Untersuchungen zur Pathogenese subpialer kortikaler Läsionen bei Multipler Sklerose und bei Marmosetten mit experimenteller autoimmuner Enzephalomyelitis

Experiments on the pathogenesis of subpial cortical lesions in Multiple Sclerosis and in Marmosets with Experimental autoimmune encephalomyelitis

by Katharina Zimmermann née Neid
Doctoral thesis
Date of Examination:2015-07-15
Date of issue:2015-06-30
Advisor:Dr. Dr. Christiane Theodossiou-Wegner
Referee:Prof. Dr. Wolfgang Brück
Referee:Prof. Dr. Alexander Flügel
Referee:Prof. Dr. Margarete Schön
Persistent Address: http://dx.doi.org/10.53846/goediss-5151

 

 

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Abstract

English

Lately, evidence has accumulated the extensive grey matter involvement in multiple sclerosis (MS). It is known that subpial cortical demyelination (SCD) accounts for the greatest proportion of demyelinated cortex in progressive MS – but it can also be found in early MS and in marmosets with experimental autoimmune encephalomyelitis (EAE). Cerebral cortex shows a distinct endogenous propensity for remyelination. But the pathogenesis of SCD and the way of remyelination is not well understood. In the first part of the present study we investigated whether and, if so, which meningeal inflammatory cells are associated with early SCD in marmosets with EAE. Our data showed significantly increased T cells paralleled by elevated plasma cells in meninges adjacent to SCD, but unaltered B cell numbers compared with normal appearing cortex in marmosets with EAE. The meninges overlying normal appearing cortex displayed similarly low T, B and plasma cell numbers as control cortex. Follicle-like B cell structures could not be found. Our findings suggest that meningeal T and plasma cell infiltration contributes to the pathogenesis of SCD in marmosets with EAE. The second objective of this study was to characterize mature NogoA+ oligodendrocytes and Olig2+ oligodendrocyte precursor cells in SCD and in normal appearing cortex in chronic MS as well as in control cortex. NogoA+ and Olig2+ cells were significantly reduced in subpial cortical lesions compared to normal appearing cortex in patients with chronic MS. Our data indicate that missing remyelination is not just because of a lack of oligodendrocyte precursor cells but also because of a disturbed proliferation and differentiation in chronic cortical MS-lesions.
Keywords: Multiple sclerosis; Cortical demyelination; Oligodendrocytes; Oligodendrocyte precursors

Other Languages

Multiple sclerosis · Cortical demyelination · Oligodendrocytes · Oligodendrocyte precursors · Targeted cortical EAE
 
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