Fig. 7: RHBDL4 in the context of an APP transgenic AD model.
From: Loss of the APP regulator RHBDL4 preserves memory in an Alzheimer’s disease mouse model
RHBDL4 ablation in an AD model increases APP expression and the production of amyloidogenic processing markers (β-CTFs and Aβ40). This confirms the relevance of RHBDL4 as a physiologically relevant modulator of APP. However, early in the pathology, β-catenin activity is normalized, and cognition is maintained in the absence of RHBDL4, despite the expected deleterious effects of the Aβ accumulation on cognition. These findings are in concordance with increased RHBDL4 expression in late-stage AD patients (Fig. 1), which negatively correlates with cognition. Thus, RHBDL4 may influence cognition by balancing the amounts of APP processing versus β-catenin signaling.
