Alpha-synuclein fibrils amplified from multiple system atrophy and Parkinson's 
disease patient brain spread after intracerebral injection into mouse brain

Zhang, Shuyu; Dauer, Karina; Strohäker, Timo; Tatenhorst, Lars; Gomes, Lucas Caldi; Mayer, Simon; Jung, Byung Chul; Kim, Woojin S. S.; Lee, Seung-Jae; Becker, Stefan; Liesche-Starnecker, Friederike; Zweckstetter, Markus; Lingor, Paul

doi:10.1111/bpa.13196

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Alpha-synuclein fibrils amplified from multiple system atrophy and Parkinson's disease patient brain spread after intracerebral injection into mouse brain

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Becker, Stefan
Department of NMR Based Structural Biology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Zweckstetter, Markus
Department of NMR Based Structural Biology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;
Research Group of Protein Structure Determination using NMR, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Brain Pathology - 2023 - Zhang.pdf
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引用

Zhang, S., Dauer, K., Strohäker, T., Tatenhorst, L., Gomes, L. C., Mayer, S., Jung, B. C., Kim, W. S. S., Lee, S.-J., Becker, S., Liesche-Starnecker, F., Zweckstetter, M., & Lingor, P. (2023). Alpha-synuclein fibrils amplified from multiple system atrophy and Parkinson's disease patient brain spread after intracerebral injection into mouse brain. Brain Pathology, 33(5):. doi:10.1111/bpa.13196.

引用: https://hdl.handle.net/21.11116/0000-000D-BEA4-4

要旨

Parkinson's disease (PD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB) are neurodegenerative disorders with alpha-synuclein (α-syn) aggregation pathology. Different strains of α-syn with unique properties are suggested to cause distinct clinical and pathological manifestations resulting in PD, MSA, or DLB. To study individual α-syn spreading patterns, we injected α-syn fibrils amplified from brain homogenates of two MSA patients and two PD patients into the brains of C57BI6/J mice. Antibody staining against pS129-α-syn showed that α-syn fibrils amplified from the brain homogenates of the four different patients caused different levels of α-syn spreading. The strongest α-syn pathology was triggered by α-syn fibrils of one of the two MSA patients, followed by comparable pS129-α-syn induction by the second MSA and one PD patient material. Histological analysis using an antibody against Iba1 further showed that the formation of pS129-α-syn is associated with increased microglia activation. In contrast, no differences in dopaminergic neuron numbers or co-localization of α-syn in oligodendrocytes were observed between the different groups. Our data support the spreading of α-syn pathology in MSA, while at the same time pointing to spreading heterogeneity between different patients potentially driven by individual patient immanent factors.