Familial Alzheimer’s disease mutations in PSEN1 lead to premature human stem cell neurogenesis
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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.
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The reduction in amyloid beta production by NB-360 in oligodendrocytes is similar to what has previously been shown in human iPSC-derived neurons upon administration of NB-360 or similar BACE inhibitors.
“Notably, this reduction in Aβ production is similar to what has previously been shown in human iPSC-derived neurons upon administration of NB-360 or similar BACE inhibitors [21–24]”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [23]
The Results section on secretase inhibition reports treating iPSC-derived neural precursors with the BACE inhibitor LY2886721, but reports effects on proliferation and neurogenesis, not Aβ production. The Methods describe an Aβ42 assay without linking it to an inhibitor-induced reduction. Searches for NB-360 and reduced Aβ after BACE inhibition found no passage establishing the claimed neuronal result. (LLM, conf=0.72)
Experimental — accuracy not yet measuredPSEN1 mutations can affect neuronal differentiation in iPS cell-derived systems, such as cerebral organoids, through reduced Notch signaling and premature aging phenotypes.
“PSEN1 mutations can affect neuronal differentiation in iPS cell-derived systems, such as cerebral organoids, through reduced Notch signaling and premature aging phenotypes (Arber et al., 2021).”
From APOE3 Christchurch modulates β-catenin/Wnt signaling in iPS cell-derived cerebral organoids from Alzheimer’s cases (2024) · cites this paper as Arber et al., 2021
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- Authors
- Arber, C., Lovejoy, C., Harris, L., Willumsen, N., Alatza, A., Casey, J. M., Lines, G., Kerins, C., Mueller, A. K., Zetterberg, H., Hardy, J., Ryan, N. S., Fox, N. C., Lashley, T., & Wray, S.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- The Francis Crick Institute (GB)
- National Hospital for Neurology and Neurosurgery (GB)
- Sahlgrenska University Hospital (SE)
- UK Dementia Research Institute (GB)
- Corresponding author
- Arber, Charles
- Wray, Selina
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 34
- Issue
- 2
- Pages
- 108615
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC7809623
- OpenAlex
- W3121043932
- Cited by
- 116
- References
- 76
- Citations by year
- 2026: 19 · 2025: 23 · 2024: 29 · 2023: 17 · 2022: 17 · 2021: 11
- FWCI
- 6.92
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- Alzheimer’s Research UK
- Alzheimer's Society
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- familial Alzheimer's disease, PSEN1 mutations, presenilin 1, gamma-secretase, Notch signaling, induced pluripotent stem cells, brain organoids, cortical differentiation, adult hippocampal neurogenesis, neural stem cells, aging
- MeSH terms
- Alzheimer Disease, Cells, Cultured, Humans, Mutation, Receptors, Notch, Presenilin-1, Amyloid Precursor Protein Secretases, Neurogenesis, Induced Pluripotent Stem Cells, Neural Stem Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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