ArticleCell reports2024
Development of MAPT S305 mutation human iPSC lines exhibiting elevated 4R tau expression and functional alterations in neurons and astrocytes.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Distribution of Big Tau Isoforms in the Human Central and Peripheral Nervous System.Annals of neurology · 2026Article
- Astrocytes orchestrate neuroprotection and pathogenesis via bidirectional neuronal interactions in Parkinson's disease.Journal of physiology and biochemistry · 2026Review
- Scalable human neuronal models of tauopathy producing endogenous seed-competent 4R tau.Science advances · 2026Article
- Using iPSC models to examine neuron-glia interactions in neurodegenerative diseases.Bioscience reports · 2026Review
- circPDE4B downregulation triggers GEMIN5‑dependent translational stress response and autophagy to reduce MAPT pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Distinct tau filament folds in familial frontotemporal dementia due to thebioRxiv : the preprint server for biology · 2026Article
- Astrocytes in Parkinson's Disease: From Guardians to Accomplices.Clinical interventions in aging · 2026Review
- Mutant MAPT Induces rDNA Transcriptional Hyperactivation and Nucleolar Stress in Cellular Models.Research square · 2025Article
- Acetylation mimetic and null mutations within the filament core of P301L tau have varied effects on susceptibility to seeding and aggregation.bioRxiv : the preprint server for biology · 2025Article
- GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau.Nature communications · 2025Article
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12 authors.
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Abstract
Due to the importance of 4R tau (with four microtubule-binding-repeat domains) in the pathogenicity of primary tauopathies, it has been challenging to model these diseases in induced pluripotent stem cell (iPSC)-derived neurons, which express very low levels of 4R tau. To address this, we have developed a panel of isogenic iPSC lines carrying MAPT splice-site mutations, S305S, S305I, or S305N, derived from four different donors. All mutations significantly increase 4R tau expression in iPSC neurons and astrocytes. Functional analyses of S305 mutant neurons reveal shared disruption in synaptic signaling and maturity but divergent effects on mitochondrial bioenergetics. In iPSC astrocytes, S305 mutations promote internalization of exogenous tau that may be a precursor to glial pathology. These lines recapitulate previously characterized tauopathy-relevant phenotypes and highlight functional differences between the wild-type 4R and the mutant 4R proteins in both neurons and astrocytes. As such, these lines enable a more complete understanding of pathogenic mechanisms underlying 4R tauopathies across different cell types.
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