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3D bioengineered neural tissue generated from patient-derived iPSCs mimics time-dependent phenotypes and transcriptional features of Alzheimer’s disease
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Abstract
Several iPSC-derived three-dimensional (3D) cultures have been generated to model Alzheimer's disease (AD). While some AD-related phenotypes have been identified across these cultures, none of them could recapitulate multiple AD-related hallmarks in one model. To date, the transcriptomic features of these 3D models have not been compared with those of human AD brains. However, these data are crucial to understanding the pertinency of these models for studying AD-related pathomechanisms over time. We developed a 3D bioengineered model of iPSC-derived neural tissue that combines a porous scaffold composed of silk fibroin protein with an intercalated collagen hydrogel to support the growth of neurons and glial cells into complex and functional networks for an extended time, a fundamental requisite for aging studies. Cultures were generated from iPSC lines obtained from two subjects carrying the familial AD (FAD) APP London mutation, two well-studied control lines, and an isogenic control. Cultures were analyzed at 2 and 4.5 months. At both time points, an elevated Aβ42/40 ratio was detected in conditioned media from FAD cultures. However, extracellular Aβ42 deposition and enhanced neuronal excitability were observed in FAD culture only at 4.5 months, suggesting that extracellular Aβ deposition may trigger enhanced network activity. Remarkably, neuronal hyperexcitability has been described in AD patients early in the disease. Transcriptomic analysis revealed the deregulation of multiple gene sets in FAD samples. Such alterations were strikingly similar to those observed in human AD brains. These data provide evidence that our patient-derived FAD model develops time-dependent AD-related phenotypes and establishes a temporal relation among them. Furthermore, FAD iPSC-derived cultures recapitulate transcriptomic features of AD patients. Thus, our bioengineered neural tissue represents a unique tool to model AD in vitro over time.
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iPSC-derived neurons from individuals with AD exhibit increased production of Aβ42, active GSK-3β, phosphorylated tau, endosomal abnormalities, and oxidative stress.
“iPSC-derived neurons from individuals with AD exhibit increased production of Aβ42, active GSK-3β, phosphorylated tau, endosomal abnormalities, and oxidative stress (12–17)”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [14]
The Results section, “Aβ42/40 ratio and extracellular Aβ42 deposition are elevated in FAD cultures” (page unavailable), reports an increased Aβ42/Aβ40 ratio in patient-derived familial AD cultures compared with controls; the Discussion also reports extracellular Aβ42 deposition. These findings support the amyloid component, though an increased ratio is not the same as increased Aβ42 production. Our copy does not report active GSK-3β, phosphorylated tau in the iPSC-derived neurons, endosomal abnormalities, or oxidative stress. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLate-stage neuropathological features, such as formation of insoluble tau and neurodegeneration, have not been reported in iPSC-derived neurons from individuals with AD.
“but late-stage neuropathological features, such as formation of insoluble tau and neurodegeneration have not been reported.”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [14]
The Background says iPSC-derived neural cultures reproduce some AD phenotypes, and the Discussion reports amyloid deposition in the authors’ 3D cultures. Neither section says whether insoluble tau or neurodegeneration had been reported in AD patient-derived iPSC neurons. Searches for those terms and late-stage hallmarks found no passage establishing the claimed absence. (LLM, conf=0.70)
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Metadata
- Authors
- Lomoio, S., Pandey, R. S., Rouleau, N., Menicacci, B., Kim, W., Cantley, W. L., Haydon, P. G., Bennett, D. A., Young-Pearse, T. L., Carter, G. W., Kaplan, D. L., & Tesco, G.
- Affiliations
- Tufts University (US)
- The Jackson Laboratory for Genomic Medicine (US)
- Wilfrid Laurier University (CA)
- Rush University Medical Center (US)
- Jackson Laboratory (US)
- Corresponding author
- Tesco, Giuseppina
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2023-06-26
- Volume
- 28
- Issue
- 12
- Pages
- 5390-5401
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC11164539
- OpenAlex
- W4382024070
- Cited by
- 25
- References
- 80
- Citations by year
- 2026: 9 · 2025: 7 · 2024: 9
- FWCI
- 4.44
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Licence
- Locations
- Molecular Psychiatry (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- U.S. Department of Health & Human Services | National Institutes of Health (1R21AG065792, 5R01AG061838, P30AG10161, P30AG72975, R01AG15819, R01AG17917, U01AG46152, U01AG61356, R01AG055909, U54AG054345)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, 3D tissue engineering, familial Alzheimer's disease, silk fibroin scaffolds, collagen gel, amyloid-beta deposition, neuronal hyperexcitability, gene expression profiling, isogenic controls, disease modeling
- MeSH terms
- Alzheimer Disease, Brain, Cell Differentiation, Humans, Neuroglia, Neurons, Phenotype, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Bioengineering, Induced Pluripotent Stem Cells, Transcriptome
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