Impairments in intracellular quality control mechanisms, including autophagy, underlie various neurodegenerative pathologies. Despite numerous studies aiming to slow their progression, it remains largely unclear whether neuronal functions and intracellular quality can be reversed once impaired. Here, we investigated the reversibility of such pathologies in a novel mouse model in which autophagy can be rapidly and reversibly regulated. To develop autophagy-inducible mice, a tetracycline operator (tetO) element was inserted into the first non-coding exon of ATG101. Combined with a tetracycline-controlled transcriptional silencer (tTS), this genetic modification enabled rapid and reversible control of autophagy in the brain. Suppressing autophagy led to proteome changes and inclusion body accumulation, both of which were almost completely reversed after autophagy restoration, highlighting the high elasticity of neuronal proteostasis. Axonal swellings in Purkinje neurons were similarly ameliorated after autophagy rescue. Consistent with these cellular abnormalities, autophagy suppression caused motor and cognitive dysfunction, which was also significantly reversed upon autophagy restoration. Our findings elucidate the remarkable resilience of neuronal function and quality and provide insight into therapeutic targeting autophagy in neurodegenerative diseases.