ReviewNeurobiology of disease2020
Using human induced pluripotent stem cells (hiPSCs) to investigate the mechanisms by which Apolipoprotein E (APOE) contributes to Alzheimer's disease (AD) risk.
Review in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Using iPSC models to examine neuron-glia interactions in neurodegenerative diseases.Bioscience reports · 2026Review
- Microglia-to-neuron signaling linksProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Microglia-to-neuron signaling increases lipid droplet metabolism, enhancing neuronal network activity.bioRxiv : the preprint server for biology · 2025Article
- Advancing Care in Alzheimer's Disease: Current Treatments and Their Impact on Quality of Life.Cureus · 2025Review
- Biomimetic Approaches in the Development of Optimised 3D Culture Environments for Drug Discovery in Cardiac Disease.Biomimetics (Basel, Switzerland) · 2025Review
- Early- and Late-Onset Alzheimer's Disease: Two Sides of the Same Coin?Diseases (Basel, Switzerland) · 2024Review
- TFR1 knockdown alleviates iron overload and mitochondrial dysfunction during neural differentiation of Alzheimer's disease-derived induced pluripotent stem cells by interacting with GSK3B.European journal of medical research · 2024Article
- Potential use of iPSCs for disease modeling, drug screening, and cell-based therapy for Alzheimer's disease.Cellular & molecular biology letters · 2023Review
- Potential Modifying Effect of theInternational journal of molecular sciences · 2023Article
- PINE-TREE enables highly efficient genetic modification of human cell lines.Molecular therapy. Nucleic acids · 2023Article
- The Multifaceted Role of WNT Signaling in Alzheimer's Disease Onset and Age-Related Progression.Cells · 2023Review
- Ethical Aspects of Human Induced Pluripotent Stem Cells and Alzheimer's Disease: Potentials and Challenges of a Seemingly Harmless Method.Journal of Alzheimer's disease reports · 2023Article
- Building in vitro models of the brain to understand the role ofLife science alliance · 2022Review
- Exploring the Role of Lipid-Binding Proteins and Oxidative Stress in Neurodegenerative Disorders: A Focus on the Neuroprotective Effects of Nutraceutical Supplementation and Physical Exercise.Antioxidants (Basel, Switzerland) · 2022Review
- Therapeutic potential of glial cell line-derived neurotrophic factor and cell reprogramming for hippocampal-related neurological disorders.Neural regeneration research · 2022Review
- Apolipoprotein E and Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022Review
- The role of Alzheimer's disease risk genes in endolysosomal pathways.Neurobiology of disease · 2022Review
- Article
- APOE2 mitigates disease-related phenotypes in an isogenic hiPSC-based model of Alzheimer's disease.Molecular psychiatry · 2021Article
- Cytosine and adenosine base editing in human pluripotent stem cells using transient reporters for editing enrichment.Nature protocols · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Although the biochemical and pathological hallmarks of Alzheimer's disease (AD), such as axonal transport defects, synaptic loss, and selective neuronal death, are well characterized, the underlying mechanisms that cause AD are largely unknown, thereby making it difficult to design effective therapeutic interventions. Genome-wide association studies (GWAS) studies have identified several factors associated with increased AD risk. Of these genetic factors, polymorphisms in the Apolipoprotein E (APOE) gene are the strongest and most prevalent. While it has been established that the ApoE protein modulates the formation of amyloid plaques and neurofibrillary tangles, the precise molecular mechanisms by which various ApoE isoforms enhance or mitigate AD onset and progression in aging adults are yet to be elucidated. Advances in cellular reprogramming to generate disease-in-a-dish models now provide a simplified and accessible system that complements animal and primary cell models to study ApoE in the context of AD. In this review, we will describe the use and manipulation of human induced pluripotent stem cells (hiPSCs) in dissecting the interaction between ApoE and AD. First, we will provide an overview of the proposed roles that ApoE plays in modulating pathophysiology of AD. Next, we will summarize the recent studies that have employed hiPSCs to model familial and sporadic AD. Lastly, we will speculate on how current advances in genome editing technologies and organoid culture systems can be used to improve hiPSC-based tools to investigate ApoE-dependent modulation of AD onset and progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.