This article is a Preprint
Preprints are preliminary research reports that have not been certified by peer review. They should not be relied on to guide clinical practice or health-related behavior and should not be reported in news media as established information.
Preprints posted online allow authors to receive rapid feedback and the entire scientific community can appraise the work for themselves and respond appropriately. Those comments are posted alongside the preprints for anyone to read them and serve as a post publication assessment.
Interactions between SARS-CoV-2 N-protein and α-synuclein accelerate amyloid formation (preprint)
biorxiv; 2021.
Preprint
in English
| bioRxiv | ID: ppzbmed-10.1101.2021.04.12.439549
ABSTRACT
First cases that point at a correlation between SARS-CoV-2 infections and the development of Parkinson's disease have been reported. Currently it is unclear if there also is a direct causal link between these diseases. To obtain first insights into a possible molecular relation between viral infections and the aggregation of -synuclein protein into amyloid fibrils characteristic for Parkinson's disease, we investigated the effect of the presence of SARS-CoV-2 proteins on synuclein aggregation. We show, in test tube experiments, that SARS-CoV-2 S-protein has no effect on -synuclein aggregation while SARS-CoV-2 N-protein considerably speeds up the aggregation process. We observe the formation of multi-protein complexes, and eventually amyloid fibrils. Microinjection of N-protein in SHSY-5Y cells disturbed the -synuclein proteostasis and increased cell death. Our results point toward direct interactions between the N-protein of SARS-CoV-2 and -synuclein as molecular basis for the observed coincidence between SARS-CoV-2 infections and Parkinsonism.
Full text:
Available
Collection:
Preprints
Database:
bioRxiv
Main subject:
Parkinson Disease
/
Parkinsonian Disorders
/
Severe Acute Respiratory Syndrome
/
Proteostasis Deficiencies
Language:
English
Year:
2021
Document Type:
Preprint
Similar
MEDLINE
...
LILACS
LIS