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-   -   Stem cell transplantation (https://www.neurotalk.org/multiple-sclerosis/13148-stem-cell-transplantation.html)

Harry Z 02-10-2007 11:46 PM

Stem cell transplantation
 
This is not good news for those who held hope in the autologous haematopoietic stem cell transplant procedure. The docs have found more evidence that the immune system may not be the cause at all for the initial problems in MS.

Harry

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http://brain.oxfordjournals.org/cgi/...tract/awl370v1


Autologous haematopoietic stem cell transplantation fails to stop demyelination and neurodegeneration in multiple sclerosis


Imke Metz1, Claudia F. Lucchinetti2, Harry Openshaw3, Antonio Garcia-Merino4, Hans Lassmann5, Marc S. Freedman6, Harold L. Atkins6, Biagio Azzarelli7, Oldrich J. Kolar7 and Wolfgang Brück1,8

1Department of Neuropathology, Georg August University, Göttingen, Germany, 2Department of Neurology, Mayo Clinic,
College of Medicine, Rochester, MN, 3Department of Neurology, City of Hope National Medical Center, Duarte, CA, USA, 4Servicio de Neurologia, Clinica Puerta de Hierro, Universidad Autonoma, Madrid, Spain, 5Center for Brain
Research, Medical University of Vienna, Austria, 6Department of Medicine, University of Ottawa, The Ottawa Hospital Research Institute, Ottawa, ON, Canada, 7Indiana University School of Medicine, Indiana University, Indianapolis, IN, USA and 8Institut für Multiple-Sklerose-Forschung, Bereich Humanmedizin der Universität Göttingen und Gemeinnütz ige Hertie-Stiftung, Göttingen, Germany

Correspondence to: Prof. Wolfgang Brück, MD, Institut für Neuropathologie, Georg-August-Universität Göttingen Robert-Koch-Str. 40, 37075 Göttingen, Germany E-mail: wbrueck@med.uni-goettingen.de



The present study analyses autopsy material from five multiple sclerosis patients who received autologous stem cell transplantation. A total of 53 white matter lesions were investigated using routine and mmunohistochemical stainings to characterize the demyelinating activity, inflammatory infiltrates, acutely damaged axons and macrophages/microgli al cells. We found evidence for ongoing active demyelination in all of the five patients. The inflammatory infiltrate within the lesions showed only very few T cells and CD8+ cytotoxic T cells dominated the T cell population. B cells and plasma cells were completely absent from the lesions. High numbers of acutely damaged axons were found in active lesion areas. Tissue injury was associated with activated macrophages/microglial cells. The present results indicate that ongoing demyelination and axonal degeneration exist despite pronounced immunosuppression. Our data parallel results from some of the clinical phase I/II studies showing continued clinical disease progression in multiple sclerosis patients with high expanded disability system scores despite autologous stem cell transplantation.


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