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Fig. 8 | Acta Neuropathologica Communications

Fig. 8

From: Oligodendrocyte-specific overexpression of human alpha-synuclein results in elevated MBP levels and inflammatory responses in TgM83 mice, mimicking the pathological features of multiple system atrophy

Fig. 8

Hypothetical mechanism that illustrates the involvement of microglia and oligodendrocyte (OL) in the process of demyelination and re-myelination in TgM83 + AAVhSNCA mouse model. Top panel: Normal OL, myelinated axon, and microglia. Second panel: alpha synuclein (αSyn) accumulation in OL causes myelin sheath to misfold and inflammation (microglia activation, astrocyte activation, T cell priming, and cytokine secretions). Third panel: Surviving OL starts to degenerate and demyelinate. Microglia is also activated in response to OL damages. Forth panel: Surviving OLs attempt to re-myelinate and expresses more myelin basic protein (MBP). Microglia activation may also participate myelin growth. Fifth panel: newly formed myelin sheath contains pre-existing αSyn, which impair oligodendrocytes’ ability to properly form functional myelin sheaths. Created in http://BioRender.com

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Acta Neuropathologica Communications

ISSN: 2051-5960

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