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zoom RSS 多発性硬化症の神経障害を修復する

<<   作成日時 : 2010/12/07 20:24   >>

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 多発性硬化症MSの神経修復法を開発中である。
 ケンブリッジとエジンバラ大研究者によるラットでの研究は、神経繊維を保護している髄鞘を再生するためにどのように幹細胞を助けたらよいかを見いだした。しかし、実際の治療法の開発には数年がかかるだろう。
 MSは体の免疫系の異常で起こり、自らの髄鞘を攻撃することで発症する。英国には約10万人の患者がいる。86%は再発緩解を繰り返す。約10%は緩解なしで進行する。さらに再発緩解型の人も二次性進行性MSにしばしば移行する。
 今回の研究により、脳の幹細胞が新たにミエリンを再生するためのシグナル経路を発見した。

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多発性硬化症の季節変動
http://kurie.at.webry.info/201009/article_1.html
多発性硬化症の新たな実験的治療
http://kurie.at.webry.info/201007/article_17.html
多発性硬化症の経口治療薬/cladribine fingolimod 冬虫夏草
http://kurie.at.webry.info/201001/article_24.html
多発性硬化症の寄生虫卵カクテル療法
http://kurie.at.webry.info/200803/article_29.html

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5 December 2010 Last updated at 18:00 GMT
Study offers hope of 'repairing' MS damage
http://www.bbc.co.uk/news/health-11913689

画像Retinoid X receptor gamma signaling accelerates CNS remyelination
Scientists have identified a way of prompting nerve system repair in multiple sclerosis (MS).

Studies on rats by Cambridge and Edinburgh University researchers identified how to help stem cells in the brain regenerate myelin sheath, needed to protect nerve fibres.
MS charities said the "exciting" Nature Neuroscience work offered hope of restoring physical functions.
But they cautioned it would be some years before treatments were developed.
MS is caused by a defect in the body's immune system, which turns in on itself, and attacks the fatty myelin sheath.
It is thought to affect around 100,000 people in the UK.
Around 85% have the relapsing/remitting form of the condition, in which "flare-ups" which cause disability, are followed by a recovery of a level of the lost physical function.
In this form of MS, there does appear to be some natural myelin repair.
However, around 10% of people are diagnosed with a progressive form of MS, where the decline continues without any periods of remission.
In addition, people with the relapsing/remitting form do often go on to develop what is called secondary progressive MS, which affects them in the same way.

'Missing link'
Scientists have been looking at how they might develop treatments for these two groups.
In MS, loss of the myelin sheaths which act as insulating layers, leads to the nerve fibres in the brain becoming damaged.
These fibres are important as they send messages to other parts of the body.
This study identified a signalling pathway in the brain which can encourage the brain's own stem cells to regenerate new myelin.

The scientists believe this will help in identifying drugs to encourage myelin repair in MS patients.
However, much more work is needed - both to test if the mechanism works in people with MS and to see what drugs might be needed to promote the effect.
Professor Charles ffrench-Constant, of the University of Edinburgh's MS Society Centre for MS Research, said: "The aim of our research is to slow the progression of MS with the eventual aim of stopping and reversing it.
"This discovery is very exciting as it could potentially pave the way to find drugs that could help repair damage caused to the important layers that protect nerve cells in the brain."
Professor Robin Franklin, director of the MS Society's Centre for Myelin Repair at the University of Cambridge, said: "Therapies that repair damage are the missing link in treating MS.
"In this study we have identified a means by which the brain's own stem cells can be encouraged to undertake this repair, opening up the possibility of a new regenerative medicine for this devastating disease."
The study was funded by the MS Society and the National MS Society in the US.
Simon Gillespie, chief executive of the MS Society, which part-funded the research, said: "For people with MS this is one of the most exciting developments in recent years.
"It's hard to put into words how revolutionary this discovery could be and how critical it is to continue research into MS."
Pam Macfarlane, chief executive of the MS Trust added: "Exploration of processes that might repair areas of damage to myelin, is another important area of MS research and this may eventually allow people to recover function that has been lost to disability.
"This is still an early study in rodents but it will be very interesting to see how it develops."

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Retinoid X receptor gamma signaling accelerates CNS remyelination

* Jeffrey K Huang, * Andrew A Jarjour, * Brahim Nait Oumesmar, * Christophe Kerninon, * Anna Williams, * Wojciech Krezel, * Hiroyuki Kagechika, * Julien Bauer, * Chao Zhao, * Anne Baron-Van Evercooren, * Pierre Chambon, * Charles ffrench-Constant * & Robin J M Franklin
* Affiliations * Contributions * Corresponding authors

Nature Neuroscience (2010) doi:10.1038/nn.2702

Received 09 July 2010, Accepted 21 October 2010, Published online 05 December 2010

Abstract

The molecular basis of CNS myelin regeneration (remyelination) is poorly understood. We generated a comprehensive transcriptional profile of the separate stages of spontaneous remyelination that follow focal demyelination in the rat CNS and found that transcripts that encode the retinoid acid receptor RXR-γ were differentially expressed during remyelination. Cells of the oligodendrocyte lineage expressed RXR-γ in rat tissues that were undergoing remyelination and in active and remyelinated multiple sclerosis lesions. Knockdown of RXR-γ by RNA interference or RXR-specific antagonists severely inhibited oligodendrocyte differentiation in culture. In mice that lacked RXR-γ, adult oligodendrocyte precursor cells efficiently repopulated lesions after demyelination, but showed delayed differentiation into mature oligodendrocytes. Administration of the RXR agonist 9-cis-retinoic acid to demyelinated cerebellar slice cultures and to aged rats after demyelination caused an increase in remyelinated axons. Our results indicate that RXR-γ is a positive regulator of endogenous oligodendrocyte precursor cell differentiation and remyelination and might be a pharmacological target for regenerative therapy in the CNS.


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