. * * window.aa needs to exist and be usable by ANY module's script, * however early it runs - main-nav's script, for one, runs near * the top of

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, well before the real search-insights.js * so the download * begins as early as before. Repeat calls share the same downloads, a * failed load is retried on the next call, and the versions / SRI * hashes live only here. * * Algolia Insights is unaffected: window.aa above is still created in * on every page and queues events until search-insights loads. * * window.loadAlgoliaLibs({ priority: 'high' }) (Oct 2026): used by the * /search page, where the first results wait on these libraries. Chrome * gives async scripts low priority, behind images and fonts; this asks * for high instead (fetchpriority). Only the first call for a library * sets its priority - later calls share that download. */ (function (win, doc) { var LIBS = [ { ready: function () { return !!win['algoliasearch/lite']; }, src: 'https://cdn.jsdelivr.net/npm/algoliasearch@5.52.1/dist/lite/builds/browser.umd.js', integrity: 'sha256-I2oYUIvhx1g6l4lTP+yoERbzLIHKzw4AKaBRQPwIeDY=' }, { ready: function () { return !!win.instantsearch; }, src: 'https://cdn.jsdelivr.net/npm/instantsearch.js@4.98.0/dist/instantsearch.production.min.js', integrity: 'sha256-ngmqZk4WBxUw257aMYZayyNBd983INngagv0jI6Ecfs=' } ]; function loadOne(lib, options) { if (lib.ready()) return Promise.resolve(); // One download per library, shared by every caller; reset on // failure so the next call retries just the library that failed. if (lib.pending) return lib.pending; lib.pending = new Promise(function (resolve, reject) { var script = doc.createElement('script'); script.src = lib.src; script.integrity = lib.integrity; script.crossOrigin = 'anonymous'; script.async = true; if (options && options.priority === 'high') script.setAttribute('fetchpriority', 'high'); script.onload = function () { lib.ready() ? resolve() : reject(new Error('Loaded but not available: ' + lib.src)); }; script.onerror = function () { script.remove(); reject(new Error('Could not load ' + lib.src)); }; doc.head.appendChild(script); }); lib.pending.catch(function () { lib.pending = null; }); return lib.pending; } win.loadAlgoliaLibs = function (options) { return Promise.all(LIBS.map(function (lib) { return loadOne(lib, options); })); }; })(window, document); . */ window.hsConversationsSettings = window.hsConversationsSettings || {}; window.hsConversationsSettings.loadImmediately = false; (function (win) { var EVENTS = ['pointerdown', 'keydown', 'touchstart', 'scroll', 'mousemove', 'wheel']; var done = false; /* 19 Oct 2026 - chat widget layout shift (field CLS). Phones fail Core Web Vitals on CLS (p75 ~0.2 site-wide in CrUX for months). Biggest cause found: HubSpot's chat container is fixed to the bottom-right corner and changes size - 100x96 launcher to 282x253 when the welcome message pops up (~5 s after load), and to full screen when a visitor opens the chat. Its top-left corner moves, so Chrome scores it as a layout shift: 0.088 per page view at 360x640 (0.044 at 412x850), on every page. Taps happen inside the chat iframe, so the parent page never sees the input and the open/close shifts count too. Fix: whenever the container's size changes it is made transparent for 400 ms (Chrome doesn't score shifts of invisible elements), then shown again at its new size. Tested on live io1001 at 360x640 in a cookie-less frame: the 0.088 shift no longer appears. The chat itself is unchanged - it just appears 0.4 s later at each resize. Relies on HubSpot's container id; if that changes this does nothing (no error). */ function cloakChatResizes() { var ID = 'hubspot-messages-iframe-container'; function watch(c) { if (c.getAttribute('data-bb-cloak')) return; c.setAttribute('data-bb-cloak', '1'); var last = c.offsetWidth + 'x' + c.offsetHeight, timer = null; new MutationObserver(function () { var size = c.offsetWidth + 'x' + c.offsetHeight; if (size === last) return; last = size; c.style.setProperty('opacity', '0', 'important'); clearTimeout(timer); timer = setTimeout(function () { c.style.removeProperty('opacity'); }, 400); }).observe(c, { attributes: true, attributeFilter: ['style', 'class'], subtree: true, childList: true }); } var found = document.getElementById(ID); if (found) { watch(found); return; } if (!document.body || !('MutationObserver' in win)) return; var mo = new MutationObserver(function () { var c = document.getElementById(ID); if (c) { mo.disconnect(); watch(c); } }); mo.observe(document.body, { childList: true }); setTimeout(function () { mo.disconnect(); }, 30000); } function loadWidget() { var api = win.HubSpotConversations; if (api && api.widget && api.widget.status && api.widget.status().loaded) return; try { cloakChatResizes(); } catch (e) {} if (api && api.widget) api.widget.load(); } function onFirstInteraction() { if (done) return; done = true; EVENTS.forEach(function (type) { win.removeEventListener(type, onFirstInteraction, { passive: true }); }); var start = function () { if (win.HubSpotConversations) loadWidget(); else (win.hsConversationsOnReady = win.hsConversationsOnReady || []).push(loadWidget); }; if ('requestIdleCallback' in win) win.requestIdleCallback(start, { timeout: 1500 }); else setTimeout(start, 200); } EVENTS.forEach(function (type) { win.addEventListener(type, onFirstInteraction, { passive: true }); }); })(window);

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ioGABAergic Neurons APP V717I/V717I
Human iPSC-derived Alzheimer's disease model in human GABAergic neurons
AB42 ratio data in london mutation homhet-1
Disease model cells express key GABAergic neuron-specific markers comparably to the isogenic control
Alzheimer's disease models in GABAergic Neurons form structural neuronal networks
Gene expression analysis demonstrates that wild type and disease models in GABAergic Neurons
Human iPSC-derived Alzheimer's disease model in human GABAergic neurons
AB42 ratio data in london mutation homhet-1
Disease model cells express key GABAergic neuron-specific markers comparably to the isogenic control
Alzheimer's disease models in GABAergic Neurons form structural neuronal networks
Gene expression analysis demonstrates that wild type and disease models in GABAergic Neurons

cat no | io1082

ioGABAergic Neurons APP V717I/V717I

Human iPSC-derived Alzheimer's disease model

  • Cryopreserved human iPSC-derived cells powered by opti-ox, that are ready for experiments in days
  • Engineered to enable investigations into the effect of the mutant APP protein on Alzheimer's disease
  • Disease-related phenotype demonstrated by increased amyloid beta production vs. wild-type control

Place your order

Human iPSC-derived Alzheimer's disease model in human GABAergic neurons

Human iPSC-derived GABAergic neurons Alzheimer's disease model

AB42 ratio data in london mutation homhet-1

Increased ratio of A�42:40 seen in ioGABAergic Neurons APP V717I (London), as observed in Alzheimer’s disease

ioGABAergic Neurons APP V717I/V717I disease model (HOM) cells show a trend of increased production of Að�›½38 peptides and Að�›½42 (involved in the amyloidogenic pathway), with minimal difference seen for Að�›½40 (A).  This results in a significantly increased ratio of Að�›½42:40 and no change in the Að�›½42:38 ratio (B).

  • ioGABAergic neurons (WT, CL54, CL65, CL59, CL70) were seeded at 150,000 cells/cm2 in 24 well plates and cultured for 30 days according to the user manual.

  • Supernatant was collected at days 10, 20, and 30 to quantify levels of Að�›½38, Að�›½40, Að�›½42 peptides using the V-PLEX Aβ Peptide Panel ELISA kit (MSD K15200E-1).

  • Concentrations of Að�›½38, Að�›½40, Að�›½42 were normalised to the calculated total number of cells per well.

  • Data were obtained from two independent experiments and are shown as mean ± SEM. Data were analysed statistically (at days 20 and 30) using one-way ANOVA with Tukey’s post-hoc analysis. * p<0.05 ** p<0.01 ***p<0.001 **** p<0.0001

Disease model cells express key GABAergic neuron-specific markers comparably to the isogenic control

Disease model cells express key GABAergic neuron-specific markers comparably to the isogenic control

Immunofluorescent staining on day 12 post-revival demonstrates similar homogenous expression of the pan-neuronal marker, MAP2 and GABAergic neuron-specific marker, GABA in both disease model clones compared to the wild-type (WT) isogenic control. 100X magnification.

Alzheimer's disease models in GABAergic Neurons form structural neuronal networks

Disease model cells form structural neuronal networks by day 12

Both disease model clones mature rapidly and form structural neuronal networks over 12 days, with neurons identified by day 3 and visible neuronal networks being observed by day 10 post-thaw, similarly to the WT isogenic control. Day 1 to 12 post thawing; 100X magnification.

Gene expression analysis demonstrates that wild type and disease models in GABAergic Neurons

Disease model cells demonstrate gene expression of neuronal and GABAergic-specific markers following deterministic programming

Gene expression analysis demonstrates that both disease model clones and the WT isogenic control lack the expression of pluripotency markers (NANOG and OCT4) at day 12 post-thaw, whilst robustly expressing pan-neuronal (TUBB3) and GABAergic-specific markers, GAD1, GAD2, VGAT, DLX1, and DLX2. Gene expression levels were assessed by RT-qPCR (data expressed relative to the parental hiPSC control (iPSC Control), normalised to GAPDH). Data represents day 12 post-revival samples.

Vial limit exceeded

A maximum number of 20 vials applies. If you would like to order more than 20 vials, please contact us at orders@91̽»¨.

Human iPSC-derived Alzheimer's disease model

ioGABAergic Neurons APP V717I/V717I are opti-ox deterministically programmed GABAergic neurons, also known as inhibitory interneurons, carrying a genetically engineered homozygous V7171 (London) mutation in the APP gene encoding the amyloid precursor protein. This mutation is linked to familial early-onset Alzheimer's disease (AD).

These cells offer a functional, rapidly maturing, and disease relevant system in inhibitory neurons to study the role of the APP V717I (London) mutation in early-onset AD, alongside a genetically matched wild-type control.

Two clones are available, all genetically matched to the wild type control (ioGABAergic Neurons). The disease model cells and the wild-type control offer a physiologically relevant model to investigate the impact of the APP V717I mutation on cellular and molecular mechanisms and function in early-onset AD.

Benchtop benefits

comparison_0

Make true comparisons

Pair the ioDisease Model Cells with the genetically matched wild-type ioGABAergic Neurons to directly investigate the effect of the mutant APP protein on early-onset AD.

pure_0

Highly pure

>99% of cells express key GABAergic markers within 4 days post-thaw, allowing consistent and reproducible results from every vial.

culture_0

Co-culture compatible

Suitable for co-culture and tri-culture studies with ioGlutamatergic Neurons and astrocytes.

Cells arrive ready to plate


91̽»¨_ioGABAergic Neurons_timeline_horizontal_withoutdox

ioGABAergic Neurons APP V717I/V717I are delivered in a cryopreserved format and are programmed to rapidly mature upon revival in the recommended media. The protocol for the generation of these cells is a two-phase process: Induction, which is carried out at 91̽»¨, Stabilisation for 3 days (Phase 1), and Maintenance (Phase 2) during which the ioGABAergic Neurons mature. Phases 1 and 2 after revival of cells are carried out at the customer site.

Product specifications

Starting material

Human iPSC line

Karyotype

Normal (46, XY)

Seeding compatibility

6, 12, 24, 96 and 384 well plates

Shipping info

Dry ice

Donor

Caucasian adult male, age 55-60 years old (skin fibroblast),
Genotype APOE 3/4

Vial size

Small: >3 x 10� viable cells

Quality control

Sterility, protein expression (ICC) and gene expression (RT-qPCR)

Differentiation method

opti-ox deterministic cell programming

Recommended seeding density

150,000 cells/cm²

User storage

LN2 or -150°C

Format

Cryopreserved cells

Product use

ioCells are for research use only

Genetic modification

Homozygous V717I mutation in the APP gene

Applications

Alzheimer's disease modelling
Drug discovery and development
MEA analysis
Co-culture studies
ASO screening

Available clones

io1081S: ioGABAergic Neurons APP V717I/V717I (CL59)
io1082S: ioGABAergic Neurons APP V717I/V717I (CL70)

 

Scale your study with volume pricing

Enabling scientists to use human cells in their research, running additional experiments without rationing cells or limiting experimental scale

 

Order quantity Total vials received Pricing tier 
1 - 9 packs 3 - 27 vials Standard price
10 - 33 packs 30 - 99 vials Automatic 10% discount
> 34 packs > 100 vials > Contact us for a quote

 

Academic pricing: Academic users can purchase any ioCells in 3-vial packs ($/€/£ 999 per pack), available year-round with any cell type combination.
Technical data

Disease related phenotype

Increased ratio of A�42:40 seen in ioGABAergic Neurons APP V717I (London), as observed in Alzheimer’s disease

AB42 ratio data in london mutation homhet-1

ioGABAergic Neurons APP V717I/V717I disease model (HOM) cells show a trend of increased production of Að�›½38 peptides and Að�›½42 (involved in the amyloidogenic pathway), with minimal difference seen for Að�›½40 (A).  This results in a significantly increased ratio of Að�›½42:40 and no change in the Að�›½42:38 ratio (B).

  • ioGABAergic neurons (WT, CL54, CL65, CL59, CL70) were seeded at 150,000 cells/cm2 in 24 well plates and cultured for 30 days according to the user manual.

  • Supernatant was collected at days 10, 20, and 30 to quantify levels of Að�›½38, Að�›½40, Að�›½42 peptides using the V-PLEX Aβ Peptide Panel ELISA kit (MSD K15200E-1).

  • Concentrations of Að�›½38, Að�›½40, Að�›½42 were normalised to the calculated total number of cells per well.

  • Data were obtained from two independent experiments and are shown as mean ± SEM. Data were analysed statistically (at days 20 and 30) using one-way ANOVA with Tukey’s post-hoc analysis. * p<0.05 ** p<0.01 ***p<0.001 **** p<0.0001

Highly characterised and defined

Disease model cells express key GABAergic neuron-specific markers comparably to the isogenic control

ioGABA APP V717I Hom ICC panel FINAL compressed

Immunofluorescent staining on day 12 post-revival demonstrates similar homogenous expression of the pan-neuronal marker, MAP2 and GABAergic neuron-specific marker, GABA in both disease model clones compared to the wild-type (WT) isogenic control. 100X magnification.

Disease model cells form structural neuronal networks by day 12

ioGABA APP V717I Hom Morphology panel

Both disease model clones mature rapidly and form structural neuronal networks over 12 days, with neurons identified by day 3 and visible neuronal networks being observed by day 10 post-thaw, similarly to the WT isogenic control. Day 1 to 12 post thawing; 100X magnification. 

Disease model cells demonstrate gene expression of neuronal and GABAergic-specific markers following deterministic programming

ioGABA APP V717I Hom RT-qPCR

Gene expression analysis demonstrates that both disease model clones and the WT isogenic control lack the expression of pluripotency markers (NANOG and OCT4) at day 12 post-thaw, whilst robustly expressing pan-neuronal (TUBB3) and GABAergic-specific markers, GAD1, GAD2, VGAT, DLX1, and DLX2. Gene expression levels were assessed by RT-qPCR (data expressed relative to the parental hiPSC control (iPSC Control), normalised to GAPDH). Data represents day 12 post-revival samples.

Technical data

Expected increase of Aβ42:40 ratio measured by MSD assay

Increased ratio of A�42:40 seen in ioGABAergic Neurons APP V717I (London), as observed in Alzheimer’s disease

AB42 ratio data in london mutation homhet-1

ioGABAergic Neurons APP V717I/V717I disease model (HOM) cells show a trend of increased production of Að�›½38 peptides and Að�›½42 (involved in the amyloidogenic pathway), with minimal difference seen for Að�›½40 (A).  This results in a significantly increased ratio of Að�›½42:40 and no change in the Að�›½42:38 ratio (B).

  • ioGABAergic neurons (WT, CL54, CL65, CL59, CL70) were seeded at 150,000 cells/cm2 in 24 well plates and cultured for 30 days according to the user manual.

  • Supernatant was collected at days 10, 20, and 30 to quantify levels of Að�›½38, Að�›½40, Að�›½42 peptides using the V-PLEX Aβ Peptide Panel ELISA kit (MSD K15200E-1).

  • Concentrations of Að�›½38, Að�›½40, Að�›½42 were normalised to the calculated total number of cells per well.

  • Data were obtained from two independent experiments and are shown as mean ± SEM. Data were analysed statistically (at days 20 and 30) using one-way ANOVA with Tukey’s post-hoc analysis. * p<0.05 ** p<0.01 ***p<0.001 **** p<0.0001

How to culture ioGABAergic Neurons

 

In this video, our scientist will take you through the step-by-step process of how to thaw, seed and culture ioGABAergic Neurons.

Frequently Asked Questions (FAQs)

Do ioGABAergic Neurons APP V717I/V717I cells display disease-relevant phenotypes?

ioGABAergic Neuron APP V717I homozygous disease model cells show a trend of increased production of Aβ38 and Aβ42 peptides with minimal differences observed for Aβ40. This results in a significantly increased Aβ42:Aβ40 ratio as observed in Alzheimer's disease patients with this mutation.

 

How can I utilise the wild-type and APP V717I homozygous disease model ioGABAergic Neurons in my research?

The V717I mutation and genetically-matched wild-type control offer a physiologically relevant, functional, and rapidly maturing model to study the role of the APP V717I (London) mutation in early-onset Alzheimer's disease.

 

Do ioGABAergic Neurons APP V717I/V717I cells display disease-relevant phenotypes?

ioGABAergic Neuron APP V717I homozygous disease model cells show a trend of increased production of Aβ38 and Aβ42 peptides with minimal differences observed for Aβ40. This results in a significantly increased Aβ42:Aβ40 ratio as observed in Alzheimer's disease patients with this mutation.

 

The Potential of RNA Therapies in Autism Spectrum Disorder

In this webinar, Dr Rodney Bowling, CSO of Everlum Bio, offers an expert discussion on their use of ioGABAergic neurons for the screening of antisense oligonucleotide (ASO) based RNA therapeutics to accelerate the discovery of novel personalised therapies for rare autism spectrum disorders (ASD).

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Co-culture human excitatory and inhibitory neurons to model neurodegenerative disease
Build mutation matching functional excitatory - inhibitory in vitro cultures
Choose defined, consistent glutamatergic neurons with matching APP V717I mutations
Expand your research
Build mutation matching functional excitatory - inhibitory in vitro cultures
Choose defined, consistent glutamatergic neurons with matching APP V717I mutations
Co-culture human excitatory and inhibitory neurons to model neurodegenerative disease

Build neuronal co-cultures with matching Alzheimer's disease mutations to more accurately represent the complexity of the human brain and model disease. Glutamatergic and GABAergic neurons are crucial to help maintain stable ratios of excitatory and inhibitory populations throughout your MEA experiments. 

Explore ioGlutamatergic Neuron APP V717I Disease Models

GABAergic neurons combined with other neuronal and glial cells to generate complex multi-cell cultures.
Generate functional in vitro models of the CNS
Highly pure human iPSC-derived cells to build complex multi-cell cultures
Expand your research
Generate functional in vitro models of the CNS
Highly pure human iPSC-derived cells to build complex multi-cell cultures
GABAergic neurons combined with other neuronal and glial cells to generate complex multi-cell cultures.

ioGABAergic Neurons are highly pure, defined and consistent, a great companion for your CNS model. 

Combine them with other neuronal and glial ioCells to generate complex multi-cell cultures.

ioGlutamatergic Neurons 
ioMicroglia
ioAstrocytes
ioOligodendrocyte-like cells

CRISPR-ready human iPSC-derived cells for CRISPR studies and CRISPR screens.
Register your interest for new product development
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Looking for CRISPRko-Ready ioGABAergic Neurons?
CRISPR-ready human iPSC-derived cells for CRISPR studies and CRISPR screens.

Interested in simple gene knockouts and CRISPR screens? 
Register your interest for CRISPRko-Ready ioGABAergic Neurons.
 
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Engineer disease-relevant mutations in human iPSC-derived cells.
Custom cell development
Generate custom disease models or reporter lines
Expand your research
Custom cell development
Generate custom disease models or reporter lines
Engineer disease-relevant mutations in human iPSC-derived cells.
Build your custom disease model or reporter line to pair with wild-type ioGABAergic Neurons as the genetically matched control.

Throughout the custom process, our experts will bring your project to life, and be on hand to support you with any technical queries.

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