One of the most popular stories we've ever published here at This is MS was entitled: Multiple Sclerosis may not be an Auto-Immune Disease. It was shocking to most people that after so many decades of intense research, such a fundamental question remained wide open: whether MS developed as a result of the immune system turning renegade against its own central nervous system, or whether an environmental trigger or other unknown process was actually the culprit, and the easily observed immune response "merely" a secondary reaction. Obviously, answering this question is not just for fun-- ultimately resolving Multiple Sclerosis will more than likely require determining just what the disease *is* in the first place.
A new survey publication coming out of Australian research labs will help to keep this debate simmering. Through a survey of recent findings based on study of MS lesions soon after they form, they conclude that an alternate explanation for the development of multiple sclerosis is highly feasible, and proceeds something like the following:
- The oligodendrocytes, the highly specialized cells that produce myelin, begin to die (through the process of apoptosis-- programmed cell death) for as-yet unknown reasons.
- As a RESULT of these cell deaths, the immune system THEN comes in and tries to clean things up, creating inflammation and the familiar lesions seen on MRI.
- Over a long period of time, the immune system process becomes "automated" and happens all on its own-- explaining the progressive course of the illness (without acute exacerbations) as seen in secondary-progressive MS and primary-progressive MS.
Contrast this order of events to the autoimmune theory of MS where the immune system itself attacks the myelin and/or oligodendrocytes, and you can see the critical implications for therapy development.
The debate will continue, and we should be happy that there is a debate in the first place as, one might imagine, there is quite a bit of established momentum behind the long-accepted autoimmune theory. This must be undone to give serious credence to the theory posited above.
Please click "read more" to read the abstract from this highly relevant research paper.
Full Abstract
The pathology of multiple sclerosis: a paradigm shift.
Barnett MH, Sutton I.
aBrain and Mind Research Institute, University of Sydney, NSW, Australia bSt George Hospital, Kogarah, NSW, Australia cGarvan Institute of Medical Research, Darlinghurst, NSW, Australia dSt Vincent's Hospital, Darlinghurst, NSW, Australia.
PURPOSE OF REVIEW: Detailed immunopathological assessment of multiple sclerosis tissue remains the research tool most likely to elucidate the major processes involved in disease pathogenesis and tissue injury. Such studies steer and provide the impetus for refining cellular/molecular investigations and developing more relevant disease models in animals. RECENT FINDINGS: Recent observations in early multiple sclerosis lesions challenge the traditional hypothesis that multiple sclerosis arises as the result of a primary autoimmune process that specifically targets myelin antigen(s). A new multiple sclerosis paradigm proposes that oligodendrocyte apoptosis is the earliest change in newly forming lesions and that tissue injury is amplified by the subsequent recruitment of a systemic immune response. Over months to years the pathology of multiple sclerosis is transformed and the changes which accompany the late phase of the disease suggest that the inflammatory response becomes progressively 'compartmentalized' and therefore largely isolated from systemic influence with time. SUMMARY: Recent pathological studies raise important questions regarding the aetiology of oligodendrocyte apoptosis, the mechanisms by which the accompanying inflammatory response amplifies tissue injury and the regulation of central nervous system immunity. An improved understanding of these processes is essential for advancing therapeutic interventions applicable to different stages of the disease.
PMID: 16702829 [PubMed - as supplied by publisher]
Links:
PubMed Link
