Overexpression of TRPML1, or treatment with AMPK inhibitors and mTOR activators can downregulate ALR-associated proteins, improve recognition and memory impairment, and alleviate neuronal apoptosis, suggesting that TRPML1 participates in the pathogenesis of AD by modulating autophagy through AMPK-mTOR signaling [197]. This evidence concerns the gene MCOLN1 and Alzheimer disease.