Although QPS is complying with all government regulations for social distancing and allowing employees who can, to work from home, QPS Neuropharmacology is up and running. Please feel free to contact us any time to discuss your research needs.
QPS Neuropharmacology is the division of QPS that focuses on preclinical studies in CNS diseases, Rare Diseases and Mental Disorders. The on-site availability of highly predictive disease models and unparalleled experience with studies performed for biopharmaceutical companies of all sizes makes QPS Neuropharmacology the first choice for most CNS drug development needs.
Validated transgenic and non-transgenic in vitro and in vivo models cover most targets of Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Amyotrophic Lateral Sclerosis (ALS), Frontotemporal Dementia (FTD), Niemann-Pick Disease (NPC1), Gaucher Disease, Autism Spectrum Disorder (ASD), Schizophrenia, Frontotemporal Lobar Degeneration (FTLD) and other neurodegenerative and rare diseases.
QPS is a global contract research organization (CRO) providing discovery, preclinical and clinical drug development services since 1995. Our mission is to accelerate pharmaceutical breakthroughs across the globe by delivering custom-built research services. An award-winning leader in the CRO industry, QPS is known for proven quality standards, technical expertise, a flexible approach to research, client satisfaction and turnkey laboratories and facilities.
QPS Neuropharmacology provides research services with numerous standardized cell culture systems including transgenic and non-transgenic cell lines, glial cells, primary chicken and rat peripheral and central nervous system neurons of different developmental stages and organotypic brain slices. New models are developed and validated on request.
As a leading CRO for CNS drug development, QPS Neuropharmacology is the premier provider for services with transgenic animals. We have more than 20 years of experience in generating, characterizing, and maintaining transgenic disease models and applying them for drug testing projects.
QPS Neuropharmacology's expertise lies within the field of neurodegenerative diseases. We provide a state of the art research environment (AAALAC certified) for testing and evaluating new potential treatment approaches.
QPS Neuropharmacology's well characterized and validated in vivo models are useful tools to push your CNS drug discovery research forward. We are happy to support your research activities with sample material from our biobank composed of various specimen derived from our in-house in vivo models.
Experimental autoimmune encephalomyelitis (EAE) shows many pathological similarities to Multiple Sclerosis (MS) and is therefore often used as model to mimic MS by injecting Myelin-Oligodendrocyte-Glycoprotein (MOG) in combination with pertussis toxin (PTX).
C57Bl/6 mice develop clinical signs about two weeks after MOG + PTX treatment. Fingolimod (Fingo) was able to reduce clinical signs reaching significance after 2 weeks of treatment (Fig. 1a). Evaluation of all animals in the Open Field test showed that MOG + PTX treatment resulted in a completely diminished rearing behavior. Fingolimod was not able to rescue this phenotype (Fig.1b). Analysis of muscle strength in the Wire suspension test showed a severely reduced hanging time of MOG + PTX treated mice. This phenotype could be partially rescued by Fingolimod (Fig.1c). Motor coordination of MOG + PTX treated animals was thus also strongly impaired as analyzed in the RotaRod test. Fingolimod was also able to partially rescue this phenotype (Fig.1d).
MOG + PTX treated mice closely mimic EAE symptoms and are therefore a good model for Multiple Sclerosis. The model is widely used as primary screening tool for new MS compounds.
Figure 1: Clinical signs and motor deficits of EAE mice. EAE induced C57Bl/6 mice were tested for clinical signs (A), rearing activity in the Open Field test (B), muscle strength in the Wire suspension test (C) and motor coordination in the RotaRod test (D) compared to vehicle treated and EAE + Fingo treated mice. n = 13-16 per group; Mean + SEM; Kruskal-Wallis One-way ANOVA followed by Dunn‘s multiple comparisons post hoc test; *p<0.05; **p<0.01; ***p<0.001. *EAE-Vehicle vs. Sham-Vehicle; #EAE-Fingo vs. EAE-Vehicle. Fingo = Fingolimod.