Figure 7. Potential APP or Aβ-mediated mechanisms in neurodegeneration.

The figure shows a schematic of the mechanism by which APP or Aβ may be inducing neuropathology development in AD. The results described here imply that APP or Aβ (in an APP-dependent manner) induces phosphorylation and/or expression of proteins that play a role in cell cycle (PCTAIREs) or transcriptional (P-Histone H4) dysregulation in neurons. This could potentially lead to additional phosphorylation on Tau or APP, contributing to neurofibrillary tangle formation or plaque pathology development, or promote expression of genes that play a role in AD pathology development. Interfering with these signaling cascades might prevent APP-dependent activation and promotion of neurodegeneration by these downstream targets of APP.