ArticleMolecular neurodegeneration2014
Stem cell derived basal forebrain cholinergic neurons from Alzheimer's disease patients are more susceptible to cell death.
Article in Molecular neurodegeneration, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed.
- Advancements in differentiation of induced pluripotent stem cells into specialized neuronal subtypes.Neural regeneration research · 2026Article
- Cholinergic Basal Forebrain Atrophy Accelerates Cognitive Decline via Cortical Thinning: The Moderating Role of Amyloid-β Pathology in Preclinical Alzheimer's Disease.Research square · 2026Article
- Cholinergic basal forebrain atrophy accelerates cognitive decline via cortical thinning: The moderating role of amyloid-β pathology in preclinical Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2025Article
- Single-nucleus analysis reveals oxidative stress in Down syndrome basal forebrain neurons at birth.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Single-nucleus analysis reveals oxidative stress in Down syndrome basal forebrain neurons at birth.bioRxiv : the preprint server for biology · 2025Article
- Mapping the future of oxidative RNA damage in neurodegeneration: Rethinking the status quo with new tools.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Subtype-specific neurons from patient iPSCs display distinct neuropathological features of Alzheimer's disease.Cell regeneration (London, England) · 2024Article
- Locomotor and gait changes in the LPS model of neuroinflammation are correlated with inflammatory cytokines in blood and brain.Journal of inflammation (London, England) · 2024Article
- Neuroprotective mechanism of trans,trans-Farnesol in an ICV-STZ-induced rat model of Alzheimer's pathology.Inflammopharmacology · 2024Article
- A systematic review of clinical efficacy and safety of cell-based therapies in Alzheimer's disease.Dementia & neuropsychologia · 2024Review
- Alzheimer's disease and synapse Loss: What can we learn from induced pluripotent stem Cells?Journal of advanced research · 2023Review
- 3D bioprinting patient-derived induced pluripotent stem cell models of Alzheimer's disease using a smart bioink.Bioelectronic medicine · 2023Article
- The Breakthroughs and Caveats of Using Human Pluripotent Stem Cells in Modeling Alzheimer's Disease.Cells · 2023Review
- Therapeutic function of a novel rat induced pluripotent stem cell line in a 6‑OHDA‑induced rat model of Parkinson's disease.International journal of molecular medicine · 2022Article
- Building in vitro models of the brain to understand the role ofLife science alliance · 2022Review
- Unraveling pathological mechanisms in neurological disorders: the impact of cell-based and organoid models.Neural regeneration research · 2022Review
- Advances in Recapitulating Alzheimer's Disease Phenotypes Using Human Induced Pluripotent Stem Cell-Based In Vitro Models.Brain sciences · 2022Review
- Article
- Cell models for Down syndrome-Alzheimer's disease research.Neuronal signaling · 2022Review
- Human iPSC-Derived Neural Models for Studying Alzheimer's Disease: from Neural Stem Cells to Cerebral Organoids.Stem cell reviews and reports · 2022Review
28 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
An early substantial loss of basal forebrain cholinergic neurons (BFCNs) is a constant feature of Alzheimer's disease (AD) and is associated with deficits in spatial learning and memory. Induced pluripotent stem cells (iPSCs) derived from patients with AD as well as from normal controls could be efficiently differentiated into neurons with characteristics of BFCNs. We used BFCNs derived from iPSCs to model sporadic AD with a focus on patients with ApoE3/E4 genotypes (AD-E3/E4). BFCNs derived from AD-E3/E4 patients showed typical AD biochemical features evidenced by increased Aβ42/Aβ40 ratios. AD-E3/E4 neurons also exhibited altered responses to treatment with γ-secretase inhibitors compared to control BFCNs or neurons derived from patients with familial AD. BFCNs from patients with AD-E3/E4 also exhibited increased vulnerability to glutamate-mediated cell death which correlated with increased intracellular free calcium upon glutamate exposure. The ability to generate BFCNs with an AD phenotype is a significant step both for understanding disease mechanisms and for facilitating screening for agents that promote synaptic integrity and neuronal survival.
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