Interactions between SARS-CoV-2 N-Protein and α-Synuclein Accelerate Amyloid Formation.
ACS Chem Neurosci
; 13(1): 143-150, 2022 01 05.
Article
in English
| MEDLINE | ID: covidwho-1637498
Preprint
This scientific journal article is probably based on a previously available preprint. It has been identified through a machine matching algorithm, human confirmation is still pending.
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This scientific journal article is probably based on a previously available preprint. It has been identified through a machine matching algorithm, human confirmation is still pending.
See preprint
ABSTRACT
First cases that point at a correlation between SARS-CoV-2 infections and the development of Parkinson's disease (PD) have been reported. Currently, it is unclear if there is also a direct causal link between these diseases. To obtain first insights into a possible molecular relation between viral infections and the aggregation of α-synuclein protein into amyloid fibrils characteristic for PD, we investigated the effect of the presence of SARS-CoV-2 proteins on α-synuclein aggregation. We show, in test tube experiments, that SARS-CoV-2 spike protein (S-protein) has no effect on α-synuclein aggregation, while SARS-CoV-2 nucleocapsid protein (N-protein) considerably speeds up the aggregation process. We observe the formation of multiprotein complexes and eventually amyloid fibrils. Microinjection of N-protein in SH-SY5Y cells disturbed the α-synuclein proteostasis and increased cell death. Our results point toward direct interactions between the N-protein of SARS-CoV-2 and α-synuclein as molecular basis for the observed correlation between SARS-CoV-2 infections and Parkinsonism.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Alpha-Synuclein
/
Coronavirus Nucleocapsid Proteins
/
Amyloid
Limits:
Humans
Language:
English
Journal:
ACS Chem Neurosci
Year:
2022
Document Type:
Article
Affiliation country:
Acschemneuro.1c00666
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