Demyelinating Disease
Demyelinating diseases encompass a range of conditions that exert a substantial impact on the global economy and society. With our pioneering efforts in demyelinating disease research, we are at the forefront of developing cutting-edge diagnostic tools and therapeutics to facilitate the effective management of demyelinating disease. As your reliable partner in demyelinating disease research, we offer unmatched support to fulfill your scientific research needs.
Introduction to Demyelinating Disease
Demyelinating diseases encompass a group of neurological disorders characterized by the damage or loss of the myelin sheath surrounding nerve fibers in the central nervous system (CNS) or peripheral nervous system (PNS). These diseases can have a significant impact on the proper functioning of the nervous system, leading to a wide range of symptoms and functional impairments. Based on published estimates, there are currently 2.8 million individuals worldwide living with demyelinating diseases, indicating an incidence rate of approximately 35 cases per 100,000 population.
Fig. 1 Schematic mechanisms of demyelination. (Bando, Yoshio., 2019)Pathogenesis of Demyelinating Disease
The pathogenesis of demyelinating diseases is multifactorial and involves complex interactions between genetic, environmental, and immunological factors. The following is a list of the pathogenesis of some demyelinating diseases.
| Disease | Category | Pathogenesis |
|---|---|---|
| Pelizaeus-Merzbacher disease | CNS | Mutations in the proteolipid protein 1 (PLP1) gene are associated with Pelizaeus-Merzbacher disease, a rare X-linked disorder characterized by hypomyelination. |
| Multiple Sclerosis (MS) | CNS | Viral infections, including Epstein-Barr virus and human herpesvirus 6, have been implicated in the development of MS. These viruses may trigger an immune response that targets the myelin sheath. |
| Guillain-Barre Syndrome (GBS) | PNS | The majority of GBS cases are linked to infections caused by microorganisms found in the gastrointestinal and upper respiratory tracts, including Campylobacter jejuni, Mycoplasma pneumoniae, cytomegalovirus, etc. |
| Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) | PNS | In CIDP, the immune system mistakenly identifies components of the myelin sheath, the protective covering of the nerves, as foreign and launches an immune attack against it. This immune response leads to inflammation and damage to the myelin, resulting in demyelination and impaired nerve conduction. |
Diagnostics Development of Demyelinating Disease
Diagnostic methods for demyelinating diseases are becoming increasingly abundant, mainly involving imaging examinations, biochemical tests, and genetic testing.
Imaging Examinations
MRI plays a crucial role in the diagnosis and monitoring of demyelinating diseases by detecting characteristic abnormalities, such as white matter lesions, that indicate CNS demyelination.
Biochemical Tests
Biochemical test helps diagnose demyelinating diseases by identifying specific biomarkers. Cerebrospinal fluid analysis can help identify the presence of specific antibodies or inflammatory markers associated with certain demyelinating diseases.
Genetic Testing
Genetic testing may be warranted in cases where a hereditary component is suspected. Identifying specific genetic mutations can aid in confirming the diagnosis and providing prognostic information for affected individuals.
Therapeutics Development of Demyelinating Disease
- Targets of Demyelinating Disease Therapy Development
Inflammation and Immune Response
Targeting the immune response and modulating the inflammatory processes are key strategies in therapeutic development. Drugs such as corticosteroids and disease-modifying therapies, including interferons and monoclonal antibodies, are commonly used to suppress the immune response and reduce inflammation.
Remyelination and Axonal Protection
Promising targets for promoting remyelination in demyelinating diseases include growth factors like insulin-like growth factor-1 (IGF-1) and signaling pathways crucial for oligodendrocyte precursor cell differentiation and myelin formation. Preserving neuronal function through enhanced axonal protection is crucial and serves as a significant strategy in the development of therapies.
- Types of Demyelinating Disease Therapy Development
- Cell Therapy Development
Stem cells, including embryonic stem cells, induced pluripotent stem cells (iPSCs), and mesenchymal stem cells (MSCs), have shown potential for differentiating into oligodendrocyte precursor cells and promoting myelin repair.
- Gene Therapy Development
Gene replacement or gene editing strategies aim to provide a functional copy of the mutated gene or correct the genetic defect to restore normal myelin production, which may be effective for diseases caused by specific gene mutations.
Our Services
With years of extensive involvement in rare disease research, our company boasts a highly skilled team and vast expertise. We harness state-of-the-art technology to drive the development of innovative diagnostic tools, enabling early detection of demyelinating disease. By establishing animal models and conducting in-depth investigations into demyelinating disease pathogenesis and targets, we advance therapeutic drug development.
Research Platforms for Demyelinating Disease
Our Services
Animal Models of Demyelinating Disease
| Experimental Autoimmune Encephalomyelitis (EAE) Models | ||||
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| EAE can be induced in rodents, such as mice and rats, by immunization with myelin proteins or peptides. This leads to an immune response that targets the myelin sheath, resulting in inflammation and demyelination. | ||||
| Virus Induction Models | ||||
| Our company specializes in utilizing viral infections to induce animal models of demyelinating diseases. For instance, viral strains such as Theiler's murine encephalomyelitis virus (TMEV), Semliki forest virus (SFV), Borna disease virus (BDV), can elicit an immune response that results in demyelination, effectively replicating the characteristic features of human demyelinating diseases. | ||||
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| Chemical Induction Models | ||||
| Cuprizone is a copper chelator that, when administered to rodents, causes selective demyelination in the central nervous system. This model allows researchers to investigate the process of demyelination and remyelination and study the effects of potential therapeutic interventions. | ||||
| Transgenic Models | ||||
| Our company is dedicated to the development of transgenic animal models for demyelinating diseases. Our scientists have achieved success by introducing specific genetic mutations associated with demyelinating diseases using gene knockout, knock-in, or transgenic technology. These techniques allow us to create highly accurate animal models that closely resemble the characteristics of human demyelinating diseases. | ||||
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| Optional Species | Mice, Rats, Others | |||
No matter what stage of research you are at, we can provide you with corresponding research services. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.
References
- Kamil, Khidhir, et al. "Peripheral demyelinating diseases: from biology to translational medicine." Frontiers in neurology 10 (2019): 87.
- Bando, Yoshio. "Myelin morphology and axon pathology in demyelination during experimental autoimmune encephalomyelitis." Neural regeneration research 10.10 (2015): 1584-1585.
- Torre-Fuentes, L., et al. "Experimental models of demyelination and remyelination." Neurología (English Edition) 35.1 (2020): 32-39.
All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
