Multiple Sclerosis,
Antimyelin Antibodies
and Mimicry in a new BM&L debate this week
In the July 10 Number of
the New England Journal of Medicine, three extremely intriguing articles on
Multiple Sclerosis (MS) rise a very interesting debate, which BRAIN MIND &
LIFE INTERNATIONAL will dedicate the next week-end workshop session.
For participation
information, please write to info@brainmindlife.org, subject:
INTERNATIONAL: Antimyelin Antibodies in MS.
An article by Jack
P. Antel, M.D., and Amit Bar-Or, M.D. (Do Myelin-Directed Antibodies Predict Multiple Sclerosis? Vol 349: 107-109, Number 2, July 10,
2003)
introduces the problem of the early axonal injury depending on the primary
lesion directed at the myelin itself or its cell of origin, the
oligodendrocyte, and discusses the role of myelin-directed antibodies in
predicting the developing of MS. The research article by Thomas
Berger, M.D., Paul Rubner, M.D., Franz Schautzer, M.D., Robert Egg, M.D., Hanno
Ulmer, Ph.D., Irmgard Mayringer, M.D., Erika Dilitz, M.D., Florian
Deisenhammer, M.D., and Markus Reindl, Ph.D. (Antimyelin
Antibodies as a Predictor of Clinically Definite Multiple Sclerosis after a
First Demyelinating Event. Vol 349: 139-145, Number 2, July 10,
2003) suggests a new diagnostic
tool for MS. Here we report the entire abstract:
Background Most patients
with multiple sclerosis initially present with a clinically isolated
syndrome. Despite the fact that clinically definite multiple
sclerosis will develop in up to 80 percent of these patients, the
course of the disease is unpredictable at its onset and requires
long-term observation or repeated magnetic resonance imaging (MRI).
We investigated whether the presence of serum antibodies against
myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein
(MBP) in patients with a clinically isolated syndrome predicts the
interval to conversion to clinically definite multiple sclerosis.
Methods A total of 103 patients with a clinically isolated syndrome, positive
findings on cerebral MRI, and oligoclonal bands in the cerebrospinal
fluid were studied. At base line, serum samples were collected to
test for anti-MOG and anti-MBP antibodies with Western blot
analysis, and the lesions detected by cerebral MRI were quantified.
Neurologic examinations for relapse or disease progression (defined
as conversion to clinically definite multiple sclerosis) were
performed at base line and subsequently every three months.
Results Patients with anti-MOG and anti-MBP antibodies had relapses more
often and earlier than patients without these antibodies. Only 9 of
39 antibody-seronegative patients (23 percent) had a relapse, and
the mean (±SD) time to relapse was 45.1±13.7 months. In contrast, 21
of 22 patients (95 percent) with antibodies against both MOG and MBP
had a relapse within a mean of 7.5±4.4 months, and 35 of 42 patients
(83 percent) with only anti-MOG antibodies had a relapse within
14.6±9.6 months (P<0.001 for both comparisons with
antibody-seronegative patients). The adjusted hazard ratio for the
development of clinically definite multiple sclerosis was 76.5 (95
percent confidence interval, 20.6 to 284.6) among the patients who
were seropositive for both antibodies and 31.6 (95 percent
confidence interval, 9.5 to 104.5) among the patients who were
seropositive only for anti-MOG antibodies, as compared wit
seronegative patients.
Conclusions Analysis of antibodies against MOG and MBP in patients with
a clinically isolated syndrome is a rapid, inexpensive, and precise
method for the prediction of early conversion to clinically definite
multiple sclerosis. This finding may be important for the counseling
and care of patients with a first demyelinating event suggestive of
multiple sclerosis.
The third article is written
by Hartmut Wekerle, M.D., and Reinhard Hohlfeld, M.D. (Molecular Mimicry in Multiple Sclerosis. Vol
349: 185-186, Number 2, July 10, 2003). A recent research by Lang and his
colleagues, centred on molecular mimicry, newly attracted the attention
on this mechanism for the pathogenesis of MS. In fact, most researchers believe
that multiple sclerosis is an autoimmune disease in which T cells
recognize and attack components of the axonal myelin sheath and
other features of the central nervous system, destroying myelin and
the underlying axon. Although self-reactive T cells are present in
the immune system of people with multiple sclerosis, they are also
found in a quiescent state in perfectly healthy people. Their
pathogenic potential is realized only on acute activation, which can
occur through different mechanisms. Molecular mimicry is believed
one of the presumed triggers of autoimmunity.