ReviewNeurochemical research2018
Modelling Sporadic Alzheimer's Disease Using Induced Pluripotent Stem Cells.
Review in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- From mice to clinical relevance: humanizing neuroscience with human-based model systems.Frontiers in cellular neuroscience · 2026Review
- In reply to Letter to the Editor from Paudel: Comment on "Changes in iPSC-Astrocyte Morphology Reflect Alzheimer's Disease Patient Clinical Markers".Stem cells (Dayton, Ohio) · 2025Article
- Exploring the role of HIF-1α on pathogenesis in Alzheimer's disease and potential therapeutic approaches.Inflammopharmacology · 2025Review
- PheSeq, a Bayesian deep learning model to enhance and interpret the gene-disease association studies.Genome medicine · 2024Article
- Effect of Honokiol on culture time and survival of Alzheimer's disease iPSC-derived neurons.BioImpacts : BI · 2024Article
- The use of induced pluripotent stem cells as a platform for the study of depression.Frontiers in psychiatry · 2024Review
- Low glucose induced Alzheimer's disease-like biochemical changes in human induced pluripotent stem cell-derived neurons is due to dysregulated O-GlcNAcylation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Altered O-GlcNAcylation and mitochondrial dysfunction, a molecular link between brain glucose dysregulation and sporadic Alzheimer's disease.Neural regeneration research · 2023Article
- Single cell transcriptomic profiling of a neuron-astrocyte assembloid tauopathy model.Nature communications · 2022Article
- Cell models for Down syndrome-Alzheimer's disease research.Neuronal signaling · 2022Review
- Therapeutic potential of glial cell line-derived neurotrophic factor and cell reprogramming for hippocampal-related neurological disorders.Neural regeneration research · 2022Review
- Human iPSC-Derived Neural Models for Studying Alzheimer's Disease: from Neural Stem Cells to Cerebral Organoids.Stem cell reviews and reports · 2022Review
- Neurons derived from individual early Alzheimer's disease patients reflect their clinical vulnerability.Brain communications · 2022Article
- Astrocytes and microglia in neurodegenerative diseases: Lessons from human in vitro models.Progress in neurobiology · 2021Review
- Alzheimer's disease treatment: The share of herbal medicines.Iranian journal of basic medical sciences · 2021Review
- Prospects of Directly Reprogrammed Adult Human Neurons for Neurodegenerative Disease Modeling and Drug Discovery: iN vs. iPSCs Models.Frontiers in neuroscience · 2020Review
- A post-translational modification signature defines changes in soluble tau correlating with oligomerization in early stage Alzheimer's disease brain.Acta neuropathologica communications · 2019Article
- Astroglial atrophy in Alzheimer's disease.Pflugers Archiv : European journal of physiology · 2019Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Developing cellular models of sporadic Alzheimer's disease (sAD) is challenging due to the unknown initiator of disease onset and the slow disease progression that takes many years to develop in vivo. The use of human induced pluripotent stem cells (iPSCs) has revolutionised the opportunities to model AD pathology, investigate disease mechanisms and screen potential drugs. The majority of this work has, however, used cells derived from patients with familial AD (fAD) where specific genetic mutations drive disease onset. While these provide excellent models to investigate the downstream pathways involved in neuronal toxicity and ultimately neuronal death that leads to AD, they provide little insight into the causes and mechanisms driving the development of sAD. In this review we compare the data obtained from fAD and sAD iPSC-derived cell lines, identify the inconsistencies that exist in sAD models and highlight the potential role of Aβ clearance mechanisms, a relatively under-investigated area in iPSC-derived models, in the study of AD. We discuss the development of more physiologically relevant models using co-culture and three-dimensional culture of iPSC-derived neurons with glial cells. Finally, we evaluate whether we can develop better, more consistent models for sAD research using genetic stratification of iPSCs and identification of genetic and environmental risk factors that could be used to initiate disease onset for modelling sAD. These considerations provide exciting opportunities to develop more relevant iPSC models of sAD which can help drive our understanding of disease mechanisms and identify new therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
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.