In recent years, studies have shown that the gene editing ability of NSCs provides an important platform for the study of AD pathomechanisms, and potential therapeutic targets can be screened by editing AD risk genes, such as APP and PSEN1, and mimicking the process of β-amyloid deposition and abnormal phosphorylation of tau proteins in mouse and human cell models (Yeapuri et al., 2025). This evidence concerns the gene PSEN1 and Alzheimer disease.