Document Detail


Cell death and birth in multiple sclerosis brain.
MedLine Citation:
PMID:  9168159     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The hallmark of the brain pathology in multiple sclerosis is the white matter plaque, characterized by myelin destruction and oligodendrocyte loss. To examine the role that cell death plays in the development of MS lesions, we used the in situ TUNEL technique, a method that sensitively detects DNA fragmentation associated with death at the single cell level. We found that patchy areas within acute MS lesions have massive numbers of inflammatory and glial cells undergoing cell death. The punched out areas of some long-standing chronic lesions also had labeled glial cells showing that the attack was not a single event. Immunocytochemical identification of the dying cells with glial specific marker co-labeling showed that 14-40% were the myelin-sustaining oligodendroglial cell. Confocal microscopic evaluation of fluorescein-labeled TUNEL positive cells revealed nuclei with morphologic characteristics of apoptosis, and electrophoresed MS brain DNA produced a ladder characteristic of apoptotic DNA cleavage confirming that substantial numbers of labeled cells, but not necessarily all, were dying by apoptotic mechanisms rather than cell necrosis. Companion studies using a marker for cell proliferation on MS lesions revealed that unexpectedly large populations of perivascular inflammatory cells and parenchymal glial cells had entered the cell proliferation cycle. These findings establish that two opposing glial cell responses - relentless cell death and coincident brisk cellular proliferation - are important features of MS pathology. In the end, however, glial cell loss prevails, and we suspect apoptosis may be the critical death mechanism responsible for the depletion of myelin observed in this condition.
Authors:
P Dowling; W Husar; J Menonna; H Donnenfeld; S Cook; M Sidhu
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Journal of the neurological sciences     Volume:  149     ISSN:  0022-510X     ISO Abbreviation:  J. Neurol. Sci.     Publication Date:  1997 Jul 
Date Detail:
Created Date:  1997-07-10     Completed Date:  1997-07-10     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375403     Medline TA:  J Neurol Sci     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  1-11     Citation Subset:  IM    
Affiliation:
Department of Veterans Affairs, New Jersey Health Care System, East Orange 07018, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Autopsy
Biological Markers
Brain / pathology*
Cell Nucleus / pathology,  ultrastructure
Central Nervous System Diseases / pathology
Child
DNA Fragmentation
Encephalomyelitis, Autoimmune, Experimental / pathology
Glial Fibrillary Acidic Protein / analysis
Humans
Immunoenzyme Techniques
Ki-67 Antigen / analysis
Multiple Sclerosis / pathology*
Myelin Sheath / pathology,  ultrastructure
Neuroglia / pathology
Neurons / pathology*
Oligodendroglia / pathology,  ultrastructure
Rats
Rats, Inbred Lew
Sensitivity and Specificity
Spinal Cord / pathology*
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Glial Fibrillary Acidic Protein; 0/Ki-67 Antigen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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