Neuroinflammation Assay Services for Alzheimer’s Disease R&D
Alzheimer's Disease Preclinical Research Solutions
Online Inquiry

Neuroinflammation Assay Services for Alzheimer’s Disease R&D

Inquiry

At Ace Therapeutics, we recognize that neuroinflammation is not just a bystander in Alzheimer's disease (AD)—it's a driving force behind neurodegeneration. Our preclinical neuroinflammation assays are designed to dissect the complex interplay between microglia, astrocytes, and neurons, helping you identify compounds that modulate inflammatory pathways without compromising neuroprotection.

Why Neuroinflammation Assays Matter in AD Drug Development

Neuroinflammation in Alzheimer's involves dysregulated microglial activation, astrocyte reactivity, and cytokine storms that exacerbate amyloid-beta (Aβ) and tau pathology. Traditional models often overlook human-specific immune responses, leading to failed translation. Our assays address this by

  • Replicating AD-specific neuroinflammatory environments using human iPSC-derived cells.
  • Quantifying functional outcomes like phagocytosis, cytokine release, and synaptic pruning.
  • Identifying off-target risks early to avoid costly late-stage attrition.

Core Neuroinflammation Assay Services

Disease-Relevant Neuroinflammatory Models

Human-relevant systems to study AD-specific inflammation.

  • iPSC-derived microglia-astrocyte co-cultures with APOE3/APOE4 genotypes.
  • 3D neuroinflammatory spheroids incorporating Aβ plaques and tau tangles.
  • Primary rodent microglia assays for cross-species validation.

Mechanistic Target Engagement Assays

Evaluate compound effects on key inflammatory pathways.

  • NLRP3 inflammasome activation screening via caspase-1 activity and IL-1β release.
  • TREM2 receptor signaling assays using CRISPR-edited R47H mutant cell lines.
  • TLR4/NF-κB inhibition studies with luciferase reporter systems.

High-Content Functional Profiling

Capture dynamic inflammatory responses at single-cell resolution.

  • Live-cell imaging of microglial morphological changes (ramified vs. amoeboid).
  • ROS/RNS detection in Aβ-stimulated microglial cultures.
  • Synaptic pruning assays in neuron-microglia co-cultures.

Custom Biomarker Panels & Analytics

Tailored solutions for your therapeutic strategy.

  • Multiplex cytokine profiling (IL-6, TNF-α, IL-10).
  • Spatial transcriptomics in post-mortem AD brain slices.
  • AI-driven image analysis for quantifying IBA1+/GFAP+ cell activation.

Key Technologies

At Ace Therapeutics, we deploy cutting-edge tools to unravel the complexities of neuroinflammation in Alzheimer's disease—where microglial overactivation, cytokine storms, and impaired phagocytosis converge. Our technologies are engineered to mirror human-specific inflammatory cascades, from NLRP3 inflammasome dynamics to TREM2-dependent signaling. Below, explore the platforms that power our assays, combining scalability, precision, and translational relevance to transform your preclinical neuroinflammation research.

Technology Application
CRISPR-edited TREM2 models Study AD risk variants (e.g., R47H) in microglial function and phagocytosis.
Organ-on-chip neurovascular units Model BBB-immune interactions in neuroinflammatory environments.
High-content imaging (HCI) Track microglial migration and chemotaxis in real time.
Spatial transcriptomics Map cytokine expression gradients in 3D spheroids.

Why Partner with Ace Therapeutics?

  • Human-Relevant Precision
  • Scalability
  • Cross-Disciplinary Expertise
  • Regulatory-Grade Data

Neuroinflammation is a double-edged sword in Alzheimer's—too little impedes plaque clearance, too much accelerates neurodegeneration. Ace Therapeutics equips you with the tools to strike the right balance. Contact us today to design a preclinical strategy that turns your anti-inflammatory candidate into a disease-modifying therapy.

Frequently Asked Questions (FAQ)

What cell types do you support for neuroinflammation studies

We offer iPSC-derived microglia, astrocytes, and neurons, as well as primary rodent microglia. Custom co-cultures (e.g., neuron-microglia-astrocyte) are available.

Can you profile compounds targeting the NLRP3 inflammasome

Yes. Our assays measure caspase-1 activation, IL-1β release, and ASC speck formation in Aβ-stimulated models.

How much compound is required for screening

Most HTS assays require 1–5 mg for small molecules or 0.5–2 mg for biologics. Microscale options reduce material needs by 50%.

Do you provide data on reactive astrocytes (A1 vs A2)

Absolutely. We use RNA-seq and protein markers (C3, PTX3) to classify astrocyte polarization states.

What turnaround times can I expect

High-throughput screens take 3–4 weeks. Custom 3D spheroid or organ-on-chip studies require 6–8 weeks.

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

HOW WE WORK

Make Order

Make Order

Experimental Scheme

Experimental Scheme

Implementation

Implementation

Conclusion

Conclusion

Ace Therapeutics is a specialized team of scientists and technical professionals committed to working closely with clients worldwide. We offer comprehensive preclinical testing solutions to support the development of novel therapies and medications across a range of disease areas.