Charcot Marie Tooth Disease Type 1A

C3-PMP22 Mouse Model

Mutations in the PMP22 gene cause several forms of neuropathies such as Charcot-Marie-Tooth Disease Type 1A 

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Charcot Marie Tooth Disease Type 1A (CMT1A) is a hereditary, demyelinating peripheral neuropathy, leading to progressive skeletal muscle atrophy, weakenss and subsequent walking diabilities and sensory impairments. This autosomal, dominantly inherited disease is caused by a duplication of a segment on chromosome 17p11.2 containing the gene encoding peripheral myelin protein 22 (PMP22). 

To help accelerate CMT1A research to clinic, InnoSer offers specialized preclinical research services using the C3-PMP22 mouse model (Verhamme et al. 2011) of CMT1A. Transgenic C3-PMP22 mice carry multiple copies of the wild-type human PMP22 gene. The C3-PMP22 mouse model shows a mild disease phenotype that more closely resembles the human disease pathophysiology. As part of our services, InnoSer offers you with efficacy studies in the C3-PMP22 mouse model of CMT1A, focusing on functional readouts such as sciatic nerve conduction electrophysiology and motor function assessments, as well as histopathology analyses. 

InnoSer’s scientists have extensive experience in performing efficacy studies in the C3-PMP22 mouse model of CMT1A and have published numerous papers using this mouse model (Michailidou et al. 2023 and Prior et al. 2024).

InnoSer’s neurology expert team possesses relevant experience in working with multiple therapy types ranging from small molecules, peptides, enzymes, oligonucleotides, and gene therapy (viral vectors – e.g.. AAVs). 

C3-PMP22 model key characteristics:

  • The C3-PMP22 mouse model reverts back to the original C22-PMP22 model on its own after being bred with C57BL/6J mice.
  • Model contains 3 to 4 copies of the human PMP22 gene.
  • In comparison to the original C22-PMP22 model, the C3-PMP22 model shows a milder disease phenotype, better resembling the human disease course of CMT1A.

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Key readouts in the C3-PMP22 mouse model

Test the efficacy of your treatments in the following battery of behavioural tests: 

Neuromuscular function
  • Compound muscle action potential (CMAP) 
  • Sensory nerve conduction velocity (SNCV) 
Test the efficacy of your treatments with the following biological readouts:

  • Sciatic nerve histology

Example data featuring the C3-PMP22 mouse model

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AAALAC Accreditation

InnoSer has earned the AAALAC accreditation, demonstrating our commitment to responsible animal care and use. AAALAC International is a nonprofit organization that promotes the humane treatment of animals in science through voluntary accreditation and assessment programs. Our accreditation is valid for three years, incl. 2023. Read more about the AAALAC accreditation programme here.

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Animal Welfare

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References

  • Michailidou I, Vreijling J, Rumpf M, Loos M, Koopmans B, Vlek N, Straat N, Agaser C, Kuipers TB, Mei H, Baas F. The systemic inhibition of the terminal complement system reduces neuroinflammation but does not improve motor function in mouse models of CMT1A with overexpressed PMP22. Current Research in Neurobiology. 2023 Jan 1;4:100077. 

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