ArticleCell death & disease2021
Genetically engineered MAPT 10+16 mutation causes pathophysiological excitability of human iPSC-derived neurons related to 4R tau-induced dementia.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Tau pathology in epilepsy: emerging mechanisms and translational opportunities.Brain : a journal of neurology · 2026Review
- Bezafibrate treatment rescues neurodevelopmental and neurodegenerative defects in 3D cortical organoid model of MAPT frontotemporal dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Immunization targeting diseased proteins in synucleinopathy and tauopathy: insights from clinical trials.Translational neurodegeneration · 2025Review
- Astrocytic RNA editing regulates the host immune response to alpha-synuclein.Science advances · 2025Article
- Brain neurons internalise polymeric micron-sized capsules: Insights fromMaterials today. Bio · 2025Article
- Modeling and correction of protein conformational disease in iPSC-derived neurons through personalized base editing.Molecular therapy. Nucleic acids · 2025Article
- miR-92a-3p and miR-320a are Upregulated in Plasma Neuron-Derived Extracellular Vesicles of Patients with Frontotemporal Dementia.Molecular neurobiology · 2025Article
- Understanding retinal tau pathology through functional 2D and 3D iPSC-derived in vitro retinal models.Acta neuropathologica communications · 2025Article
- Development of MAPT S305 mutation human iPSC lines exhibiting elevated 4R tau expression and functional alterations in neurons and astrocytes.Cell reports · 2024Article
- A cell autonomous regulator of neuronal excitability modulates tau in Alzheimer's disease vulnerable neurons.Brain : a journal of neurology · 2024Article
- Ferritin nanocage-enabled detection of pathological tau in living human retinal cells.Scientific reports · 2024Article
- Synaptic gene expression changes in frontotemporal dementia due to themedRxiv : the preprint server for health sciences · 2024Article
- Conserved gene signatures shared amongFrontiers in molecular biosciences · 2023Article
- Defective proteostasis in induced pluripotent stem cell models of frontotemporal lobar degeneration.Translational psychiatry · 2022Article
- Deciphering tau-related dementia using human iPSC lines: electrophysiological perspectives of future studies.Neural regeneration research · 2022Article
- Protein aggregation and calcium dysregulation are hallmarks of familial Parkinson's disease in midbrain dopaminergic neurons.NPJ Parkinson's disease · 2022Article
- Presenilin-1 F105C mutation leads to tau accumulation in human neurons via the Akt/mTORC1 signaling pathway.Cell & bioscience · 2022Article
- Human Induced Pluripotent Stem Cell Models of Frontotemporal Dementia With Tau Pathology.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Human iPSC lines represent a powerful translational model of tauopathies. We have recently described a pathophysiological phenotype of neuronal excitability of human cells derived from the patients with familial frontotemporal dementia and parkinsonism (FTDP-17) caused by the MAPT 10+16 splice-site mutation. This mutation leads to the increased splicing of 4R tau isoforms. However, the role of different isoforms of tau protein in initiating neuronal dementia-related dysfunction, and the causality between the MAPT 10+16 mutation and altered neuronal activity have remained unclear. Here, we employed genetically engineered cells, in which the IVS10+16 mutation was introduced into healthy donor iPSCs to increase the expression of 4R tau isoform in exon 10, aiming to explore key physiological traits of iPSC-derived MAPT IVS10+16 neurons using patch-clamp electrophysiology and multiphoton fluorescent imaging techniques. We found that during late in vitro neurogenesis (from ~180 to 230 days) iPSC-derived cortical neurons of the control group (parental wild-type tau) exhibited membrane properties compatible with "mature" neurons. In contrast, MAPT IVS10+16 neurons displayed impaired excitability, as reflected by a depolarized resting membrane potential, an increased input resistance, and reduced voltage-gated Na
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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.