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bioRxiv · 10.1101/2025.08.08.669385

Modulation of Aβ1-42 Aggregation by a SARS-COV-2 Protein Fragment

Premathilaka, M. B.·Hansmann, U. H. E.
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Abstract

A number of studies have pointed out to the possibility that SARS-COV-2 infections could trigger amyloid diseases such as Parkinsons disease or type-II diabetes. In the present study we probe this question for Alzheimers disease which is connected with presence of amyloids rich in A{beta}-peptides. For this purpose, we study by way of molecular dynamics simulations the interaction between the fragment FKNIDGYFKI of the Spike protein with A{beta}1-42 monomer and two fibril models, one patient-derived and one synthetic. Our results are compared with previous studies of other amyloid-forming proteins to identify commonalities and differences in the modulation of amyloid-formation by the viral protein fragment. Table of Contents Figure O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=111 SRC="FIGDIR/small/669385v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@e9d5e7org.highwire.dtl.DTLVardef@1da47baorg.highwire.dtl.DTLVardef@19b1ad4org.highwire.dtl.DTLVardef@1fe5832_HPS_FORMAT_FIGEXP M_FIG C_FIG

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Premathilaka, M. B., Hansmann, U. H. E.. 2025-08-11. Modulation of Aβ1-42 Aggregation by a SARS-COV-2 Protein Fragment. https://doi.org/10.1101/2025.08.08.669385

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