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Guillain-Barre Syndrome (GBS)

Guillain-Barré Syndrome (GBS) is an infrequent disorder where the nervous system gets demyelinated, and the immune system attacks peripheral nerves. The condition can occur within a person of any age; however, it is more prevalent among adult males. GBS can be life threatening. There is also need for novel and specialized services in drug development and therapy for GBS which can help boost the pace of GBS research. Our company is capable of meeting your needs in GBS therapy development as well.

Introduction to Guillain-Barre Syndrome

Guillain-Barre Syndrome is uncommonly diagnosed, but, potentially, the most damaging autoimmune disease as it can cause death due to uncontrollable systemic paralysis within a matter of days due the body fighting off the peripheral nerves attacking the body’s undergo; it typically follows an assault on the body like influenza or severed gastrointestinal diseases. It’s estimated that about 0.84 to 1.91 people per year in a population of 100,000 get it. It does have a slight increase in rates of prevalence with an estimated increase of 6.4 percent cases from the year 1990 to 2019.

Pathogenesis of Guillain-Barre Syndrome

Neurological GBS primarily results from an autoimmune response to particular infections. A common mechanism is molecular mimicry in which an antibody to the infectious agent also reacts with structures within the nerve such as gangliosides. Numerous infectious agents can initate this response, the most well known being the Campylobacter jejuni which is strongly associated with the worst form of the GBS, the axonal subtype 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

Antibodies against sulfatide are potential biomarkers which when further studied are capable of diagnosing GBS at faster rates. The capability of these biomarkers is GBS is greatly identified allowing valuable solo treatment options before the patient reaches more severe stages. The identification of elevated protein in the CSF without a corresponding increase in cells was a hallmark of GBS. Now, albuminocytological dissociation is a feature is well known as increased cell count in CSF with GBS. This is one of the main criteria which are often observed about 1-2 weeks after the onset of symptoms.

Therapy Development of Guillain-Barre Syndrome

Small Molecule Drugs

For treatment of GBS, molecular drugs at the lowest levels continue to be the most important. A standard treatment is the intravenous immunoglobulin (IVIG) therapy where the massive pool of donor antibodies is infused to suppress the autoimmune responses against the nervous system. In conjunction, patients can undergo plasma exchange where the blood is filtered and antibodies are removed, as well as replacing the plasma with donor plasma.

Cell Therapies

MSCs stem cells are under investigation for their capacity to immunomodulate and promote nerve tissue repair. Those cells may have a substantial positive impact by lessening nerve impairment, thereby enhancing recovery. Also, T regulatory cells (Tregs), which are known to immunomodulate, are being studied to see whether they can prevent the inappropriate self immune attacks seen in GBS.

Monoclonal Antibodies

Contrary, monoclonal antibodies are a more refined methodology to tackling GBS by lessening the aggressive actions of the immune system. Eculizumab, an antibody that stops the activation of a complement system, is considered to reduce neuronal inflammation. If a person produces autoantibodies against GM1 ganglioside, the solution will be formulating healing monoclonal antibodies targeting these autoantibodies to mitigate the damage inflicted to the peripheral nerves.

Gene Therapies

The use of gene therapy can yield positive results in treating GBS. Certain techniques like gene silencing and RNA interference (RNAi) would be able to selectively inhibit the synthesis of detrimental inflammatory molecules and antibodies. The capacity of correcting genetic predispositions or immune function in affected patients with autoimmune conditions such as GBS may one day be achieved by powerful gene editing technology.

Our Services

Our company follows a partnership model. Working together with the clients, we develop creative GBS therapies and provide active assistance for the duration of the treatment, and as necessary afterward.

Platforms of Guillain-Barre Syndrome Therapy Development

Animal Models of Guillain-Barre Syndrome

We have developed the necessary animal models that accurately reflect the disease and the response to therapy. This allows us to assess the safety and potential efficacy of the candidate 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, 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, we offer surgery services in models that focus on specific pathways and the most promising 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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