In those days it was not possible to separate the kinds of glia, and I did not count the papers about "glia" or "glioma", or C6 cells. But with the help of GFAP, many more kinds of experiments were possible, and for a time astrocytes predominated. At this time the neurons are taking off again. But oligodendrocytes never did predominate in spite of the seemingly endless numbers of papers on oligodendrocyte lineage. So, again, these comparisons did not support the perception that myelin rules the ASN.

So why did this perception come about? I think it was because the myelin sessions were quite visible. A number of colorful characters who were very possessive of their own findings were involved. Although, at the first ASN meeting in Albuquerque there was no myelin session, the stage had already been set. About six years earlier at a New York Academy of Science meeting which I and others in this room attended, a lot of myelin work was presented for the first time. Bill Norton reported on a method for purifying myelin, and presented a lipid composition for this structure. Marian Kies also reported another myelin purification method, and also a lipid composition, Marjorie Lees described her studies with the proteolipid protein, and this was all very friendly. Three different people, however, E.J. Fields, Marian Kies' laboratory, and Elizabeth Roboz-Einstein reported the partial purification of an encephalitogenic protein which was extractable in 0.1 N HCl. They all appeared to have the same protein, but in different stages of purification. There was much argument about dialysis time, and "what do you mean by dialyzable?", and other details, and some of the remarks were not very polite.

In the next six years the proteins became much better purified, but at the Albuquerque meeting, where there was no myelin session, a new character appeared on the scene, Ed Eylar. In a protein session he described a new protein which he called A1. It was encephalitogenic, and was fairly pure. If, however, the tryptophane group was blocked, the encephalitogenic activity was blocked. This work was presented as if the A1 was a new protein, with no attempt to relate his protein to that already described in the literature. Needless to say, this was quite irritating.

At the next ASN meeting in Hershey,where there was a myelin session, Ed was not in it. Instead, at a protein session he reported the complete sequence of his A1 protein, which was especially irritating, because he had beaten everyone else to it. Over the years, many others jumped into fray of myelin basic protein (MBP) as it came to be called, including Steve Brostoff, George Hashim, Fred Wolfgram, Bob Kibler, and Catherine McPherson, and later on, in the proteolipid protein (PLP) field, originally dominated by Jordi Folch-Pi and Marjorie Lees, there were Mario Moscarello, and John Trotter. The myelin basic protein sessions were especially wild. There was much discussion about who discovered the protein, who purified it first, how pure it was, as well as whether MBP in imcomplete adjuvant would protect against subsequent immunization with complete Freund's adjuvant. The discussions were stormy, critical, and very rude, with insults hurled around the room. Sometimes it was a bit embarrassing to the non-participants in the controversies.

For a while it was thought that the proteins PLP and MBP were the main proteins in myelin. The Wolfgram Protein was added shortly after, which was found subsequently by Terry Sprinkle to contain enzymatic activity, as well as other constituents. Then Dick Quarles found and described a new protein which he called the myelin-associated glycoprotein (MAG). He had a difficult time getting his findings accepted because it had already been published by Ed Eylar that there were no glycoproteins in myelin. Then when Dick, in company with Jean-Marie Matthieu found two forms of the MAG it was almost too much. Even Marjorie Lees did not escape critical comment. When her group showed that the PLP was encephalitogenic, it was widely disbelieved, and was said to be due to contaminating MBP in the preparation. It wasn't until her group identified the encephalitogenic peptide, synthesized it, and injected it into an animal which developed EAE, that her critics were finally convinced that her PLP was not contaminated with MBP.

So why was this such a big deal? Why were the workers in the myelin field so emotional? At that time it was, and still is, terribly important to solve the problem of multiple sclerosis, and at the time it was not realized how very complex multiple sclerosis as well as EAE are. At first, everyone thought that MBP was the key to MS, and if MBP was manipulated in certain ways, MS could be cured. Naturally everyone wanted to be the one who succeeded. So, here we are, thirty years later, with hundreds of millions of dollars spent by the NIH and the MS Society, and the cure for MS, though much closer, is not yet at hand. I think, however, that our members have contributed greatly to the unraveling of the mysteries of myelin and to a better understanding of MS. Many of the breakthroughs have been announced on our platforms, and certainly this meeting is no exception. Myelin papers are still coming on, and we hope, due to our meetings, we will reach a much better understanding of the field, maybe better treatments, or even a cure. Certainly there is much potential out there.