SARS CoV-2 link to Parkinson's, N protein α-synuclein interaction

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Recent research highlights a concerning link between COVID-19 and an increased risk of developing Parkinson's disease (PD). Studies indicate that while the SARS-CoV-2 spike protein does not influence α-synuclein aggregation, the nucleocapsid protein (N-protein) significantly accelerates this process. Experiments reveal that the N-protein disrupts α-synuclein proteostasis and promotes cell death in neuronal cells. This interaction suggests a molecular basis for the observed correlation between COVID-19 infections and Parkinsonism. Additionally, the N-protein's stability makes it a potential target for vaccine development, though its implications for long-term neurological health warrant caution. Overall, the findings emphasize the need for further investigation into the long-term effects of SARS-CoV-2 on neurodegenerative diseases.
artis
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While researching S protein interactions I stumbled across a couple of recent papers studying the increased risk of developing Parkinson's after a Covid infection and the possible mechanism that plays a role there.
https://pubmed.ncbi.nlm.nih.gov/34860005/
here is the full version of the study in the link above
https://pubs.acs.org/doi/10.1021/acschemneuro.1c00666#.
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.
Neurodegenerative diseases such as Alzheimer’s disease (AD) and PD are protein aggregation diseases in which specific proteins, tau and Aβ peptide in AD and α-synuclein (αS) in PD, assemble into amyloid aggregates. Once started, the aggregation process spreads from cell to cell and the formed aggregates and deposits hamper brain function
In the absence of additional proteins, the onset of aggregation of αS is observed at time scales >240 h,In the presence of N-protein, we see a strong decrease in the time to the onset of aggregation which reduces to <24 h

The N-protein is also considered as a target for vaccine development because in the SARS family of viruses, the N-protein gene is more conserved and stable than the S-protein gene
Well I guess no more...

Our results point toward a direct interaction between the N-protein of SARS-CoV-2 and αS as a molecular basis for the observed relations between virus infections and Parkinsonism. The observed molecular interactions thus suggest that SARS-CoV-2 infections may have long-term implications and that caution is required in considering N-protein as an alternative target in vaccination strategies.

https://parkinsonsnewstoday.com/202...-alpha-synuclein-buildup-parkinsons-hallmark/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8150712/
 
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@artis, I think that your post presents a grim report, and that nevertheless it's a likeworthy post.
 
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Likes Oldman too and artis
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