News
Two Recent Research Breakthroughs We've Funded
MS may lead to lower cancer risk researchers at Karolinksa Institute have discovered. Click here for more information.
A group of 12 proteins associated with pediatric MS has been discovered for the first time by a team of neurology and pathology researchers at Stony Brook University Medical Center. Click here for more information.
Promising Results for New MS Drug
Genetech and Biogen Idec recently presented promising results from a Phase II clinical study of Rituxan® (Rituximab) and its effects on multiple sclerosis. Rituxan® (Rituximab) is a therapeutic antibody that targets and depletes CD20-positive B-cells. Currently, the drug is used to treat several forms of CD20-positive B-cell non-Hodgkin’s lymphoma, diffuse large B-cell lymphoma, and rheumatoid arthritis and is also being tested for its effects on other diseases such as lupus nephritis. The new study suggests that B-cells may play a prominent role in the initiation and development of MS, which is contrary to the traditional perception that the disease is singularly T-cell mediated. These initial tests show positive results for the drug as a treatment option for MS although its use is not without side effects. Evaluation of the data will be taking place throughout the upcoming months to analyze the safety of Rituxin and its overall effectiveness. For more information on Rituxan® (Rituximab) please visit www.gene.com or call 1-800-821-8590.
Take Action!
Challenge
Multiple sclerosis (MS) is a potentially debilitating and
unpredictable chronic neurological disease that affects more than one
million Americans nationwide. The nature and severity of the disease can
vary greatly from person to person, and even over the course of an
individual’s illness. An MS survivor may be prone to periodic relapses
that render him/her temporarily incapable of working.
Many MS survivors work when they are healthy, but during periods of disability are denied the very benefits for which their own Social Security Disability Insurance (SSDI) taxes are collected. Decades-old Social Security Administration (SSA) guidelines, testing that fails to detect “hidden” symptoms of illnesses such as MS (like fatigue and dizziness) and lengthy bureaucratic procedures conspire to make it difficult for chronic illness survivors to attain benefits.
While current SSA guidelines recognize "permanent disability," there is no current solution for those who are "temporarily disabled" because of chronic illness. Individuals who are awarded SSDI benefits risk losing them if they return to work. They must reapply for benefits through an application process that can take years, or give up working altogether.
What can be done??
Bob Guidara, of the United Citizens Assistance
Network and an MS survivor himself, has initiated a much-needed petition
for Social Security Reform at acceleratedcure.org. With the amendment of SSA
regulations, victims of chronic illnesses can enjoy:
- Immediate temporary SSDI benefits
- Benefits that are renewable in case of relapse
- The ability to work with peace of mind when health permits
Temporary SSDI benefits are also more cost-effective than providing permanent permanent disability insurance benefits to people who are often willing and able to work. Clearly this is also a quality of life issue.
Please sign the SSA Disability "Chronic Illness" Insurance Petition in order to help create fairer SSDI guidelines and benefits for survivors of MS and other chronic illnesses. And please let your family members, friends and colleagues know about the petition. It is time for change!
MS GENE IS IDENTIFIED
Article: Nature Genetics 37 , 486 - 494 (2005)Published online: 10 April 2005; | doi:10.1038/ng1544
MHC2TA is associated with differential MHC molecule expression and susceptibility to rheumatoid arthritis, multiple sclerosis and myocardial infarction
Antigen presentation to T cells by MHC molecules is essential for adaptive immune responses. To determine the exact position of a gene affecting expression of MHC molecules, we finely mapped a previously defined rat quantitative trait locus regulating MHC class II on microglia in an advanced intercross line. We identified a small interval including the gene MHC class II transactivator ( Mhc2ta ) and, using a map over six inbred strains combined with gene sequencing and expression analysis, two conserved Mhc2ta haplotypes segregating with MHC class II levels. In humans, a -168A G polymorphism in the type III promoter of the MHC class II transactivator ( MHC2TA ) was associated with increased susceptibility to rheumatoid arthritis, multiple sclerosis and myocardial infarction, as well as lower expression of MHC2TA after stimulation of leukocytes with interferon-. We conclude that polymorphisms in Mhc2ta and MHC2TA result in differential MHC molecule expression and are associated with susceptibility to common complex
diseases with inflammatory components.
Authors: Maria Swanberg1, Olle Lidman1, Leonid Padyukov2, Per Eriksson3, Eva Åkesson4, Maja Jagodic1, Anna Lobell1, Mohsen Khademi1, Ola Börjesson2, Cecilia M Lindgren5, Pia Lundman6, Anthony J Brookes7, Juha Kere5, Holger Luthman8, Lars Alfredsson9, Jan Hillert4, Lars Klaresko2, Anders Hamsten3, Fredrik Piehl1 & Tomas Olsson1
1 Department of Clinical Neuroscience, Neuroimmunology Unit, Karolinska Institute, Stockholm, Sweden.
2 Department of Medicine, Rheumatology Unit, King Gustaf V Research Institute, Karolinska Institute, Stockholm, Sweden.
3 Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institute, Stockholm, Sweden.
4 Department of Neurology, Neurotec, Karolinska Institute, Huddinge, Sweden.
5 Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
6 Department of Medicine, Danderyd's Hospital, Stockholm, Sweden.
7 Center for Genomics and Bioinformatics, Karolinska Institute, Stockholm, Sweden.
8 Lund University, Department of Clinical Sciences, Malmö, Sweden.
9 Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.
10 These authors contributed equally to the work. Correspondence should be addressed to Tomas Olsson | tomas.olsson@cmm.ki.se