Development and characterisation of a robust in vitro disease model to study tauopathies
In this poster, Charles River Laboratories assessed how MAPT N279K and MAPT P301S mutations affect Tau hyperphosphorylation, a hallmark of frontotemporal dementia, in precision reprogrammed iPSC-derived glutamatergic neuron disease models from bit.bio. The data demonstrate that beta-amyloid oligomers induce Tau phosphorylation in the wild type ioGlutamatergic Neurons. It also shows that compared to an isogenic control, Tau is hyperphosphorylated in ioGlutamatergic Neurons MAPT N279K and ioGlutamatergic Neurons MAPT P301S.
In this poster, you will explore:
- How ioGlutamatergic Neurons MAPT N279K and MAPT P301S were assessed for their relevance as an in vitro disease model of frontotemporal dementia.
- How ioGlutamatergic Neurons from bit.bio form an isogenic control for the MAPT disease models, allowing the authors to directly compare the effect of MAPT mutations on FTD-associated phenotypes.
- Data showing how a homozygous MAPT P301S mutation and a heterozygous MAPT N279K mutation in ioGlutamatergic Neurons both lead to the hyperphosphorylation of Tau compared to the isogenic control.
Laila Ritsma et al.
Charles River Laboratories & bit.bio