cat no | io1061
A rapidly maturing, physiologically relevant, functional system for investigating the role of the APP Swedish mutation in early-onset Alzheimer's disease (AD). This in vitro disease cell model recapitulates an overall increase in the production of amyloid beta peptides, as observed in AD.
ioGlutamatergic Neurons APP KM670/671NL / WT are opti‑ox deterministically programmed glutamatergic neurons carrying a genetically engineered heterozygous double mutation in the APP gene encoding amyloid precursor protein.
This disease model is part of an Alzheimer's disease panel of human iPSC-derived cells that can be incorporated into translational research and drug discovery workflows. Two additional clones for the APP KM670/671NL het mutation are available for scientists who wish to repeat their experiments in multiple independent clones, please enquire. All disease models are genetically matched to the wild-type control, ioGlutamatergic Neurons. Additional mutations in the AD panel include homozygous APP KM670/671NL, and heterozygous and homozygous APP V717I and PSEN1 M146L, alongside AD-relevant mutations in ioGABAergic Neurons and ioMicroglia.
Confidently investigate your phenotype of interest across multiple clones with our disease model clone panel. Detailed characterisation data (below) and bulk RNA sequencing data (upon request) help you select specific clones if required.
per vial
A maximum number of 20 vials applies. If you would like to order more than 20 vials, please contact us at orders@bit.bio.
Disease related phenotype
Overall increase in the production of amyloid beta peptides compared to the wild type control, measured by immunoassay.
Make True Comparisons
Pair the ioDisease Model Cells with the genetically matched wild-type ioGlutamatergic Neurons to investigate the impact of the APP double point mutation on early-onset AD.
Quick
The disease model cells and isogenic control are experiment ready as early as 2 days post revival, and form structural neuronal networks at 11 days.
Increased overall production of A𝛽38, A𝛽40 and A𝛽42 shown in ioGlutamatergic Neurons APP KM670/671NL (Swedish), as observed in Alzheimer’s disease
ioGlutamatergic Neurons APP KM670/671NL het express neuron-specific markers comparably to the genetically matched control
ioGlutamatergic Neurons APP KM670/671NL het form structural neuronal networks by day 11
ioGlutamatergic Neurons APP KM670/671NL het demonstrate gene expression of neuronal-specific and glutamatergic-specific markers following deterministic programming
Disease-related APP is expressed in ioGlutamatergic Neurons APP KM670/671NL het following deterministic programming
bit.bio
V11
bit.bio
2024
Professor Deepak Srivastava
Professor of Molecular Neuroscience and Group Leader, MRC Centre for Developmental Disorders
King’s College London
Emmanouil Metzakopian | Vice President, Research and Development | bit.bio
Javier Conde-Vancells | Director Product Management | bit.bio
Chakraborty et al
Nature Communications
2023
Featuring ioGlutamatergic Neurons
Dr Ania Wilczynska | Head of Computational Genomics | Non-Clinical | bit.bio
Innovation showcase talk at ISSCR
Marius Wernig MD, PhD | Stanford
Mark Kotter, MD, PhD | bit.bio
Oosterveen, et al
bit.bio & Charles River Laboratories
2023
Qiaojin Lin et al
The EMBO Journal
2023
Featuring opti-ox powered hiPSC-derived glutamatergic neurons with constitutive expression of Cas9
Mark Kotter | CEO and founder | bit.bio
Marius Wernig | Professor Departments of Pathology and Chemical and Systems Biology | Stanford University
Madeleine Garrett | Field Application Specialist | bit.bio
Read this blog on glutamatergic neuron cell culture for our top tips on careful handling, cell plating and media changes to achieve success from the outset.
Further your disease research by pairing our wild type cells with isogenic disease models.