Abstract
We used double immunocytochemistry for α-synuclein and markers of sympathoexcitatory neurons, oligodendrocytes, iron metabolism, and autophagy to study putative neuropathological interactions in multiple system atrophy. We focused in the rostral ventrolateral medulla as a prototype vulnerable region. We found that loss of C1 neurons and oligodendrocytes related to glial cytoplasmic inclusion accumulation, downregulation of iron transport, and upregulation of autophagy and ferritin expression in these area.
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Acknowledgments
Selective cell vulnerability in MSA: insight from cases with associated lewy body disease, funded by the CurePSP foundation and Mayo Funds.
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The authors declare that they have no conflict of interest. Study approved by the Mayo Clinic IRB#08-000783.
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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
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Informed consent was obtained from all individual participants included in the study.
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Benarroch, E.E., Schmeichel, A.M., Parisi, J.E. et al. Putative neuropathological interactions in MSA: focus in the rostral ventrolateral medulla. Clin Auton Res 25, 77–80 (2015). https://doi.org/10.1007/s10286-015-0273-2
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DOI: https://doi.org/10.1007/s10286-015-0273-2