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Main text (Cell Stem Cell 31, 1162–1174.e1–e9; August 1, 2024) Our original manuscript erroneously listed the concentration of SB431542 as 10 mM instead of 10 μM in the dopamine neuron differentiation section of the Method details section. We apologize for this error, which has been corrected in the original version. The corrected manuscript also includes additional changes to comply with the open access policy requirements of the funder (Aligning Science Across Parkinson’s disease).
Highlights • CRISPR screen uncovers candidate mediators of cellular aging and neurodegeneration • Inhibiting neddylation in hPSC-derived neurons induces age-associated phenotypes • Neddylation and genetic vulnerability synergize to trigger late-onset pathologies • Strategy is applied to modeling late-onset phenotypes in hPSC models of AD and PD Summary Aging is the biggest risk factor for the development of Alzheimer’s disease (AD).
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