C1, an mTOR-independent activator of TFEB, efficiently reduces APP, APP C-terminal fragments (CTF-β/α), Aβ and Tau aggregates in three AD animal models, such as beta-amyloid precursor protein pathology (5xFAD mice), tauopathy (P301S mice) and the APP/Tau combined pathology (3xTg-AD mice). This evidence concerns the gene TFEB and Alzheimer disease.