Alzheimer's Disease Preclinical Research Solutions

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All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

Human iPSC-Derived Models of Alzheimer's Disease

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Alzheimer's disease (AD) remains one of the most challenging neurodegenerative disorders, with complex pathologies spanning amyloid-beta (Aβ) plaques, tau neurofibrillary tangles, and neuroinflammation. Traditional animal models often fall short in replicating human-specific disease mechanisms. At Ace Therapeutics, we harness the power of human iPSC-derived models of Alzheimer's disease to deliver clinically relevant insights, accelerating therapeutic discovery from bench to bedside.

Why Human iPSC Models?

Human induced pluripotent stem cell (iPSC) models bridge critical gaps in AD research by capturing genetic diversity, cell-type-specific interactions, and human-like disease progression. Unlike rodent systems, iPSC-derived neurons, glia, and 3D organoids enable researchers to

Study sporadic and familial AD mechanisms in a human genetic context.
Recapitulate Aβ oligomer toxicity, tau hyperphosphorylation, and synaptic dysfunction with high fidelity.
Investigate neuroimmune crosstalk and mitochondrial dysfunction in disease-relevant cell populations.

Our models are engineered to mirror the complexity of human AD, offering unparalleled translational value for preclinical studies.

Our Core Services

3D Cerebral Organoids with AD Pathology

Our iPSC-derived brain organoids replicate key AD hallmarks, including Aβ plaque-like aggregates, tau tangles, and neuroinflammation. These 3D systems incorporate neurons, astrocytes, and microglia to model cell-cell interactions in a dynamic microenvironment. Applications include

Testing anti-Aβ antibodies and tau aggregation inhibitors.
Studying neuroinflammatory pathways driven by microglial activation.
Assessing drug penetration across blood-brain barrier analogs.

Neuro-Glial Co-Culture Systems

AD progression involves intricate interactions between neurons and glia. Our tri-culture platforms combine iPSC-derived neurons, astrocytes, and microglia to study

Synaptic pruning and dendritic spine loss in AD.
Cytokine-driven neurotoxicity and its modulation by therapeutics.
The role of APOE4 in exacerbating glial dysfunction.

Drug Screening & Target Validation

Our iPSC-based platforms streamline preclinical drug development through

High-throughput screens of BACE1 inhibitors, γ-secretase modulators, and neuroprotective compounds.
Functional assays measuring Aβ oligomer toxicity, mitochondrial ROS production, and synaptic vesicle recycling.
Multi-omics integration (RNA-seq, proteomics) to identify novel biomarkers and therapeutic targets.

Aging & Mitochondrial Dysfunction Models

Aging is the primary risk factor for sporadic AD. We simulate age-related neurodegeneration using

Progerin-induced senescence to accelerate neuronal aging.
Mitochondrial stress assays to study metabolic dysregulation and oxidative damage.
Models expressing SHMOOSE microprotein to explore mitochondrial DNA contributions to AD.

Applications in AD Research

Our models are trusted for

Mechanistic studies of Aβ-tau cross-talk and neuroinflammation.
Preclinical validation of disease-modifying therapies (DMTs).
Biomarker discovery for early diagnosis and treatment monitoring.

Partner with Ace Therapeutics to unlock the potential of human iPSC models in your Alzheimer's research. Contact us to design a customized preclinical study today.

Frequently Asked Questions (FAQ)

How do iPSC models improve AD drug discovery compared to animal models?

Human iPSC systems capture species-specific pathways, such as APOE4 effects and neuroimmune interactions, reducing translational failures.

Can your organoids model late-stage AD pathology?

Yes. Long-term cultures (6+ months) develop mature Aβ aggregates, tau tangles, and glial activation resembling advanced AD.

What types of genetic modifications do you offer?

We engineer familial AD mutations (e.g., APP, PSEN1), risk alleles (APOE4), and novel variants linked to sporadic AD.

How long does a typical drug screening study take?

High-throughput screens in 2D neuronal cultures can yield results in 2–4 weeks, while organoid studies may require 8–12 weeks.

Are your models suitable for studying neuroinflammation?

Absolutely. Our tri-culture systems include microglia and astrocytes to model cytokine release, phagocytosis, and synaptic pruning.

Our products and services are for research use only and can not be used for diagnostic or other purposes.