Modulation of Abeta(1-42) Aggregation by a SARS-COV-2 Protein Fragment

Abstract

A number of studies have pointed out to the possibility that SARS-COV-2 infections could trigger amyloid diseases such as Parkinson’s disease or type-II diabetes. In the present study we probe this question for Alzheimer’s disease which is connected with presence of amyloids rich in Ab- peptides. For this purpose, we study by way of molecular dynamics simulations the interaction between the fragment FKNIDGYFKI of the Spike protein with Ab1-42 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.