Fig. 8.

Minimal mechanism for nucleation of amyloid at the surface of an amorphous aggregate. In this model the amorphous aggregate surface presents a certain number of sites (shown by an X) that are capable of binding monomer from the bulk phase to generate an amyloid structural state. This process is governed by a second-order rate constant, $k_{n{\left(A\right)}_S}$. This surface amyloid nucleus is itself capable of binding more monomer to grow the surface amyloid, governed by the second-order kinetic constant, $k_{g{\left(A\right)}_S}$. The surface amyloid is capable of shrinkage via loss of monomer from the end of the fiber or by fracture of the fiber with loss of the free fractured component to the bulk phase. For completeness, the surface amyloid is also considered able to join with bulk phase fibers governed by the second-order rate constant, $k_{j{\left(A\right)}_S}$. (Translated and reprinted with full permission from Hirota and Hall (2019), CMC Publishing Corporation)