By Sheldon F. Gottlieb
A.J.S. Rayl's article on the possibility of an oral treatment for multiple sclerosis1 (MS) once again points out the need for new thinking about the causes and treatments for MS. For over 50 years, the public has been inundated with incomplete and misleading information about the nature of MS, its origins, and potential treatments. The "MS industry" has been touting either the infectious (bacterial or viral) or immunological etiology of the disease along with the experimental autoimmune encephalomyelitis (EAE) as the paradigm of the animal model.2,3
The much-touted EAE model is nothing more than a model for inducing immunological reactions, not for mimicking MS. One specific example should suffice to substantiate this claim: In MS, perivascular infiltration and cellular inflammatory response follow myelin destruction, whereas in EAE infiltration and inflammation precede the breakdown of myelin, as one would expect in any experimentally induced immunological reaction against myelin or one of its derivatives. These differences between the actual disease process and the induced disease may provide the basis as to why the various immunological agents proposed as treatments for MS have not had the success the EAE model would predict. This includes copolymer 1 and Betaseron (interferon beta-1b).
With respect to the infectious concept of MS, not once has a bacterium or virus been isolated from an MS lesion that produces the disease in any animal and that meets Koch's postulates.2,4 Contrast these long-term negative results with the rapidity with which the AIDS virus was isolated and identified.
The desideratum in MS research is new ideas based on solid observations of the actual disease process. One of the prominent features of the MS lesion is the involvement of the cerebral vasculature; the lesion is primarily perivenule. Thus, concepts pertaining to the etiology of MS perhaps should focus on this vascular relationship. The Gottlieb-Neubauer vascular-ischemic model3 of MS provides an explanation for the immunological changes being viewed as a response to, rather than a basis for, the MS disease process. It also explains why there has been an unending failure to isolate an infectious agent from the brains of MS patients. The Gottlieb-Neubauer concept that MS may be viewed as a wound in the central nervous system resulting from a vascular dysfunction provides the basis for a rational therapy that, in double-blind studies, has shown to be effective in decreasing rates of exacerbation and increasing the times of remission, especially when applied early in the disease and continued throughout life.2,3,5
The time is ripe for the members of the "MS industry" to open their minds to new concepts and new approaches to treating this debilitating and demoralizing6 disease and not repackage old and barely useful therapiess based on fallacious concepts.
Sheldon F. Gottlieb, Ph.D.
10418 Utopia Circle East
Boynton Beach, FL 33437
The Scientist 13:12, Sep. 13, 1999
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