To better understand why people develop Parkinson’s disease and Huntington’s disease we established human models using iPSCs from patients with these diseases. We were specifically interested in understanding how proteostasis, a pathway used by the cell to degrade proteins, is disrupted in these diseases. We used single cell longitudinal analysis to probe the role of components of the proteostasis network including autophagy in the patient cells. Furthermore using transcriptomic analysis and bioinformatic interrogation, we were able to identify components of the proteostasis network that were modulated in the patient cells. This work highlights targets that could lead to novel therapeutic strategies for treating these diseases.