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

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