醫學持續不斷的進步, 也希望每個醫療團隊都能夠用開放的心和態度共同合作,真正的解決問題.
基因/免疫方面:
英國劍橋大學科學家發現29種和多發性硬化症（MS）有關的新變體基因.
在「自然」（Nature）期刊今天刊登的研究中，研究者表示他們發現T細胞和化學物質「白細胞介素」（interleukins）對於使人殘廢的多發性硬化症而言相當重要。T細胞是1種白血細胞，負責免疫反應。
經歷多年時間，研究團隊在１５個國家和地區收集了９７７２名多發性硬化症患者的脫氧核糖核酸，並與１．７萬名健康人的脫氧核糖核酸比對，結果新發現２９種與這種病症存在關聯的基因和５種可能存在關聯的“嫌疑基因”。
先前，生物醫學界已確認２３種致病基因，加上新發現的２９種基因和５種可疑基因，引發多發性硬化症的基因范圍已擴展至５７種。
鎖定基因種類有助于診斷和治療多發性硬化症。
可疑基因已經初步確認, 但是否只針對白種人? 不知是否有無東方人的基因資料庫納入研究?確認基因是第一步, 之後還要找出可以控制的方法, 以及動物實驗, 人體實驗.. 再加油!!
藥物實驗方面:
神經退化性疾病的基因治療有了新突破！馬偕醫院小兒遺傳科主任林達雄醫師發表基因治療腦白質退化症的動物實驗研究結果刊登於國際著名期刊「分子遺傳與代謝」（Molecular Genetics and Metabolism）， 並且獲選為八月的封面故事。
此次研究主要是因為利用了神經軸突傳導神經信息物質至遠端神經元的特性，經由以腺病毒相關病毒為載體攜帶正常基因，直接注射入實驗動物的中樞神經的神經軸突聚集處，此正常基因即可在進入細胞後，被送達遠方細胞，並且製造出正常酵素蛋白，治療中樞神經系統的病變與發炎。
此 次研究同時找到小腦與脊髓神經退化的療法。藉由適當的基因療法，構成完整的治療基因網絡，同時保護小腦與脊髓的神經纖維髓鞘與神經軸突，成功遏止了小腦與 脊髓的髓鞘退化與神經軸突病變。這對於諸如小腦萎縮症、多發性硬化症、脊髓性肌肉萎縮症等疾病， 將會是未來治療的新契機。
動物實驗有曙光, 人體實驗還要時間, 也許還要5年, 再加油!看來這些許多中樞神經病變的疾病都有機會復原或阻止.
靜脈血管窄化方面:
來自聖地牙哥的神經學家 Dr David Hubbard 給出了目前的較為清晰的解釋和思路:
靜脈血管窄化會增加血管內血液的壓力,當中樞神經系統內血管壓力升高對於血腦屏障本身的防禦能力產生缺陷, 血液中的物質有很大的機會突破血腦屏障進入組織當中, 所以也更容易讓病毒突破此屏障而進入中樞神經系統. 同時免疫系統對於這樣的缺陷也變得敏感, 會進一步造成組織的發炎反應. 同樣的情形也出現在腿部
CCSVI Update
A clear understanding of Multiple sclerosis has proved elusive for generations of doctors and scientists.
The first suggestion that there could be a vascular component to the disease dates back 180 years to Sir Robert Carswell from Glasgow. He was drawing an image of a post mortem sample of brain tissue from an MS patient and commented that "there appears to be vascular lesions here".
Dr Franz Schelling from Austria has been a lone voice for many years in promoting this theory and I spent an intriguing half hour with Franz as he drew the various venous sinuses on napkins at the CCSVI conference in Poland this year. It was Franz who convinced Paulo Zamboni to explore this field and the results of that collaboration has changed the world of medicine. The recent discovery of the importance of CCSVI has filled in many of the gaps in our understanding of the disease.
At the International Society of Neurovascular Disease meeting in Bologna in March this year, Dr David Hubbard, a consultant neurologist from San Diego, gave the clearest description of MS that I have ever heard. He described how leakage of blood products across the blood brain barrier caused the initial damage in the brain tissue. The immune system became aware of this damage and was triggered to respond as a secondary event. I sought him out later to congratulate him on his presentation and particularly the clarity of his description of how the vascular and immune parts of the disease interact. This made sense on many levels and explained why most current treatments are only partially effective as they are aimed at the secondary and not the primary driver of the disease. This new paradigm does not exclude the immune system and immune modulating drugs as part of a treatment regime but this new understanding gives new possibilities for treatment with the possibility of improved outcomes.
Treating venous pressure by means of angioplasty could be a relatively safe and easy way of improving outcomes in MS if this theory is proven to be correct. A recent study by Ivo Petrov from Bulgaria, presented a series of over 461 CCSVI procedures carried out in Sofia, showed no major complications which confirmed the safety of angioplasty in MS (1).
A new paper published in the Journal 'Brain' in June 2011 appears to support this new paradigm (2). A research team from Vienna examined post mortem samples of 30 MS patients and 25 controls who died of other causes. For the first time, they have shown that the most recent MS lesions were associated with oxidative stress damage consistent with leakage across the blood brain barrier. Older lesions showed the T lymphocyte infiltration typical of an immune response.
A good demonstration of the damage that blood products can produce is in cellulitis in legs associated with varicose veins. As the veins enlarge, the increased pressure in the vessel causes the junction between endothelial cells lining the vein to widen allowing blood products to leak into the leg tissues. This causes inflammation in the tissues with the classic inflammatory signs of redness, heat, swelling and pain as seen in this image.
The brain has the relative protection of the blood brain barrier but this is simply a tighter connection between endothelial cells, thirty proteins joining the cells as opposed to the usual ten. Increased venous pressure in the deep veins of the brain will eventually loosen even these tight junctions and when the blood products leak into brain tissue the damage will be similar to that seen in leg cellulitis. The secondary immune response is triggered to try in an attempt to limit this damage but in itself, this response can increase inflammation.
After seven years of successfully using LDN in the management of MS, I knew that the immune system was an important factor in all types of the disease. Paulo Zamboni, Franz Schnelling, David Hubbard and others are helping us to understand the complex interplay between the immune system and the venous system in MS. A combined approach to the management of the disease is a logical way forward.
Like any new paradigm, this will take some time to be accepted by all of those involved in treating and raising the awareness of this condition but as the research stacks up, it will become clear that a major step towards understanding and successfully treating MS has taken place.
There is still much to learn and many unanswered questions but CCSVI has taken us a long way towards better understanding and treatment of this complex condition.
參考文獻:
- Petrov I, Grozdinski L, Kaninski G, Iliev N, Iloska M, Radev A. J Endovasc Ther. 2011 Jun;18(3):314-23. Safety profile of endovascular treatment for chronic cerebrospinal venous insufficiency in patients with multiple sclerosis.
- Haider et al. Oxidative damage in Multiple Sclerosis Lesions. Brain 7th june 2011
醫學持續不斷的進步, 也希望每個醫療團隊都能夠用開放的心和態度共同合作,真正的解決問題.
都加油吧~
MS疾病和相關研究的進展更新
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