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Guillain-Barre Syndrome (GBS)

Guillain-Barré syndrome (GBS) is a rare condition in which a person's immune system attacks the peripheral nerves. People of all ages can be affected, but it is more common in adults and in males. It's potentially life-threatening. Specialized drug and therapy development services are essential to enhance and expedite GBS research. Our company is well-equipped to address your drug and therapy development requirements in GBS therapy.

Introduction to Guillain-Barre Syndrome

Guillain-Barre Syndrome is a rare autoimmune disorder that leads to rapid, progressive paralysis due to the immune system attacking peripheral nerves following infections such as influenza or gastrointestinal diseases. Globally, the incidence rate ranges from 0.84 to 1.91 per 100,000 people annually. The prevalence has been increasing slightly, with a 6.4% rise in cases from 1990 to 2019.

Pathogenesis of Guillain-Barre Syndrome

The pathogenesis of GBS is primarily linked to an autoimmune response following certain infections. The immune system mistakenly attacks peripheral nerve components, especially the myelin sheath or axons, leading to varying degrees of paralysis and sensory disturbances. A key mechanism involves molecular mimicry, where antibodies formed against infectious agents cross-react with nerve components such as gangliosides. This response can be triggered by different pathogens, most notably Campylobacter jejuni, which is closely associated with the more severe, axonal subtype of GBS.

Immunopathogenesis of Guillain-Barre Syndrome (GBS).Fig. 1 Immunopathogenesis of GBS: molecular mimicry and antiganglioside antibodies. (van den Berg, B., et al., 2014)

Diagnosis Development of Guillain-Barre Syndrome

Biomarkers such as antibodies against sulfatide are being studied for their potential to rapidly diagnose GBS. These biomarkers could enable earlier identification of the disease, allowing for timely intervention before more severe stages develop. The recognition of albuminocytological dissociation (elevated protein without increased cell count in CSF as a hallmark of GBS was a significant advancement. This feature is now a key diagnostic criterion, typically appearing one to two weeks after symptom onset.

Therapy Development of Guillain-Barre Syndrome

Small Molecule Drugs

Small molecule drugs continue to be foundational in managing GBS. Intravenous immunoglobulin (IVIG) is widely used as a standard therapy, where a large pool of donor antibodies is administered to mitigate the autoimmune attack on the nervous system. Alongside this, plasmapheresis, or plasma exchange, removes harmful antibodies by filtering the individual's blood and replacing the plasma with donor plasma.

Cell Therapies

Mesenchymal stem cells (MSCs) are being studied for their ability to moderate the immune response and facilitate nerve repair. They could provide significant benefits by reducing nerve damage and promoting recovery. Similarly, regulatory T cells (Tregs), which naturally modulate immune responses, are being explored for their potential to suppress the inappropriate immune attacks characteristic of GBS.

Monoclonal Antibodies

Monoclonal antibodies represent a targeted approach to reducing the immune response in GBS. Eculizumab, an antibody that inhibits complement activation, is being explored for its potential to reduce nerve inflammation. In cases where individuals produce autoantibodies against the GM1 ganglioside, developing monoclonal antibodies to neutralize these autoantibodies could help minimize the attack on the peripheral nerves.

Gene Therapies

Gene therapy holds transformative potential in treating GBS. Techniques such as gene silencing and RNA interference (RNAi) could specifically suppress the production of harmful antibodies or inflammatory molecules. CRISPR/Cas9, a powerful gene-editing tool, may one day correct genetic predispositions or alter immune function in those with autoimmune disorders like GBS.

Our Services

Our company adopts a partnership-driven approach. We collaborate closely with clients to craft tailored, innovative GBS therapy strategies and ensure robust support throughout the process.

Platforms of Guillain-Barre Syndrome Therapy Development

Animal Models of Guillain-Barre Syndrome

We have established expertise in developing and utilizing relevant animal models that closely mimic the disease characteristics and response to therapy. These models enable us to evaluate the safety and efficacy of potential therapies.

Biologics Induced Models
We provide diverse model choices customized to meet specific research needs related to GBS. These models allow researchers to simulate and study the complex biological processes associated with GBS.
Optional Models
  • Experimental Allergic Neuritis Model
  • Ganglioside Injection Model
  • Anti-beta2-Glycoprotein I Induced Model
  • Cytomegalovirus Infectious Model
  • Campylobacter Jejuni Infectious Model
  • Anti-Cardiolipin Antibodies Induced Model
Genetically Engineered Models
Our expertise in genetic engineering techniques, such as CRISPR/Cas9 technology, allows us to generate accurate and reliable models that recapitulate the genetic alterations observed in human GBS.
Optional Models
  • Human GM1 Transgenic Model
  • DAF Knockout Model
  • TLR family Knockin Model
  • Tregs Regulatory Gene Knockout Model
Optional Species Mice, Rats, Non-human primates, Others

In addition to these models, our comprehensive services encompass other models that target specific signaling pathways and molecular targets.

If our services align with your goals, please contact us for more details.

References

  • van den Berg, B., et al., "Guillain-Barre syndrome: pathogenesis, diagnosis, treatment and prognosis." Nat Rev Neurol, (2014). 10(8): p. 469-482..
  • Langille, M.M., "Guillain-Barre Syndrome in Children and Adolescents." Adv Pediatr, (2023). 70(1): p. 91-103.

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

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