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Date:5/26/2009

ase severity reduced indirectly due to the dampening of the immune response. This issue required further investigation, particularly due to the ability of statins to cross the blood-brain barrier and access the CNS, and the enrichment of cholesterol in the myelin sheath."

The objective of the MNI study was to determine the direct impact of simvastatin, a statin in clinical trials, on the integrity of myelin in the brain and on the remyelination process. The study uses a model of myelin damage that has relatively little inflammation and mimics the demyelinating aspect of MS, allowing MNI researchers to determine the direct effect of long-term statin therapy on remyelination, independent of its indirect effects mediated via immune modulation.

"The results of our study indicate that simvastatin has in fact, a slightly deleterious effect on myelin under non-pathological conditions," adds Dr. Miron. "During remyelination, there is a decrease not only in myelin production but also in oligodendrocyte number as a result of simvastatin treatment. The findings also suggest that simvastatin inhibits CNS remyelination by blocking oligodendrocyte progenitor cell differentiation or maturation into myelinating oligodendrocytes."

This study underscores the necessity of monitoring the long-terms effects of CNS accessible immune therapies, particularly those that can impact cell types that are postulated to be targeted in neurological disease processes and that are implicated in any brain tissue repair processes. Understanding the underlying mechanisms of these therapies will lead to improved and enhanced treatment strategies and ultimately improved quality of life for people who suffer from a variety of neurological diseases.


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Contact: Anita Kar
anita.kar@mcgill.ca
514-398-3376
McGill University
Source:Eurekalert

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