Utilization of a stem cell‐derived 3D Alzheimer's Disease neurosphere model to investigate the role of ApoE on neuronal/Glial interaction

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Publicat a:Alzheimer's & Dementia vol. 21 (Dec 1, 2025)
Autor principal: Lee, Christopher
Altres autors: Wendt, Stefan, Lin, Ada J, Huang, Jessica, Nygaard, Haakon B.
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John Wiley & Sons, Inc.
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Accés en línia:Citation/Abstract
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022 |a 1552-5260 
022 |a 1552-5279 
024 7 |a 10.1002/alz70855_105390  |2 doi 
035 |a 3286372090 
045 0 |b d20251201 
100 1 |a Lee, Christopher  |u University of British Columbia, Vancouver, BC, Canada, 
245 1 |a Utilization of a stem cell‐derived 3D Alzheimer's Disease neurosphere model to investigate the role of ApoE on neuronal/Glial interaction 
260 |b John Wiley & Sons, Inc.  |c Dec 1, 2025 
513 |a Journal Article 
520 3 |a Background Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by a progressive deterioration in multiple facets of cognitive function. Genome‐wide association studies have confirmed that the strongest genetic risk factor for AD is polymorphism in the apolipoprotein E encoding gene APOE, with the ε3 allele being considered neutral risk, ε2 and the more recently described APOE ε3 Christchurch mutation conferring protection, and ε4 conferring risk. It is unclear exactly how APOE increases AD risk or hastens AD development, but elucidating these mechanisms is critical in developing a possible therapy. In this work we investigated APOE in an in vitro induced human pluripotent stem cell (hiPSC)‐derived 3D neurosphere model system containing neurons, astrocytes, and microglia to effectively recreate the natural cellular environment. Method Neuronal/astrocyte neurospheres were formed from hiPSCs harboring homozygous APOE variants for ε2, ε3, ε4, and ε3christchurch (ε3ch) and matured over a 60‐day period, while hiPSC‐derived microglia for the same isotypes were separately differentiated and applied to spheres. AD‐like pathology was investigated through a chronic treatment of synthetic oligomeric amyloid‐beta treated over 5‐weeks. Result Expression of ApoE rose with oligomeric amyloid‐beta treatment, and variation in resistance to chronic amyloid‐beta treatment‐induced functional degeneration was found to mimic natural resistance, with ε2 > ε4 displaying delayed decline of neuronal activity; this was observed both with‐ and without the presence of microglia. Conclusion This work provides validation of a protocol for the generation of hiPSC‐derived neurospheres consisting of neurons, astrocytes and microglia. Demonstrating its value as a disease model system for the study of ApoE and AD. 
653 |a Cognitive functioning 
653 |a Stem cells 
653 |a Alzheimer's disease 
653 |a Resistance 
653 |a Genomics 
653 |a Encoding (Cognitive process) 
653 |a Genetics 
653 |a Risk 
653 |a Deterioration 
653 |a Pathology 
653 |a Neurons 
653 |a Variants 
653 |a Encoding 
653 |a Genetic susceptibility 
653 |a Health risk assessment 
653 |a Disease 
653 |a Apolipoproteins 
653 |a Risk factors 
653 |a Medical model 
700 1 |a Wendt, Stefan  |u University of British Columbia, Vancouver, BC, Canada, 
700 1 |a Lin, Ada J  |u University of British Columbia, Vancouver, BC, Canada, 
700 1 |a Huang, Jessica  |u University of British Columbia, Vancouver, BC, Canada, 
700 1 |a Nygaard, Haakon B.  |u University of British Columbia, Vancouver, BC, Canada, 
773 0 |t Alzheimer's & Dementia  |g vol. 21 (Dec 1, 2025) 
786 0 |d ProQuest  |t Consumer Health Database 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3286372090/abstract/embedded/L8HZQI7Z43R0LA5T?source=fedsrch 
856 4 0 |3 Full Text - PDF  |u https://www.proquest.com/docview/3286372090/fulltextPDF/embedded/L8HZQI7Z43R0LA5T?source=fedsrch