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Conclusions Taken together, the development of pharmacological molecules that elevate endogenous Rab7 activity via inhibition of TBC1D15-mediated Rab7 inactivation could be beneficial in NPC1 disease and other neurological disorders with endolysosomal dysfunction, and allow advances to better understand how Rab7- and TBC1D15-related activities contribute to Charcot-Marie-Tooth type 2B and lysosome regeneration in neurodegeneration [87, 90,91,92,93,94]

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Given the central role of AMPK in coordinating mitophagy, pharmacological modulation of this energy-sensing kinase has emerged as a promising therapeutic strategy for age-related neuronal degeneration