Maternal Immune Activation (MIA) Model Development Service
Are you currently facing challenges with high variability in your animal models, long drug development cycles, or a lack of reliable translational data? Our maternal immune activation (MIA) model development Services help you accelerate your research and de-risk your drug discovery process through advanced model development, standardized protocols, and comprehensive phenotyping.
The link between maternal health and offspring neurodevelopment has been a subject of intense scientific inquiry. MIA is a state of systemic inflammation in the mother during pregnancy, which is now recognized as a significant risk factor for neurodevelopmental disorders. The prevailing hypothesis is that the resulting maternal immune response, not the pathogen itself, disrupts fetal brain development. This makes the MIA model a foundational blueprint for understanding a wide range of human conditions.
How Our MIA Model Development Services Can Assist Your Project
At Creative Biolabs, our services are meticulously designed to provide you with the critical insights needed to advance your neuroscience projects. We offer comprehensive solutions that go beyond simple model generation, helping you to accurately validate therapeutic targets, elucidate complex disease mechanisms, and generate robust, translational data. Our expertise ensures you can make informed go/no-go decisions with confidence, streamlining your path from hypothesis to breakthrough.
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Workflow
Our process is built for clarity and scientific rigor, providing a clear path from initial concept to actionable data.
| Required Starting Materials | To initiate a project, clients typically provide a detailed research hypothesis, information on the therapeutic agent being tested (if applicable), and specific neurodevelopmental endpoint requirements. |
| Final Deliverables | A comprehensive Final Report, raw data files, and a Project Summary Presentation. |
| Estimated Timeframe | The typical timeframe for a complete MIA model development project ranges from 12 to 24 weeks, depending on the complexity of the study design and the scope of behavioral and molecular analysis. |
Why Choose Us?
Choosing CBL means partnering with a team that has over 20 years of experience in the field, deeply understands the complexities of neurodevelopment, and prioritizes the scientific rigor and reproducibility of every study. We address the historical variability of MIA models by standardizing protocols, employing rigorous validation steps, and providing detailed characterization to ensure your data is robust and reliable. Our commitment to excellence allows us to provide a service that is both scientifically advanced and highly translatable.
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Customer Reviews
- "[Reproducibility & Confidence] Using CBL's MIA model development services in our research has significantly improved the reproducibility of our neurodevelopmental studies." - 2024, Dr. Jne De, Research Institute
- "[Translational Relevance] The comprehensive data package and behavioral phenotyping provided by CBL allowed us to make a more confident go/no-go decision on our lead compound." - 2024, Sah Tr, Drug Discovery Scientist
- "[Expertise & Support] The team's deep understanding of epigenetic mechanisms and their willingness to customize the study design was invaluable for our complex project." - 2025, Prf. Lke C*x, Academic Researcher
Maternal Immune Activation (MIA) Model
Epidemiological and preclinical studies have firmly established the MIA model as a powerful tool for understanding the origins of neurodevelopmental disorders (NDDs) such as schizophrenia and autism spectrum disorder (ASD). The model is based on the premise that an inflammatory insult during a critical period of gestation leads to lasting neurobiological and behavioral changes in the offspring.
Our understanding of this model is continuously evolving. Recent published data confirms that MIA induces profound epigenetic changes, particularly in DNA methylation. These alterations, which may not be immediately apparent after birth, reappear in adulthood and coincide with cognitive deficits and other disease-relevant phenotypes. This "two-hit" model, where a prenatal insult manifests much later in life, highlights the enduring impact of MIA and the importance of longitudinal studies.
The outcomes of MIA can also be sex-dependent, with males and females often exhibiting distinct behavioral and molecular profiles. Our MIA models are meticulously designed to account for these sex-specific differences, providing a more accurate and comprehensive view of disease etiology. We utilize well-established inducing agents like Poly(I:C) and LPS to precisely mimic viral and bacterial infections, respectively, allowing for controlled and reproducible studies that are essential for translational research.
Fig.1 The methylation pathway and the percentage of 5-mC changes in the PFC of offspring from poly(I:C)-treated dams at PD21 and PD35.1
What We Can Offer
- Customized, end-to-end service, tailored to your specific research questions.
- Precision-driven model development with standardized protocols that ensure high-quality and reproducible data.
- Comprehensive phenotyping platforms that go beyond basic behavioral assessments.
- Expertise in both in vivo and in vitro models, offering a flexible and integrated research approach.
- Support for a range of downstream analyses, including epigenetic, molecular, and histological assessments.
- The ability to de-risk your drug discovery pipeline by generating robust, translational data.
Related Services
To help you achieve your research goals, CBL offers a suite of complementary services that can be integrated with your MIA model project:
- Target Identification & Validation
- Compound Screening & Profiling
- Pharmacokinetic/Pharmacodynamic (PK/PD) Studies
- Neuroinflammation Research Models
FAQs
Q What makes your MIA model more reproducible than others?
Q What types of analyses can you perform on the offspring?
For more information and to discuss your project in detail, please do not hesitate to reach out to our team.
Contact Our Team for More Information and to Discuss Your Project.
Reference
- Woods, Rebecca M et al. "Developmental modulation of schizophrenia risk gene methylation in offspring exhibiting cognitive deficits following maternal immune activation." Molecular psychiatry, 10.1038/s41380-025-03147-1. 29 Aug. 2025, doi:10.1038/s41380-025-03147-1. Distributed under Open Access license CC BY 4.0, without modification.
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