Compound C1 enhances autophagy and lysosomal activity by activating TFEB, and reducing APP, APP C‐terminal fragments (CTF‐β/α), β‐amyloid peptides and tau aggregates in three AD animal models that represent β‐ APP pathology (5xFAD mice), tauopathy (P301S mice), and the APP/Tau combined pathology (3xTg‐AD mice). Here, TFEB is linked to Alzheimer disease.