ArticleFrontiers in neuroscience2019
A Human Embryonic Stem Cell Model of Aβ-Dependent Chronic Progressive Neurodegeneration.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- The Phospholipase AJournal of lipid and atherosclerosis · 2026Review
- Critical Differential Expression Assessment for Individual Bulk RNA-Seq Projects.bioRxiv : the preprint server for biology · 2024Article
- Stem Cell Therapy for Alzheimer's Disease: A Scoping Review for 2017-2022.Biomedicines · 2023Article
- Fountain of youth-Targeting autophagy in aging.Frontiers in aging neuroscience · 2023Review
- LC-MS/MS Isomeric Profiling ofBiomolecules · 2022Article
- Glutamatergic Neurons Differentiated from Embryonic Stem Cells: An Investigation of Differentiation and Associated Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We describe the construction and phenotypic analysis of a human embryonic stem cell model of progressive Aβ-dependent neurodegeneration (ND) with potential relevance to Alzheimer's disease (AD). We modified one allele of the normal APP locus to directly express a secretory form of Aβ40 or Aβ42, enabling expression from this edited allele to bypass the normal amyloidogenic APP processing pathway. Following neuronal differentiation, edited cell lines specifically accumulate intracellular aggregated/oligomeric Aβ, exhibit a synaptic deficit, and have an abnormal accumulation of endolysosomal vesicles. Edited cultures progress to a stage of overt ND. All phenotypes appear at earlier culture times for Aβ42 relative to Aβ40. Whole transcriptome RNA-Seq analysis identified 23 up and 70 down regulated genes (differentially expressed genes) with similar directional fold change but larger absolute values in the Aβ42 samples suggesting common underlying pathogenic mechanisms. Pathway/annotation analysis suggested that down regulation of extracellular matrix and cilia functions is significantly overrepresented. This cellular model could be useful for uncovering mechanisms directly linking Aβ to neuronal death and as a tool to screen for new therapeutic agents that slow or prevent human ND.
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Registered trials
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