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Written Assignment due to be handed in next Friday (October 4th): Regarding Multiple Sclerosis (or any other autoimmune disease, if you prefer) Assuming the truth of the basic generalizations written on the course web page, but don't hesitate to use facts that you have learned from other sources. This is an OPEN BOOK assignment; It is OK (and even encouraged) to read books and web pages on the subject. But it should be your own work, not a collaboration with anybody, especially not other members of this class. Please mention in the text of your report whatever ideas you may have gotten from others outside of class. Please write an at least two page single-spaced report. It can be longer, but be succinct and focused. Who knows, you might actually think of a cure.
HERE IS THE QUESTION YOU SHOULD ANSWER: The following is an outline of an example of the kind of subject (Which you could actually use, although it is better to invent your own.) Many of your essays will be read out loud in class, and discussed by everyone. I would most like to know why early attacks are usually so sudden? And what explains the almost-complete remissions that so often occur ? Furthermore, what allows neural damage and increasing paralysis to strike again, and why more and more closely spaced in time? Is some threshold reached? For example, is this caused by accumulation of anti-myelin T-lymphocytes, which perhaps need to "gang" up locally in order to produce serious damage? As to the spontaneous remissions: do the anti-myelin T-lymphocytes somehow get used up, tired, inhibited, go back to wherever they came from? Maybe the normal tolerance mechanism gets reactivated and catches up to them? Maybe the blood-brain barrier repairs itself, and blocks any more T-lymphocytes from getting into the cerebrospinal fluid, where they are not supposed to be? Maybe these T-lymphocytes re-direct their attacks to other tissues, for a while, where damage is not so apparent to the victim. Try to think of all the possibilities we can think of that might explain spontaneous remissions? For each such possibility, we should be able to invent one or two or three different ways to stimulate remission artificially, and to prolong it indefinitely. That would almost be a cure! I.e. if by some not-too unpleasant treatment the return of the disease could be delayed for 10, 20, 25 years, or more. The irregularly spaced attacks that often occur suggest to me that some process is only barely able to get re-started again. If so, then we need a method to keep the balance tipped away from a recurrence. And why is the damage concentrated in these centimeter-to half-centimeter diameter blobs you saw on the MRI photographs? For example, did anti-myelin lymphocytes get attracted there, maybe by chemotaxis? Or did a few cells quickly grow up to a large population? Do these form be enlargement from a center, outward? Or from the outer edge inward? Then What happens during the remission? For example, did the anti-myelin T lymphocytes become inactive; or did they die? What happens at the outer edge of those lesions, that prevents damage from extending farther? DOES THIS STOPPING HAVE THE SAME BASIC CAUSE AS THE REMISSIONS? After all, they are small-scale localized remissions, aren't they? And these lesions will be followed by partial repair, and by a delay of months before another attack occurs at the same location. In that sense, periodic, apparently random small attacks are like a microcosm of the effect of the disease on the whole central nervous system. Perhaps the limited size and duration of individual lesions is temporarily blocked by the same causes at cause spontaneous remission of the disease as a whole. In which case, the same treatments might suppress the sizes and time durations of individual lesions.
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