Fig. 1. A schematic representation of the minimal model of coupled Aβ aggregation and inflammation used in this study.

The following events (and related parameters) are shown: (i) generation of Aβ monomers by neurons and astrocytes (rate, $k_{+}$), (ii) clearance (degradation) of Aβ (rate constant for Aβ monomers, $k_{-}$, scaled down by factors ${\gamma }_o$ for oligomers and ${\gamma }_f$ for fibrils), (iii) primary nucleation (forward rate constant, $j_1^{n1}$, with the superscript $n1$ representing the molecular order with respect to Aβ monomers; reverse rate constant, $j_{-1}^1$, with superscript representing the molecular order of 1 with respect to Aβ oligomers), (iv) oligomer conversion (rate constant, $j_2^{\mathit{nconv},1}$, with the superscripts $\mathit{nconv}$ and 1 representing molecular orders with respect to Aβ monomers and oligomers, respectively), (v) elongation (rate constant, $j_3^{\mathrm{1,1}}$, with the superscripts 1 and 1 representing molecular orders with respect to Aβ monomers and fibrils, respectively), (vi) secondary nucleation (rate constant, $j_4^{n\mathrm{2,1}}$, with the superscripts $n2$ and 1 representing molecular orders with respect to Aβ monomers and fibrils, respectively), (vii) generation of inflammation by Aβ oligomers and fibrils (governed by the weight factors ${\delta }_o$ and ${\delta }_f$, respectively), (viii) modulation of rates of Aβ generation and clearance by inflammation, and (ix) self-inhibitory mechanisms of inflammation (represented by $k_{\mathit{infl}}$).