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• W3121043932 endingPage "108615" @default.
• W3121043932 startingPage "108615" @default.
• W3121043932 abstract "Mutations in presenilin 1 (PSEN1) or presenilin 2 (PSEN2), the catalytic subunit of γ-secretase, cause familial Alzheimer's disease (fAD). We hypothesized that mutations in PSEN1 reduce Notch signaling and alter neurogenesis. Expression data from developmental and adult neurogenesis show relative enrichment of Notch and γ-secretase expression in stem cells, whereas expression of APP and β-secretase is enriched in neurons. We observe premature neurogenesis in fAD iPSCs harboring PSEN1 mutations using two orthogonal systems: cortical differentiation in 2D and cerebral organoid generation in 3D. This is partly driven by reduced Notch signaling. We extend these studies to adult hippocampal neurogenesis in mutation-confirmed postmortem tissue. fAD cases show mutation-specific effects and a trend toward reduced abundance of newborn neurons, supporting a premature aging phenotype. Altogether, these results support altered neurogenesis as a result of fAD mutations and suggest that neural stem cell biology is affected in aging and disease." @default.
• W3121043932 created "2021-01-18" @default.
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• W3121043932 date "2021-01-01" @default.
• W3121043932 modified "2023-10-16" @default.
• W3121043932 title "Familial Alzheimer’s Disease Mutations in PSEN1 Lead to Premature Human Stem Cell Neurogenesis" @default.
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• W3121043932 doi "https://doi.org/10.1016/j.celrep.2020.108615" @default.
• W3121043932 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7809623" @default.
• W3121043932 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33440141" @default.
• W3121043932 hasPublicationYear "2021" @default.

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