Autoimmune Encephalitis (AE)
Autoimmune encephalitis (AE) defines an inflammation of the brain due to a malfunctioning immune system, and is generally regarded as a form of non-infectious encephalitis which has the potential for recovery. The diagnosis and treatment of this condition remains a problem. We have solutions in drug development and therapy for autoimmune encephalitis (AE) that will help you meet your R&D objectives in a more timely and effective manner.
Introduction to AE
AE is the Neurological Inflammatory disorder that affects the Central Nervous System, initiated by an unusual immune response to a neuronal antigen. It bears primarily damage to the CNS and is mediated by either humoral immunity or cell-mediated immunity. AE is responsible for 10-20% of all encephalitis cases, with a single year prevalence of roughly 1 per 100,000 population.
Pathogenesis of AE
Somatic theories regarding the pathogenesis of autoimmune related encephalitis (AE) etiology contend contribution of various immunological factors directed against neuronal antigens. The growing AE literature seems to suggest that an exaggerated immune reaction to certain infections, tumors, or other surrounding factors is the primary trigger of the disease pathology. This response produces autoantibodies against certain “self” proteins located at the neuronal surface or synapse, including NMDA receptors, LGI1, CASPR2, and GABAB receptors.
When autoantibodies breach blood-brain barrier his most crucial function would lead to his failure. Consequently, it would become unable to transmit impulses between neurons and modulate their structure directly and moreover develop inflammation in the brain. In addition, complementing mediated processes may intensify already existing damage to tissue and inflammatory processes in the CNS.
Fig.1 The functional network changes of NMDAR encephalitis. (Heine, J., et al., 2023)Diagnostics Development of AE
The diagnosis of AE focuses on identifying particular autoantibodies or biomarkers like NMDA receptor antibodies or LGI1 antibodies. These antibodies are identified using a method called ELISA and IFA, which helps accelerate the verification process. Further development of diagnostic accuracy is provided by live neuronal cell test and transfected cell lines that express target antigens.
Therapy Development of AE
The development of therapeutic strategies using monoclonal antibodies for AE involves the design of antibodies that bind to neuronal antigens related to the disease, such as NMDA receptors or LGI1 proteins. Considerable advances in treatment of AE have been made with the monoclonal antibody rituximab, which targets CD20 on B cells, by depleting autoantibody-producing cells and modulating the immune response.
The development of cell therapy for autoimmune encephalitis (AE) centers on investigating approaches that utilize stem cell-derived mesenchymal stem cells (MSCs) or neural progenitor cells (NPCs) to alter the immune system and enhance neural recovery. Research is being conducted on the safety and efficacy of these cell therapies on animal models of AE, with some encouraging preliminary findings suggesting their suitability for human use.
Our Services
Our firm has chosen to focus on the incorporation of teams from biotechnology, pharmaceuticals and medical devices. Our expertise represents a dependable pillar in the field of drug and therapy development which supports your research.
Platforms of AE Therapy Development
Animal Models of AE
We have sufficient experience with developing and utilizing appropriate animal models of diseases that can closely mimic the disease and its response to therapies. These models allow us to test the safety and effectiveness of potential therapy.
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| Our company specializes in developing induced animal models that faithfully replicate AE's pathology and immunological features. Experimental Autoimmune Encephalomyelitis (EAE) induces immune responses by immunizing animals with myelin proteins like MOG or MBP, mimicking AE symptoms. The antibody transfer model transfers specific antibodies from AE patients or animals, triggering neuroinflammation akin to AE's pathology. | ||
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| Genetically Engineered Models | ||
| Our expertise in genetic engineering techniques, allows us to generate accurate and reliable models that recapitulate the genetic alterations observed in human AE. | ||
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| Optional Species | Mice, Rats, Others | |
Apart from these models, our diverse services include other models that focus on certain signaling and molecular targets. Such models have substantially contributed to the study of AE pathogenesis and helped define targets and treatment strategies.
If you are considering utilizing our services, we welcome you to contact us at your convenience to discuss how we can best meet your needs and support your goals.
References
- Heine, J., et al., "Autoimmune encephalitis-An update. "Nervenarzt (2023). 94(6): p. 525-537.
- Varley, J.A., et al., "Autoimmune encephalitis: recent clinical and biological advances." J Neurol (2023). 270(8): p. 4118-4131.
All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.