English: Figure 4. Assumed effect of muscarinic acetylcholine receptor agonists such as cevimeline on the mAChRs in association with AD. The agonist-mediated activation of mAChRs result in increased activity of PKC via same pathway as described in the previous figure. The increased activity of PKC via a cascade of reactions activates ERK, which in turn activates α-secretase. The APP is cleavaged predominantely by α-secretase to produce a non-amyloidogenic P3 peptide. In addition, the activated PKC inhibits γ-secretase activity, leading to a decrease of Aβ in the amyloidogenic pathway. Abbreviations: Aβ, amyloid beta; AICD, APP intracellular domain; APP, amyloid precursor protein; CTFα (C83), C-terminal fragment α; CTFβ (C99), C-terminal fragment β; DAG, diacylglycerol; ERK, extracellular regulated kinase; Gq/11, G proteins; IP3, inositiol trisphosphate; MEK, mitogen-activated protein kinase kinase; P3, non-amyloidogenic peptidic fragment; PIP2; phosphatidylinositol 4,5-bisphosphate; PLC, phospholipase C; PKC, protein kinase C; Raf, serine/threonine specific protein kinases; Ras, small GTP-binding proteins; sAPP/α/β, secreted APP/α/β. Created with BioRender.com.