Have a read


Spikes and prions / neurodegenerative disease. I'll not say anything more. I warned you all.

Mrs Doom was ABSOLUTELY CLEAR on the risks of spikes and the brain.



[link to www.ncbi.nlm.nih.gov (secure)]




Next, we look for the interaction of S1-heparin complex to the amyloid forming HBPs (Table 2). Interestingly, the SARS-CoV-2 S1-heparin complex binds more strongly to these HBPs when compared to the docking strength of S1-HBPs complex. This result clearly suggests that heparin binding to S1 protein allows the amyloid forming HBPs to bind more strongly to S1 protein. The docking scores indicate that α-syn binds more strongly to S1-heparin complex followed by RRM > Aβ >Prion > Tau (Table 2).

Next, we calculated the binding affinities (Kd) of the docked structures using the PRODIGY server [18] (Table 1). The binding affinities of S1-complexes showed that S1-α-Syn complex has a stronger binding affinity (2.3 × 10−10 M) among other complexes, followed by S1-prion (3.9 × 10−10 M), S1-Aβ (8.5 × 10−10 M), S1-RRM (9.7 × 10−10 M), and S1-tau (3.5 × 10−9 M). This indicates that α-Syn has a more favourable binding affinity to SARS-CoV-2 S1 protein. The binding affinity of S1 to FGF2 indicates the favourable binding with the Kd of 2.2 × 10−10 M.

Further, the binding energy scores (Kd) of S1 complexes were predicted as a function of temperature. There was an obvious increase in Kd as the temperature increased from 25 °C to 40 °C, indicating a decrease in binding affinity for SARS-CoV-2 S1 protein complexes. At higher temperature also, α-Syn appeared to have stronger binding affinity for S1 protein (6.6 × 10−10 M) followed by Prion (1.1 × 10−9 M), Aβ (2.3 × 10−9 M), RRM (2.6 × 10−9 M), and Tau protein (8.8 × 10−9 M).

Furthermore, the predicted Kd for S1-α-Syn and S1-tau complex was less affected as the temperature increased from 25 °C to 40 °C, in contrast to Aβ, prion and RRM. Increase in temperature usually disrupts the noncovalent interactions between a protein-protein complex, despite that, the decrease in binding affinity across the temperatures was less apparent for the α-Syn complex with S1. This suggests a stable interaction between α-synuclein to SARS-CoV-2 S1 protein.