CRO for CNS Drug Development
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Welcome to QPS Neuropharmacology
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.
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- Customer satisfaction is our absolute priority
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Latest News
6neo mice closely mimic Pompe disease muscle pathology
The glycogen storage disease type II (GSD II) is a rare, multisystemic disease with variable rates of disease progression that is also called Pompe disease. It is caused by alterations in the acid α-glucosidase (GAA) gene, resulting in reduced levels of this enzyme that in turn leads to a reduced degradation and thus accumulation of glycogen mostly in different muscle tissues. Most common symptoms include cardiac dysfunction, muscle weakness, hypotonia, respiratory problems and a strongly reduced life expectancy. To model this lysosomal storage disease, we analyzed the 6neo mouse line that has a Gaa knockout resulting in reduced GAA enzyme levels and thus a progressive accumulation of glycogen in different muscle tissues. Our preliminary analyses of muscle and motor deficits show reduced muscle strength in the wire hanging test of 6neo mice at 24 weeks of age compared to wild type littermates (A). In the grip strength test significant differences of 6neo mice can already be observed at the age of 8 weeks that progressively worsen with age (B). Evaluation of motor deficits using the beam walk test revealed that 6neo mice slip more often compared to wild type littermates at the age of 24 weeks (C+D). Our results suggest that 6neo mice closely mimic the muscle phenotype observed in Pompe disease patients, making this mouse a useful tool to evaluate new compounds against this devastating disease.
Figure: Muscle and motor deficits in the 6neo mouse model of Pompe disease. 6neo mice at the age of 8 and 24 weeks were tested for hanging time in the wire hanging test (A), for mean grip strength in the grip strength test (B) and for number of slips (C) and slips per speed (D) in the beam walk test (C+D). WT: n = 24; 6neo: n = 48; mean + SEM; two-way ANOVA followed by Bonferroni’s multiple comparison post hoc test; **/##p<0.01, ***/###p<0.001; *significance between genotypes; #significance between age groups.
Further analyses of 6neo mouse pathological features like enzyme and substrate levels as well as survival rate are currently in progress.