ProMyelo currently focuses on two distinct research topics: First, to develop valid and easy to implement measurements for neurodegeneration in multiple sclerosis animal models. Methods currently used to study neurodegeneration in multiple sclerosis animal models include Golgi-staining, quantification of synaptic density on the single-cell level, design-based stereology, and gene-expression analysis.
Second we aim to understand the contribution of brain intrinsic degeneration for inflammatory lesion formation in multiple sclerosis. Can brain intrinsic, degenerative events trigger peripheral immune cell recruitment? In a recently published work our group was able to demonstrate that primary oligodendrocyte degeneration indeed can act as a potent trigger for peripheral immune cell recruitment into the brain (Scheld et al., 2016). In this study, mice were fed cuprizone for 3 weeks, followed by a period of 2 weeks on normal chow to induce primary oligodendrocyte apoptosis, followed by the formation of degenerative forebrain lesions. Subsequent immunization with myelin oligodendrocyte glycoprotein 35-55 peptide (MOG35-55), which induces myelin autoreactive T cells in peripheral lymphoid organs, resulted in massive immune cell recruitment into the mouse brain. On the histopathological level, such infiltrates were characterized by destruction of the perivascular glia limitans, monocyte and lymphocyte extravasation as well as demyelination. These results clearly illustrate the significance of brain-intrinsic degenerative cascades for immune cell recruitment and MS lesion formation. Additional studies have now to address the signaling cascades and mechanistic processes that form the top-down communication between the affected brain area, neurovascular unit, and peripheral immune cells. Furthermore, it remains to be verified whether neuroprotective drugs can ameliorate both multiple sclerosis aspects, relapses and disease progression.
Our novel multiple sclerosis animal model is superior to study such kind of scientific questions.

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J Neurosci. 2016 Jan 27;36(4):1410-5

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Cells. 2019 Jan 28;8(2).

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Cells. 2019 Nov 14;8(11)

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Glia. 2019 Feb;67(2):263-276

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Expert Rev Neurother. 2016;16(1)

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Mol Neurobiol. 2016 Apr;53(3):1551-64

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Br J Pharmacol. 2015 Jan;172(1):80-92

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J Immunol. 2015 Apr 1;194(7):3400-13

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J Mol Neurosci. 2013 Oct;51(2):567-72

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CNS Neurol Disord Drug Targets. 2012 Aug;11(5):570-88