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Genetically engineered MAPT 10+16 mutation causes pathophysiological excitability of human iPSC-derived neurons related to 4R tau-induced dementia.

Cell death & disease - 17 Jul 2021

Kopach Olga, Esteras Noemí, Wray Selina, Abramov Andrey Y, Rusakov Dmitri A

Abstract excerpt

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...

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Identifiers

PMID: 34274950
DOI: 10.1038/s41419-021-04007-w
PMCID: PMC8286258

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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