Multiple Sclerosis is a disease of the Central Nervous System that destroys myelin, oligodendrocytes, neurons and axons. It is among the most destructive diseases of the human brain. In the absence of cause for this devastating disease, research has historically focused on the most obvious pathological feature of MS brains - inflammatory demyelination of white matter. This presentation will summarize recent data that supports the concept that inflammation is a secondary response to an underlying CNS disease, which affects the survival of oligodendrocytes and/or neurons. The data originate from pathological analysis of post-mortem MS brains, magnetic resonance imaging studies and the natural history of the disease. From the pathological perspective, demyelination and inflammation have been spatially dissociated in the cerebral cortex of MS patients. This is quite striking in lesions that occupy both subcortical white matter and the cerebral cortex. Prineas and colleagues have recently identified areas of white matter in post-mortem MS brains which contain dying oligodendrocytes but no inflammtory cells. Both MRI and natural history studies identify inflammatory lesions and relapses as modulators, but relatively poor predictors of disease progression in MS patients. A major predictor of disease progression in MS patients is chronological age as most MS patients reach EDSS 4.0 at a similar age independent of disease course (relapsing-remitting vs primary progressive), age of onset and number of relapses. This supports the concept that MS is a primary neurodegenerative disease with a subpopulation of patients having degrees of secondary inflammatory white matter lesions.
Shayk wrote:Hi, I ’m definitely not in the "auto-immune camp".
On the flipside much of the research done to date, and the treatments which have been developed, will have been a waste of time. As usual this vile disease always has the last laugh.
But I'd like to know how many people who have had the disease for 25 or 30 years are still walking without aids
The study describes the clinical and pathological findings in 12 patients with relapsing and remitting multiple sclerosis, who died during or shortly after the onset of a relapse. Pathological changes not previously associated with the formation of new symptomatic lesions were observed in seven cases, namely, extensive oligodendrocyte apoptosis and microglial activation in myelinated tissue containing few or no lymphocytes or myelin phagocytes. No current laboratory model of multiple sclerosis, in particular, experimental allergic encephalomyelitis, is known with these features, which raises the possibility of some novel process underlying new lesion formation in multiple sclerosis.
microglia were activated focally and phagocytosed the collapsed myelin. This study demonstrates that an antibody directed against myelin-forming cells induces CNS demyelination and supports the hypothesis that autoantibodies may play a role in CNS demyelinating diseases.
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