Autophagy plays a crucial role in intracellular clearance and quality control. In mice, neuronal cell-specific deletion of autophagy genes causes neurological dysfunction with the accumulation of protein aggregates and dysfunctional organelles. One important question is whether these neurological dysfunctions due to autophagy defects can be reversed when autophagy is restored. To address this issue, we developed a novel mouse model in which autophagic activity can be rapidly and reversibly regulated in a doxycycline-dependent manner. Suppressing autophagy resulted in changes to the proteome and transcriptome, accumulation of inclusion bodies, and axonal swelling, all of which were largely ameliorated after autophagy restoration. Consistent with these cellular abnormalities, autophagy suppression caused motor and cognitive dysfunction, which was also significantly reversed by autophagy restoration. These results suggest that neurological dysfunctions caused by autophagy defects can be reversed by autophagy restoration and provide a rationale for therapeutically targeting autophagy in neurodegenerative diseases.