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Toxicity of extracellular alpha-synuclein is independent of intracellular alpha-synuclein

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F22%3A00133949" target="_blank" >RIV/00216224:14740/22:00133949 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.nature.com/articles/s41598-022-25790-2" target="_blank" >https://www.nature.com/articles/s41598-022-25790-2</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/s41598-022-25790-2" target="_blank" >10.1038/s41598-022-25790-2</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Toxicity of extracellular alpha-synuclein is independent of intracellular alpha-synuclein

  • Original language description

    Parkinson ' s disease (PD) pathology progresses throughout the nervous system. Whereas motor symptoms are always present, there is a high variability in the prevalence of non-motor symptoms. It has been postulated that the progression of the pathology is based on a prion-like disease mechanism partly due to the seeding effect of endocytosed-alpha-synuclein (ASYN) on the endogenous ASYN. Here, we analyzed the role of endogenous ASYN in the progression of PD-like pathology in vivo and in vitro and compared the effect of endocytosed-ASYN as well as paraquat and rotenone on primary enteric, dopaminergic and cortical neurons from wild-type and ASYN-KO mice. Our results show that, in vivo, pathology progression did not occur in the absence of endogenous ASYN. Remarkably, the damage caused by endocytosed-ASYN, rotenone or paraquat was independent from endogenous ASYN and related to the alteration of the host ' s mitochondrial membrane potential. Dopaminergic neurons were very sensitive to these noxae compared to other neuronal subtypes. These results suggest that ASYN-mitochondrial interactions play a major role in initiating the pathological process in the host neuron and endogenous ASYN is essential for the transsynaptical transmission of the pathology. Our results also suggest that protecting mitochondrial function is a valid primary therapeutic target.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30103 - Neurosciences (including psychophysiology)

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2022

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Nature Scientific Reports

  • ISSN

    2045-2322

  • e-ISSN

  • Volume of the periodical

    12

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    DE - GERMANY

  • Number of pages

    16

  • Pages from-to

    1-16

  • UT code for WoS article

    000971311200020

  • EID of the result in the Scopus database

    2-s2.0-85144263595