrantly - all the way until about 10 years ago. After high school she took up a job at the LAPD Department of Records. She'd do records research for police officers who called in, giving them the facts they needed on duty in the field. She dated, married a policeman for a brief time, and enjoyed her career at work and her family and friends at home. She had constructed what was, in fact, a fortunate and well-earned life.

But despite hard work and healthy living, by her late 30s, the ataxia caught up with her and began its relentless assault. Cathy developed an awkward gait. Jagged hand motions. Slurred speech. First came a cane, and then came the walker. By 51, Cathy's motor functions had deteriorated such that she suffered two auto accidents and the DMV revoked her license. Determined to be self-sufficient, she worked for another year at the LAPD, with coworkers driving her to the office. But soon her speech became so compromised she could no longer fulfill her duties. She was dismissed with reduced retirement benefits and left to face a terminal disease, medical bills, and a $2,800 a month home mortgage payment.

We bought her an electric cart and refitted her home, and for a couple of years, independent-minded Cathy cared for herself, riding around Valencia's convenient paseos - shopping, visiting, and carving out a newly motorized life. But as the disease progressed, Cathy lost her ability to walk or stand at all.

Determined not to burden others, Cathy kept secret that at home she crawled from room to room to get around. After a dangerous fall, Cathy tearfully confided with Carrie she could no longer get by alone. By God's grace and good fortune, we found "Pinkie" - a wonderful caregiver who moved in with Cathy at her home, providing 24-hour care.

Few sufferers of disabling disease have the otherwise good fortune of living in their own homes with constant care, and surrounded with loving family members. In this much, Cathy was indeed fortunate, as her family supported her completely.

Cathy's decline accelerated quickly over the past month. Last week she became fully paralyzed, unable to even swallow. Cathy passed away in her sleep on Aug. 15 at 1:50 a.m. Our family got the call from Pinkie at 2 a.m., and we met and huddled at Cathy's home. The hospice nurse arrived at 3:30 a.m. to declare her passing. The morticians followed at 6:00 a.m. Two dark-suited men respectfully carried Cathy's withered body from her bed to a gurney, and from the gurney to a white van. And then they drove Cathy away and we were left alone in Cathy's empty house. Ataxia claimed another body, but it never claimed Cathy's spirit. Just four short weeks prior, Cathy, by then mostly paralyzed, went with Pinkie by wheelchair to the Town Center Mall to see "Sex and the City." She couldn't move, but she could still see, hear - and moan out a laugh.

Our hearts are forever changed, having traveled that hard road with Cathy. We feel such empathy for the hundreds of thousands of Americans stricken by profound disease and disability - through no fault of their own. Cathy kept her dignity and meaning with the help of a loving family that had sufficient resources. But many either don't have the family or don't have the money. What becomes of these, when their bodies give out - and finances can't keep up? In my younger years, when my father suffered and died of the same disease, I saw first-hand how these people can be warehoused for death, isolated from any meaningful sense of life.

And I wonder, as our national health care debate draws front and center in the coming years, if America, for all her greatness, can't find a way to care less for war and more for its ailing citizens. Cathy served the citizens of Los Angeles for nearly 30 years and was left to fend for herself with a reduced pension.

What about all the others? Can fortunate American share maybe just a little more with our less fortunate? Isn't proper care for our sick and suffering at least as patriotic as this or that foreign adventure? Those suffering fates like Cathy give testimony to our need to rethink national priorities and sensibilities.

Gary Horton lives in Valencia. His column reflects his own views, not necessarily those of The Signal.

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2128 (ITA)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2134 (FRA)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2135 (ESP)

Translation:  Marion Clark

From:  Maria Litani

To:  babelFAmily Italia; FA_babelFAmily

Sent:  Monday, August 25, 2008, 2:48 a.m.

Subject:  [FA_babelFAmily] ITA:  Therapy with pulsed magnetic fields

Therapy with pulsed magnetic fields.

For about a month, I have had a device in my home called the Medithera Home to provide therapy with pulsed magnetic fields—I’m satisfied with it and wanted to let you all know what I’ve been able to experience personally.

I became aware of this type of therapy thanks to the information shared through BabelFAmily about the Viofor, a product distributed in France, which had been discussed on the French mailing list of AFAF [French Association for Friedreich’s Ataxia].

Sandrine, a patient with FA, informed us of the progress she had made thanks to using that device.

So I invited Daniel Cau, a French distributor, to do a presentation on this product during a meeting organized in Genoa, Italy, on May 10, 2008, by AISA-Liguria [a regional chapter of the Italian Association for Ataxic Syndromes].

The Viofor was the object of a great deal of interest, and I was planning on getting one.

In the meanwhile, I discovered that there was a product similar to the Viofor, the Medithera Home, which has a sales representative in Italy.  At that time, Medithera Home was being tested at the AISM center in Genoa [one of the Italian Multiple Sclerosis Society’s rehabilitation centers] with a double-blinded study on fatigue in patients with multiple sclerosis.

The Medithera Home consists of a control console that produces a pulsed magnetic field in the applicator, which is a mat to lie down on with a small cushion to position on the part of the body to be treated.  The treatment can be carried out in various modalities, based on the needs.

My son Stefano (FA, age 30) is using this therapy in the morning and in the evening.

Right away he noticed an improvement in the quality of his sleep.  Now he sleeps calmly, and the contractions he had in his legs, as well as the cramps, have diminished significantly.  Before, I had often needed to stretch his legs during the night.  Sometimes the contractions affected his entire body, including his hands and chest, and they could even block his diaphragm and obstruct his breathing.  Every night he took one and a half 0.25-mg tablets of Lioresal (Baclofen) along with Valium in order to sleep and to relax.

But since a month ago, he no longer takes Valium, and he even sleeps 7-8 hours in a row.  This is just the first benefit, clear and measurable.

There are other positive effects, such as the fluidity of the blood and visual flashes--Stefano no longer sees much at all—however, I still need to verify this effect in order to know if the flashes persist and if they are really a result of the pulsed magnetic fields.

I’m also using the Medithera Home myself, and starting with my first session, the headache I’d had for a full week disappeared.

Periodically I suffer with migraines and vasomotor headaches, but with this treatment, my episodes are less frequent.

In addition, I have dislocated wrists, and I have tendonitis in the left wrist.  Now the tendonitis is gone and I can use my hands to bear weight and to help my son and daughter [who also has FA] to transfer without any problems.

We also have a friend with FA, Eva Aronelius, who suffers from diabetes.  She has used the Medithera Home for over a month.  She too is now able to sleep deeply and without contractions.  In addition, she has noticed a reduction in her glycemic peaks, and she is using less insulin.

Magnetotherapy will not cure ataxia, but I have reason to believe that it contributes to a much better quality of life for ataxic persons.

Maria Litani, Italy

Biorm e pazienti con Sclerosi Multipla e fatica primaria

Associazione Italiana Sclerosi Multipla-Servizio di Riabilitazione

Consform

La fatica primaria è un sintomo frequente nella SM che colpisce il 75-95 % dei pazienti con SM.

La fisiopatologia della fatica primaria nella SM è sconosciuta. Alcuni studi affermano che il meccanismo della fatica primaria può essere in relazione con livelli multipli nell’organizzazione neuronale, essendo in connessione, allo stadio iniziale, con il funzionamento dell’attività della corteccia cerebrale e, quindi, con la contrazione muscolare. (Enoka and Stewart 1992.; Kent-Brown at al 1994.; Sandroni et al 1992.; Roelcke et al 1997).

L’obiettivo dello studio è quello di verificare l’efficacia clinica dei campi elettromagnetici pulsanti a bassa intensità nella fatica primaria nei pazienti SM.

Verranno selezionati 50 pazienti che progressivamente accedono al servizio di Riabilitazione AISM di Genova affetti da SM che lamentano il sintomo fatica, deambulanti con EDSS < 7, in fase stabile  (non ricadute da almeno 6 mesi ) di cui vengano escluse cause secondarie di fatica attraverso una valutazione anamnestica e clinica.

Verranno esclusi pazienti con patologie concomitanti che possono interferire con la partecipazione o con la sintomatologia stessa (gravi disturbi cognitivi, disturbi psichiatrici, patologie cardiovascolari, patologie respiratorie, ecc).

Lo studio è in doppio cieco e prevede che un gruppo venga trattato con BIORM (25 pazienti) e un gruppo con placebo (25 pazienti) tramite assegnazione randomizzata. Segue un periodo di wash out di 4 mesi e successivamente i pazienti che erano stati sottoposti a trattamento attivo saranno sottoposti al placebo e viceversa.

Entrambi i gruppi saranno trattati per 24 minuti per sessione, per 24 sessioni, almeno tre volte alla settimana.

I pazienti sono sottoposti prima e dopo il ciclo a: Time Walking Test, Visual Analogue Test (VAS), Modified Fatigue Impact Scale (MFIS) e Fatigue Severity Scale (FSS).

Attualmente sono stati reclutati 39 pazienti che sono in trattamento, 15 hanno terminato le sessioni e 4 sono stati i drop out.

14 pazienti riferiscono un beneficio dopo il trattamento, solo un paziente dichiara nessun effetto. I dati statistici verranno analizzati alla fine dello studio. Le motivazioni del drop out sono state: in un paziente si è evidenziato un incrementato della spasticità degli arti inferiori (Ashworth da 2 a 3); un paziente ha interrotto le sedute per motivi personali; un paziente ha interrotto per una ricaduta clinica di malattia; il quarto paziente ha riferito il manifestarsi di dolori agli arti immediatamente dopo le sedute che perduravano il giorno seguente il trattamento, inoltre, descriveva un peggioramento della ritenzione urinaria con relativa necessità di eseguire autocateterismo intermittente immediatamente dopo la seduta.

Genova, 07/08/2008

                                                                                              Il Direttore Tecnico

                                                                                              Dott.ssa M.L.Lopes de Carvalho

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2132 (ENG)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2133 (ITA)

Traducción: MariLuz González Casas

http://www.news.com.au/heraldsun/story/0,21985,24244110-662,00.html

Desarrollan una  píldora minúscula  capaz de liberar antioxidantes dentro del organismo.

Tamara McLean

26 agosto 2008

Investigadores australianos desarrollan una píldora de nanodimensiones, capaz de liberar, como un caballo de Troya, potentes antioxidantes dentro del organismo.

Esta partícula en miniatura, del grosor de una milésima de un cabello humano, ofrece nuevas esperanzas para que el organismo pueda  asimilar de forma más eficaz algunas sustancias terapéuticas presentes en alimentos como el té verde o el chocolate.

Los científicos esperan que esta píldora llegue a ser un instrumento eficaz para combatir  patologías degenerativas.

Se ha demostrado en reiteradas ocasiones que los antioxidantes , además de las vitaminas, carotenoides y flavonoides, mejoran el estado de salud, al neutralizar los efectos nocivos provocados por los radicales libres.

Pero los antioxidantes se destruyen fácilmente por los ácidos y enzimas presentes en el intestino, que  absorbe sólo un pequeño porcentaje de lo que consume.

Mientras esto es suficiente en individuos sanos, para las personas con un alto riesgo de padecer diabetes, patologías cardíacas o Alzheimer, es necesario poder acceder a una reserva continua de antioxidantes que el organismo no puede proporcionar.

El Dr. Ken Ng y  el Dr. Ian Larson,  de la Facultad de Farmacia de la Universidad  Monash de Melbourne, creen haber encontrado la solución a este problema gracias a una minúscula partícula de aspecto esponjoso, capaz de fijarse por completo al antioxidante, y que está compuesta por una sustancia extraída del caparazón del cangrejo.

 “Los antioxidantes se colocan en el interior de este minúsculo caballo de Troya, donde permanecen protegidos de los ataques de los jugos gástricos” afirma el Dr. Larson.

“Estas partículas en miniatura, una vez que llegan al intestino delgado, se vuelven viscosas y se adhieren a la pared intestinal. Liberan su contenido directamente a las células del intestino para ser absorbido inmediatamente por el flujo sanguíneo.” 

Perfeccionando esta técnica, los científicos esperan aumentar la eficacia de  los fármacos y suplementos vulnerables durante el  proceso digestivo.

Esta técnica se experimentará en ratas, con la esperanza de que en el futuro estas partículas se puedan cargar de  antioxidantes  y añadirlas a los  productos alimentarios.

 “Las personas con alto riesgo de patologías degenerativas, tales como la enfermedad de Alzheimer  y  Parkinson, o que hayan sufrido un ictus con riesgo de recaída, necesitan proteger los tejidos con antioxidantes para ralentizar el curso de la enfermedad” afirmó el Dr. Ng.

“Estamos sólo al principio, pero creemos haber descubierto un sistema nuevo para reforzar nuestro  organismo.”

http://www.ahora.cu:80/english/index.php?option=com_content&task=view&id=445&Itemid=57

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2128   (ITA)

Traduction: Henriette Champsaur

Thérapie avec champs magnétiques pulsés

Depuis environ 1 mois, j’ai à la maison un appareil pour la thérapie avec champs magnétiques pulsés, le «Medithera Home», j’en suis satisfaite et j’ai souhaité vous informer tous de ce que j’ai pu expérimenter personnellement.

J’ai eu connaissance de ce type de thérapie grâce aux informations diffusées à travers BabelFAmily sur le Viofor, un produit distribué en France et dont on parlait sur la liste de diffusion Française de l’AFAF.

Sandrine, une patiente atteinte de l’AF, nous informait des progrès obtenus grâce à l’utilisation de cet appareil.

J’ai alors invité Daniel Cau, distributeur français, à présenter ce produit à Gênes à l’occasion d’une réunion organisée par l’AISA Ligurie, le 10 Mai dernier.

Le VIOFOR a suscité beaucoup d’intérêt et j’avais l’intention de l’acquérir.

Entre temps, j’ai découvert qu’il y  avait un produit similaire au VIOFOR, qui avait un représentant en Italie, le «MEDITHERA HOME» et qu’il était expérimenté en ce moment  à Gênes (Italie) au centre AISM  avec une étude en double aveugle sur la fatigue chez les patients atteints de scléroses multiples.

Le MEDITHERA  HOME est constitué d’un instrument de contrôle qui produit un champ magnétique pulsé, d’un matelas pour s’allonger et d’ un petit coussin à positionner sur les parties à traiter.

Le traitement peut être réalisé de diverses manières, en fonction des besoins.

Matins et soirs mon fils Stefano (AF, 30 ans) utilise cette thérapie.

Il a tout de suite remarqué une amélioration de la qualité de son sommeil. Maintenant, il dort calmement et les contractions qu’il avait dans les jambes ainsi que les crampes ont diminué de manière importante. Souvent, la nuit il fallait lui  étirer les jambes. Parfois, les contractions se transmettaient à tout le corps, y compris aux mains et au thorax, et arrivaient même à bloquer le diaphragme et à gêner sa respiration. Chaque soir il prenait un cachet et demi de Lioresal (0.250mg de Baclofen) et du Valium pour dormir et se détendre.

Depuis un mois, il ne prend plus de valium et dort même 7 à 8 heures de suite. Ceci est le premier bénéfice mesurable et évident.

Il y a d’autres effets positifs comme la fluidité du sang et des flashes visuels (Stefano ne voit presque plus) que cependant je dois encore vérifier pour savoir s’ils persistent et sont vraiment produits par la thérapie magnétique.

Moi aussi j’utilise le Medithera Home et dès la première séance le mal de tête dont je souffrais en permanence depuis une semaine a disparu.

Par périodes je souffre de migraines, de céphalées vasomotrices, mais avec ce traitement les épisodes ont diminué.

De plus, j’ai les pouces luxés et j’ai une tendinite au poignet gauche. Maintenant la tendinite est passée et j’arrive à soulever du poids et à aider mon fils et ma fille à faire leurs transferts sans problème.

Nous avons aussi une amie, Eva Aronellus, AF, qui souffre de diabète. Elle utilise le Medithera Home depuis plus d’un mois. Elle aussi maintenant arrive à dormir profondément et sans contractions. De plus, elle a remarqué une réduction des pics glycémiques et elle utilise moins d’insuline.

La thérapie par  champs magnétiques ne guérit pas l’Ataxie, mais j’ai beaucoup de raisons de croire qu’elle contribue à une qualité de vie nettement meilleure pour les malades ataxiques.

Maria Litani, Italie.

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2132 (ENG)

Traduzione: Dott.ssa Stefania Grasso

http://www.news.com.au/heraldsun/story/0,21985,24244110-662,00.html

Messa a punto una minuscola pillola  in grado di liberare antiossidanti nell’organismo

Tamara McLean

26 agosto 2008

Ricercatori australiani hanno messo a punto una pillola di nanodimensioni che, come un cavallo di Troia, libera potenti antiossidanti.

Questa particella miniaturizzata, spessa un millesimo di un capello umano, offre nuove speranze per rendere più efficacemente assimilabili alcune sostanze terapeutiche presenti in alimenti quali il thé verde o il cioccolato.

Gli scienziati sperano che questa  pillola si riveli un importante strumento per combattere le patologie degenerative.

E’ stato più volte dimostrato che gli antiossidanti, inclusi vitamine, carotenoidi e flavonoidi, favoriscono una migliore salute in quanto neutralizzano gli effetti nocivi dei radicali liberi.

Gli antiossidandi vengono però distrutti facilmente da acidi ed enzimi presenti nell’intestino,  in cui viene assorbita solamente una piccola percentuale di ciò che si è consumato.

Mentre ciò è normale per gli individui sani, per le persone  ad alto rischio di sviluppare il diabete, patologie cardiache o morbo di Alzheimer è necessario poter accedere a una riserva continua di antiossidanti che l’organismo non è in grado di offire.

Il Dr Ken Ng e il Dr Ian Larson, della facoltà di farmacia dell’Università Monash di Melbourne, pensano di aver trovato la soluzione a questo problema grazie a una particella miniaturizzata di tipo spugnoso che avvolge interamente l’antiossidante, composta da una sostanza ricavata dall’esoscheletro del granchio.

Gli antiossidanti vengono collocati all’interno di questo minuscolo cavallo di Troia, dove rimangono protetti dagli attacchi dei succhi gastrici” ha affermato il Dr Larson.

“Queste particelle miniaturizzate, una volta giunte nel piccolo intestino, diventano viscose e si attaccano alla parete intestinale. Qui il loro contenuto viene versato direttamente  nelle cellule dell’intestino per poi essere assorbito interamente dal flusso sanguigno”.

Attraverso il perfezionamento di questa tecnica, gli scienziati sperano di rendere maggiormente assimilabili dall’organismo i farmaci e i complementi alimentari normalmente attaccati durante la digestione.

Questa tecnica verrà sperimentata sui topi, con la speranza che un giorno queste particelle possano essere colmate di antiossidanti e aggiunte ai prodotti alimentari.

“I soggetti ad alto rischio di patologie neurodegenerative, quali il morbo di Alzheimer o il morbo di Parkinson, o che hanno avuto un ictus e ne rischiano un altro, necessitano di proteggere i propri tessuti con gli antiossidanti per rallentare il decorso della malattia” ha affermato il Dr Ng.

“Siamo solo all’inizio ma crediamo di aver trovato un nuovo sistema per rafforzare l’organismo”.

http://www.news.com.au/heraldsun/story/0,21985,24244110-662,00.html

Scientists develop tiny pill to deliver antioxidants to the body

Tamara McLean

August 26, 2008 02:20pm

A NANO-sized pill that delivers enriching antioxidants into the body like a Trojan Horse has been developed by Australian scientists.

The miniature particle, one thousandth the thickness of a human hair, holds new hope as a vehicle to get healing substances found in foods like green tea and chocolate absorbed into the system more effectively.

Scientists hope the pill will help fortify the body against degenerative disease.

Studies have repeatedly shown that antioxidants, including vitamins, carotenoids and flavonoids, promote better health by neutralising the harmful effects of free radicals in the body.

But they are easily destroyed by acids and enzymes in the gut, leaving only a small percentage of what is consumed to be absorbed.

While this is sufficient for healthy people, those at high risk of developing diabetes, heart disease and Alzheimer's disease need a regular surge of protective antioxidants the body cannot currently get.

Dr Ken Ng and Dr Ian Larson, from the faculty of pharmacy at the Monash University in Melbourne, think they may have developed the answer with a tiny sponge-like nanoparticle made from a substance found in crab shells, that it wraps around the antioxidant.

"Antioxidants sit within this tiny Trojan Horse, protecting it from attack from digestive juices in the stomach,'' Dr Larson said.

"Once in the small intestine the nanoparticle gets sticky and bonds to the intestinal wall, and it then leaks its contents directly into the intestinal cells, which allows them to be absorbed directly into the blood stream.''

By mastering this technique, the scientists hope drugs and supplements also vulnerable to the digestive process can be better absorbed by the human body.

The technology will be tested on rats, with the hope that one day the particles could be loaded with antioxidants and added to food items.

"People who are at high risk of degenerative diseases like Alzheimer's and Parkinson's, or who have had a stroke and are at risk of another, need antioxidants in their tissues to protect them and slow the process,'' Dr Ng said.

"It's early days but we think we've got a new way to fortify the body in this way.''

http://www.therapeuticsdaily.com/news/article.cfm?contentvalue=564818&contenttype=newsarchive&channelID=30

Neurologix Initiates Recruitment for Phase 2 Parkinson's Disease Trial

From the PharmaLive.com News Archive - Aug. 19, 2008

FORT LEE, N.J.--(BUSINESS WIRE)--Aug. 19, 2008 - Neurologix, Inc. (OTCBB:NRGX), a biotechnology company engaged in the development of innovative gene therapies for the brain and central nervous system, announced today that it has received Institutional Review Board approvals to begin recruiting and enrolling participants for its Phase 2 clinical trial of the company's gene transfer approach to the treatment of advanced Parkinson's disease. The study is designed to evaluate the safety and efficacy of a novel non-dopaminergic approach for reestablishing motor function in Parkinson's patients who are sub-optimally responsive to drug therapies.

The randomized, double-blind, sham-procedure controlled trial will involve up to 10 leading academic research centers across the United States, with the first sites being Massachusetts General Hospital and Wake Forest University Health Sciences. Neurologix expects to enroll a total of 40 study participants in the trial. Twenty participants will receive an infusion of the gene-based treatment bilaterally via a catheter temporarily placed in each subthalamic nucleus (STN) (a deep brain structure that is the main target of surgery to treat Parkinson's disease) by stereotactic surgery. The other 20 participants will receive sterile saline solution into a partial thickness burr hole made into the skull, with no brain infusion.

Study participants will be assessed for treatment effects by standardized Parkinson's disease ratings at multiple time points post-procedure. The primary endpoint for the study will be a clinical assessment of motor function at 6 months using the Unified Parkinson's Disease Rating Scale (UPDRS). All participants in the study will also be monitored for safety for 12 months following the gene transfer procedure. If the primary endpoint is met following the analysis of 6 month data, then the sham-control participants will be offered the opportunity to crossover into an open label study of the Neurologix gene transfer therapy if they continue to meet all entry, medical and surgical criteria.

"Parkinson's disease is a devastating illness for those patients whose symptoms are no longer well controlled by medication alone," said John Mordock, President and Chief Executive Officer of Neurologix. "We are very pleased to initiate this study, which may offer a new therapeutic option that is potentially disease modifying and more consistent with the brain's normal metabolic activity."

For details about participating in the clinical trial, please visit http://clinicaltrials.gov/ct2/show/NCT00643890?term=neurologix&rank=1.

About the Neurologix Gene Transfer Approach to Parkinson's Disease

In Parkinson's disease, patients lose dopamine-producing brain cells, which results in substantial reductions in the activity and amount of GABA (gamma-aminobutyric acid), a major inhibitory neurotransmitter in the brain that helps 'quiet' excessive neuronal firing. This reduction in GABA causes a dysfunction in brain circuitry responsible for coordinating movement. GABA is made by a gene called glutamic acid decarboxylase, or GAD.

Neurologix's gene transfer approach to Parkinson's disease seeks to restore GABA -- and thus improve the patient's motor control -- by inserting the GAD gene back into an area of the brain called the subthalamic nucleus, a key regulatory center for movement.

About Neurologix

Neurologix, Inc. (NRGX.OB) is a clinical-stage biotechnology company dedicated to the discovery, development, and commercialization of life-altering gene transfer therapies for serious disorders of the brain and central nervous system (CNS). Neurologix's therapeutic approach is built upon the groundbreaking research of its scientific founders and advisors, whose accomplishments have formed the foundation of gene therapy for neurological illnesses. Current company programs address such conditions as Parkinson's disease, epilepsy and Huntington's chorea, all of which are large markets not adequately served by current therapeutic options. For more information, please visit the Neurologix website at http://www.neurologix.net.

Cautionary Statement Regarding Forward-looking Statements

This news release includes certain statements of the Company that may constitute "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, and which are made pursuant to the Private Securities Litigation Reform Act of 1995. These forward-looking statements and other information relating to the Company are based upon the beliefs of management and assumptions made by and information currently available to the Company. Forward-looking statements include statements concerning plans, objectives, goals, strategies, future events, or performance, as well as underlying assumptions and statements that are other than statements of historical fact. When used in this document, the words "expects," "promises," "anticipates," "estimates," "plans," "intends," "projects," "predicts," "believes," "may" or "should," and similar expressions, are intended to identify forward-looking statements. These statements reflect the current view of the Company's management with respect to future events. Many factors could cause the actual results, performance or achievements of the Company to be materially different from any future results, performance or achievements that may be expressed or implied by such forward-looking statements, including, but not limited to, the following:

-- The Company is still in the development stage and has not generated any revenues. From inception through June 30, 2008, it incurred net losses and negative cash flows from operating activities of approximately $31.3 million and $25.0 million, respectively. Management believes that the Company will continue to incur net losses and cash flow deficiencies from operating activities for the foreseeable future. Because it may take years to develop, test and obtain regulatory approval for a gene-based therapy product before it can be sold, the Company likely will continue to incur significant losses for the foreseeable future. Accordingly, it may never be profitable and, if it does become profitable, it may be unable to sustain profitability.

-- At June 30, 2008, the Company had cash and cash equivalents of approximately $21.6 million, which management believes will be sufficient to fund the Company's operations through at least December 31, 2009. The Company does not know whether additional financing will be available when needed, or if available, will be on acceptable or favorable terms to it or its stockholders.

-- The Company will need to conduct future clinical trials for treatment of Parkinson's disease using the Company's NLX technology. If the trials prove unsuccessful, future operations and the potential for profitability will be materially adversely affected and the business may not succeed.

-- There is no assurance as to when, or if, the Company will be able to successfully receive approval from the FDA on its Investigational New Drug Application to commence a Phase 1 clinical trial for the treatment of epilepsy.

Other factors and assumptions not identified above could also cause the actual results to differ materially from those set forth in the forward-looking statements. Additional information regarding factors that could cause results to differ materially from management's expectations is found in the section entitled "Risk Factors" in the Company's 2007 Annual Report on Form 10-KSB. Although the Company believes these assumptions are reasonable, no assurance can be given that they will prove correct. Accordingly, you should not rely upon forward-looking statements as a prediction of actual results. Further, the Company undertakes no obligation to update forward-looking statements after the date they are made or to conform the statements to actual results or changes in the Company's expectations.

Contact

Neurologix, Inc.
Marc Panoff, 201-592-6451
Chief Financial Officer, Treasurer and Secretary
marcpanoff@...
or
Kureczka/Martin Associates
Joan Kureczka, 415-821-2413 (Media)
Jkureczka@...

See also: http://health.groups.yahoo.com/group/FA_babelFAmily/message/1777 (ENG)

°°°°°°

  http://www.nature.com/gt/journal/v15/n17/full/gt2008117a.html

J W Bainbridge¹ and R R Ali¹

¹Department of Molecular Therapy, Institute of Ophthalmology, University College London, Bath Street, London EC1V 9EL, UK

Terapia con campi magnetici pulsanti

Da circa un mese ho in casa un apparecchio per la terapia con campi magnetici pulsanti, il Medithera Home,  ne sono soddisfatta ed è mio desiderio informare tutti voi di quanto ho potuto personalmente sperimentare.

Ero venuta a conoscenza di questo tipo di terapia dalle informazioni diffuse attraverso babelFAmily sul Viofor, un prodotto distribuito in Francia e del quale si parlava nella mailing-list francese dell’AFAF.

Sandrine, una paziente affetta da Atassia di Friedreich, informava dei progressi ottenuti grazie all’utilizzo di questo apparecchio.

Ho invitato allora Daniel Cau, distributore francese, a presentare il prodotto a Genova durante un meeting organizzato da AISA Liguria, il 10 Maggio scorso.

Il Viofor ha suscitato notevole interesse ed ero intenzionata ad acquistarlo.

Ho scoperto nel frattempo che c’era un prodotto simile al Viofor, che aveva un referente in Italia, il Medithera Home e che veniva sperimentato a Genova al Centro AISM con uno studio in doppio cieco sulla fatica per pazienti affetti da Sclerosi multipla. 

Il Medithera Home è costituito da uno strumento di controllo che produce un campo magnetico pulsante nell’applicatore, che è una stuoia su cui coricarsi e un cuscinetto da posizionare sulle parti da trattare.

Il trattamento può essere azionato con modalità diverse, a seconda delle necessità.

Mattina e sera mio figlio Stefano (di 30 anni, con AF) fa questa terapia.

Si è evidenziato subito un miglioramento nella qualità del sonno. Ora dorme sereno  e le contrazioni alle gambe ed i crampi sono diminuiti notevolmente. Spesso di notte aveva bisogno di fare stretching alle gambe. Le contrazioni a volte passavano a tutto il corpo, comprese mani e torace, arrivando anche a bloccare il diaframma ed ostacolando la respirazione. Ogni sera assumeva una pastiglia e mezza di Lioresal  da 0,250 mg (Baclofene) e in aggiunta il Valium per dormire e rilassarsi.

Da un mese non prende più Valium e dorme anche 7- 8 ore di seguito.

Questo è il primo beneficio, misurabile ed evidente.

Ci sono altri effetti come fluidità del sangue e flash visivi, che però devo ancora verificare per capire se sono stabili e realmente prodotti dalla terapia magnetica.

Sto usando anche io il Medithera Home e dalla prima applicazione mi è passato il mal di testa che avevo costantemente da una settimana.

Io soffro da tempo di emicranie, cefalee vasomotorie, ma con questa terapia gli episodi si sono ridotti.

Inoltre ho i polsi lussati ed una tendinite al polso sinistro. Ora la tendinite è passata, riesco anche a sollevare pesi e ad aiutare i miei figli negli spostamenti, senza problemi.

Anche una nostra amica, Eva Aronelius, che soffre di diabete in AF, sta usando da più di un mese il Medithera Home. Anche lei ora riesce a riposare profondamente e senza contrazioni. Inoltre, avendo riscontrato una riduzione dei picchi glicemici, sta assumendo meno insulina.

La terapia con i campi magnetici non risolve l’atassia, ma ho motivo di credere che contribuisca a una qualità di vita nettamente migliore per i pazienti atassici.

Maria Litani

http://www.ncbi.nlm.nih.gov:80/pubmed/18716706

1: Pediatr Cardiol. 2008 Aug 21. [Epub ahead of print]

The Longitudinal Course of Cardiomyopathy in Friedreich's Ataxia During Childhood.

Kipps A, Alexander M, Colan SD, Gauvreau K, Smoot L, Crawford L, Darras BT, Blume ED.

Department of Cardiology, 300 Longwood Avenue, Boston, MA, 02115, USA, alaina.kipps@...

Background: Clinical heart disease was recognized in the first descriptions of Friedreich's ataxia (FA). Cardiac manifestations reported for this progressive neurologic disease include hypertrophic cardiomyopathy, dilated cardiomyopathy, and electrophysiologic disturbances. Longitudinal data for childhood cases are limited. This study aimed to define the longitudinal course of the cardiac abnormalities with FA diagnosed during childhood and to correlate the presence of cardiomyopathy with clinical and genetic factors.

Methods: A retrospective chart review was conducted, with prospective, blinded interpretation of echocardiograms and electrocardiograms. All the patients with a diagnosis of FA referred to the cardiology department of a single institution from 1974 to 2004 were included in the study.

Results: This study investigated a total of 113 echocardiograms for 28 patients. Overall, the group had left ventricular hypertrophy and normal systolic function, with a median mass z-score of 2.48 (range, -3.8 to 35.6) and a median ejection fraction (EF) of 61% (range, 23-81%). Of the 28 patients, 23 (82%) had two or more echocardiograms. The median follow-up time to the most recent echocardiogram was 5.1 years (range, 0.4-16.5 years). Many in this longitudinal follow-up cohort (57%) showed hypertrophic cardiomyopathy on at least one echocardiogram, with the last follow-up assessment showing systolic dysfunction for 38% of these patients. There was a slow nonlinear decline in systolic function over time, with the mean EF decreasing more rapidly as age increased (p = 0.02) and maintenance of EF in the normal range until the age of 22 years. Of the 12 patients with systolic dysfunction and follow-up echocardiograms, 10 showed improvement to the normal EF range on at least one echocardiogram, and 5 remained normal through the last study. None of the trends in cardiac function and morphology correlated with frataxin GAA repeat length (the primary genetic defect in FA) or ambulatory status. One patient required an implantable defibrillator. There were no deaths or heart transplantations.

Conclusions: Overall, patients with FA have preserved cardiac function with increased mass throughout childhood. Because many patients who experience depressed systolic function show improvement in subsequent studies, evaluation for potentially reversible causes of heart failure should be conducted. Relative clinical stability during childhood and maintenance of normal systolic function into the second decade may be helpful for parent and patient education.

PMID: 18716706 [PubMed - as supplied by publisher]

See also:

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2121 (ITA)

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2124 (FRA)

°°°°°

http://www.ncbi.nlm.nih.gov/pubmed/18716623

1: Nature. 2008 Aug 17. [Epub ahead of print]

An intrinsic mechanism of corticogenesis from embryonic stem cells.

Gaspard N, Bouschet T, Hourez R, Dimidschstein J, Naeije G, van den Ameele J, Espuny-Camacho I, Herpoel A, Passante L, Schiffmann SN, Gaillard A, Vanderhaeghen P.

IRIBHM (Institute for Interdisciplinary Research).

The cerebral cortex develops through the coordinated generation of dozens of neuronal subtypes, but the mechanisms involved remain unclear. Here we show that mouse embryonic stem cells, cultured without any morphogen but in the presence of a sonic hedgehog inhibitor, recapitulate in vitro the major milestones of cortical development, leading to the sequential generation of a diverse repertoire of neurons that display most salient features of genuine cortical pyramidal neurons. When grafted into the cerebral cortex, these neurons develop patterns of axonal projections corresponding to a wide range of cortical layers, but also to highly specific cortical areas, in particular visual and limbic areas, thereby demonstrating that the identity of a cortical area can be specified without any influence from the brain. The discovery of intrinsic corticogenesis sheds new light on the mechanisms of neuronal specification, and opens new avenues for the modelling and treatment of brain diseases.

PMID: 18716623 [PubMed - as supplied by publisher]

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2121 (ITA)

http://www.lemonde.fr/sciences-et-environnement/article/2008/08/18/du-cortex-cerebral-fabrique-in-vitro-a-partir-de-cellules-souches_1084950_3244.html?xtor=RSS-3244

Du cortex cérébral a été fabriqué in vitro à partir de cellules souches

LE MONDE | 18.08.08 | 15h22  •  Mis à jour le 18.08.08 | 19h07

Les investissements effectués dans la recherche sur les cellules souches se traduisent en résultats de plus en plus spectaculaires, à un rythme toujours plus rapide. Quelques jours après la création in vitro de neurones moteurs issus de cellules de peau de personnes souffrant d'une maladie neurodégénérative et la constitution de lignées de cellules souches porteuses des stigmates d'une dizaine d'affections de diverses origines (Le Monde des 2 et 10 août), une nouvelle étape vient d'être franchie: des chercheurs sont parvenus à fabriquer in vitro du cortex cérébral, à partir de cellules souches embryonnaires de souris. 

L'équipe de biologistes dirigée par Pierre Vanderhaeghen et Nicolas Gaspard (Université libre de Bruxelles), travaillant en collaboration avec le docteur Afsaneh Gaillard (université de Poitiers, CNRS), présente ces résultats, dimanche 17 août, sur le site de la revue Nature. Mieux encore, les cellules nerveuses corticales ainsi créées ont ensuite été greffées chez des souriceaux et se sont connectées de façon appropriée avec le système nerveux central du receveur. Les auteurs de cette première estiment qu'elle ouvre de nouvelles perspectives dans la recherche sur les affections neurologiques qui trouvent leur origine dans différents dysfonctionnements du cortex cérébral humain.

Le cortex est la structure la plus complexe du cerveau des mammifères. Chez l'homme, les cellules qui constituent ce tissu cérébral sont impliquées dans les plus fréquentes des maladies neurologiques, neurodégénératives, neurovasculaires et psychiatriques. Les auteurs de la publication de Nature ont mis au point une technique novatrice. Ils ont, dans un premier temps, démontré que des cellules souches multipotentes prélevées à un stade précoce du développement embryonnaire pouvaient être aisément transformées in vitro dans les différentes catégories de cellules qui constituent le cortex cérébral. "Nous sommes parvenus à ce résultat au moyen d'un procédé ridiculement simple en n'agissant pratiquement pas, et ce de manière quelque peu paradoxale, sur le milieu de culture des cellules embryonnaires", explique Pierre Vanderhaeghen.

Bien que créées en dehors du cerveau, ces cellules apparaissent alors fonctionnelles et ressembler en tout point aux neurones du cortex. Cette observation a été expérimentalement confirmée : la greffe de ces neurones dans des cerveaux de jeunes souris a bien pris. "Une telle "corticogenèse" in vitro constitue un outil novateur pour la recherche pharmaceutique et médicale, souligne Pierre Vanderhaeghen. Pour la première fois, nous avons accès à une source illimitée et hautement fiable de neurones spécifiques du cortex, qui peuvent être utilisés pour modéliser les maladies neurologiques et tester de nouveaux médicaments."

Les auteurs de cette publication ajoutent que leur méthode pourra par ailleurs constituer une alternative à certaines expérimentations animales ou humaines. A plus long terme, ce travail ouvre la perspective de greffes intracérébrales visant à lutter contre les différentes affections ayant pour siège le cortex.

"Cette publication est très intéressante à bien des égards, estime le docteur Hervé Chneiweiss, directeur du laboratoire plasticité gliale du Centre Paul-Broca (Paris). Il importe toutefois de préciser que le milieu de culture qui a été utilisé n'a rien de "ridiculement simple". C'est un milieu désormais considéré comme classique et dénommé N2, mis au point par Gordon Sato en 1979. Il visait déjà à faire pousser des neurones foetaux de souris."

Pour le docteur Chneiweiss, ce milieu de culture diffère des milieux de prolifération de cellules souches in vitro, qui contiennent généralement du sérum de veau foetal ou des facteurs moléculaires de croissance. A ce titre, il pourrait à terme faciliter le passage à des essais cliniques expérimentaux chez l'homme. "Ce qui me surprend en fait le plus dans ce travail, confie le docteur Chneiweiss, ce sont les expériences de greffe. Voir, comme le montre cette publication, des axones pousser sur de telles distances et sur une période de quatre semaines seulement ne peut pas ne pas étonner." "Mais attention, prévient-il, l'expérience porte sur la souris et, pour diverses raisons techniques, ces résultats ne peuvent être immédiatement transposables à l'homme."

Jean-Yves Nau

See also:

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2114 (ENG)

°°°°°°°°°°

http://www.ncbi.nlm.nih.gov/pubmed/17928358

1: FASEB J. 2008 Mar;22(3):703-12. Epub 2007 Oct 10.

Methylene blue delays cellular senescence and enhances key mitochondrial biochemical pathways.

Atamna H, Nguyen A, Schultz C, Boyle K, Newberry J, Kato H, Ames BN.

Nutrition & Metabolism Center, Children's Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA 94609-1673, USA. hatamna@...

Methylene blue (MB) has been used clinically for about a century to treat numerous ailments. We show that MB and other diaminophenothiazines extend the life span of human IMR90 fibroblasts in tissue culture by >20 population doubling (PDLs). MB delays senescence at nM levels in IMR90 by enhancing mitochondrial function. MB increases mitochondrial complex IV by 30%, enhances cellular oxygen consumption by 37-70%, increases heme synthesis, and reverses premature senescence caused by H2O2 or cadmium. MB also induces phase-2 antioxidant enzymes in hepG2 cells. Flavin-dependent enzymes are known to use NAD(P)H to reduce MB to leucomethylene blue (MBH2), whereas cytochrome c reoxidizes MBH2 to MB. Experiments on lysates from rat liver mitochondria suggest the ratio MB/cytochrome c is important for the protective actions of MB. We propose that the cellular senescence delay caused by MB is due to cycling between MB and MBH2 in mitochondria, which may partly explain the increase in specific mitochondrial activities. Cycling of MB between oxidized and reduced forms may block oxidant production by mitochondria. Mitochondrial dysfunction and oxidative stress are thought to be key aberrations that lead to cellular senescence and aging. MB may be useful to delay mitochondrial dysfunction with aging and the decrease in complex IV in Alzheimer disease.

PMID: 17928358 [PubMed - indexed for MEDLINE]