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Cited by 276

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Seeding induced by α‐synuclein oligomers provides evidence for spreading of α‐synuclein pathology

Danzer, Karin M., Krebs, Simon K., Wolff, Michael, Birk, Gerald, Hengerer, Bastian·2009·Journal of Neurochemistry
DOI 10.1111/j.1471-4159.2009.06324.x
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Abstract

Lewy bodies, α‐synuclein (α‐syn) immunopositive intracellular deposits, are the pathological hallmark of Parkinson’s disease (PD). Interestingly, Lewybody‐like structures have been identified in fetal tissue grafts about one decade after transplantation into the striatum of PD patients. One possible explanation for the accelerated deposition of α‐syn in the graft is that the aggregation of α‐syn from the host tissue to the graft is spread by a prion disease‐like mechanism. We discuss here an in vitro model which might recapitulate some aspects of disease propagation in PD. We found here that in vitro ‐generated α‐syn oligomers induce transmembrane seeding of α‐syn aggregation in a dose‐ and time‐dependent manner. This effect was observed in primary neuronal cultures as well as in neuronal cell lines. The seeding oligomers were characterized by a distinctive lithium dodecyl sulfate‐stable oligomer pattern and could be generated in a dynamic process out of pore‐forming oligomers. We propose that α‐syn oligomers form as a dynamic mixture of oligomer types with different properties and that α‐syn oligomers can be converted into different types depending on the brain milieu conditions. Our data indicate that extracellular α‐syn oligomers can induce intracellular α‐syn aggregation, therefore we hypothesize that a similar mechanism might lead to α‐syn pathology propagation.

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Crossref · 10.1111/j.1471-4159.2009.06324.x

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7 of 7 references verified0 citation errors · 0 not checkable

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  • Oligomeric α-Syn species appear prone to uptake and spread from cell-to-cell in a prion-like manner, leading to templated misfolding of native α-Syn and formation of aggregates throughout the brain.

    “Particularly, the oligomeric α-Syn species appear to be prone to uptake and spread from cell-to-cell in a prion-like manner, leading to the templated misfolding of the native forms of α-Syn and formation of α-Syn aggregates throughout the brain, which are the defining pathological features of Parkinson’s disease (PD) and dementia with Lewy body (DLB) [12–19].”

    From LRP1 is a neuronal receptor for α-synuclein uptake and spread (2022) · cites this paper as [16]

Citations

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Research works printed but not linked: 33

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  16. Krueger R., 1998, Ala30Pro mutation in the gene encoding alpha‐synuclein in Parkinson's disease, Nat. Genet., 18, 106, 10.1038/ng0298-106 · DOI · Paper page
  17. 10.1074/jbc.M107045200 · DOI
  18. 10.1523/JNEUROSCI.0692-05.2005 · DOI
  19. 10.1016/j.biocel.2008.01.017 · DOI · Paper page
  20. 10.1523/JNEUROSCI.6202-08.2009 · DOI
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  33. 10.2174/138620706777452447 · DOI

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Metadata

Authors
Danzer, K. M., Krebs, S. K., Wolff, M., Birk, G., & Hengerer, B.
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2009-09-14
Volume
111
Issue
1
Pages
192-203
ISSN
  • 0022-3042
  • 1471-4159
DOI
10.1111/j.1471-4159.2009.06324.x
Cited by
276
References
7
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)

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