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Significance Ubiquitin C-terminal hydrolase L1 (UCH-L1) is important for neuronal development. Mechanistically, UCH-L1 has an inhibitory effect on mTOR-containing complexes thereby controlling protein synthesis and degradation. Neurodegeneration arising from UCH-L1 deficiency is the result of an early increased protein turnover (synthesis and decay), which strains neurons by increasing energy requirement and endoplasmic reticulum stress. Rapamycin treatment during a critical developmental period partially rescues motor degeneration in adulthood.

Ubiquitin C-terminal hydrolase L1 (UCH-L1) loss causes neurodegeneration by altering protein turnover in the first postnatal weeks