ArticleStem cell reports2015
Distinct Neurodegenerative Changes in an Induced Pluripotent Stem Cell Model of Frontotemporal Dementia Linked to Mutant TAU Protein.
Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 99 citations in OpenAlex.
- Review
- Multi-omic phenotyping of MAPT V337M neurons reveals early changes in axonogenesis and tau phosphorylation.NPJ dementia · 2026Article
- Elevated SGK1 increases Tau phosphorylation and microtubule instability in Alzheimer's patient-derived cortical neurons.Molecular psychiatry · 2026Article
- Multi-omic phenotyping of iPSC-derived neurons harboring thebioRxiv : the preprint server for biology · 2025Article
- Generation of human induced pluripotent stem cell-derived cortical neurons expressing the six tau isoforms.Journal of Alzheimer's disease : JAD · 2025Article
- Article
- Single-cell transcriptomic and neuropathologic analysis reveals dysregulation of the integrated stress response in progressive supranuclear palsy.Acta neuropathologica · 2024Article
- A pathogenic mutation in the ALS/FTD gene VCP induces mitochondrial hypermetabolism by modulating the permeability transition pore.Acta neuropathologica communications · 2024Article
- iPSC-induced neurons with the V337M MAPT mutation are selectively vulnerable to caspase-mediated cleavage of tau and apoptotic cell death.Molecular and cellular neurosciences · 2024Article
- Xenografted human iPSC-derived neurons with the familial Alzheimer's disease APPActa neuropathologica · 2024Article
- Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons.Cell stem cell · 2024Article
- MAPT Mutations V337M and N297K Alter Organelle Trafficking in Frontotemporal Dementia Patient-Specific Motor Neurons.Biomedicines · 2024Article
- Decoding Neurodegeneration: A Comprehensive Review of Molecular Mechanisms, Genetic Influences, and Therapeutic Innovations.International journal of molecular sciences · 2023Review
- Intraneuronal tau aggregation induces the integrated stress response in astrocytes.Journal of molecular cell biology · 2023Article
- A 3D human co-culture to model neuron-astrocyte interactions in tauopathies.Biological procedures online · 2023Article
- RNA methyltransferase NSun2 deficiency promotes neurodegeneration through epitranscriptomic regulation of tau phosphorylation.Acta neuropathologica · 2023Article
- Defective proteostasis in induced pluripotent stem cell models of frontotemporal lobar degeneration.Translational psychiatry · 2022Article
- DNA methylation signatures of Alzheimer's disease neuropathology in the cortex are primarily driven by variation in non-neuronal cell-types.Nature communications · 2022Article
- Modelling the Human Blood-Brain Barrier in Huntington Disease.International journal of molecular sciences · 2022Article
- Recapitulation of endogenous 4R tau expression and formation of insoluble tau in directly reprogrammed human neurons.Cell stem cell · 2022Article
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
Frontotemporal dementia (FTD) is a frequent form of early-onset dementia and can be caused by mutations in MAPT encoding the microtubule-associated protein TAU. Because of limited availability of neural cells from patients' brains, the underlying mechanisms of neurodegeneration in FTD are poorly understood. Here, we derived induced pluripotent stem cells (iPSCs) from individuals with FTD-associated MAPT mutations and differentiated them into mature neurons. Patient iPSC-derived neurons demonstrated pronounced TAU pathology with increased fragmentation and phospho-TAU immunoreactivity, decreased neurite extension, and increased but reversible oxidative stress response to inhibition of mitochondrial respiration. Furthermore, FTD neurons showed an activation of the unfolded protein response, and a transcriptome analysis demonstrated distinct, disease-associated gene expression profiles. These findings indicate distinct neurodegenerative changes in FTD caused by mutant TAU and highlight the unique opportunity to use neurons differentiated from patient-specific iPSCs to identify potential targets for drug screening purposes and therapeutic intervention.
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