Contact Us Services

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.

Welcome to QPS Neuropharmacology

QPS Neuropharmacology is the division of QPS that focuses on preclinical studies in CNS diseases, Orphan 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, Autism Spectrum Disorder (ASD), Schizophrenia, Lewy Body Dementia (LBD) and other neurodegenerative 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.

Why Choose Us?

  • Customer satisfaction is our absolute priority
  • Your timeline is our timeline
  • Every study is custom-built
  • Scientific input to study design and data interpretation
  • Extensive experience with virtually all drug targets and treatment types
  • Wide range of validated models and techniques for comprehensive compound tests from a single source
  • AAALAC certification ensures highest quality standards


Latest News

In vitro model to study A53T α-synuclein in PD

Different preformed recombinant human α-synuclein (α-syn) fibrils were evaluated for their toxicity and seeding properties on primary cortical neurons in vitro.

Our results show that monomeric human α-syn has no impact on cell viability, while preformed wild type and A53T human α-syn fibrils have toxic effects on primary cortical neurons. This toxic effect was exceeded by oligomeric isoforms (Fig.1A). Only A53T α-syn fibrils of the tested isotypes showed seeding properties in cortical neurons (Fig.1B).

cell viability

Figure 1. In vitro assessment of α-syn preformed fibrils on mouse primary neurons. Toxicity (A) as well as seeding (B) properties of different preformed recombinant human α-syn species (Stressmarq) on mouse primary cortical neurons. (A) Neurons treated with α-syn species, and assessed for cell viability by MTT assay. (B) Neurons treated with α-syn species and immunocytochemically analyzed for murine α-syn. Mean+SD. One-way ANOVA with Bonferroni post hoc test (vs vehicle control: VC). ** p<0.01, *** p<0.001.


Figure 2. Representative images of endogenous murine α-syn accumulation after seeding with different preformed recombinant human α-syn species (Stressmarq). Neurons were treated with (A) monomeric and (B) A53T preformed fibrils and after incubation immunocytochemically stained for murine α-syn. Nuclear stain DAPI = blue; murine α-syn = red; scale bar 100 µM.


In vivo mouse model expressing α-synuclein with A53T mutation

hA53T-Sud mice express A53T mutant human α-synuclein under the control of the murine Thy-1 promoter. This line M53 is bred on a C57BL/6J background (Chandra et al.2005).

Animals show the following phenotype:

  • 10 – 20 -fold higher α-synuclein levels compared to wild type mice (Chandra et al.,2005)
  • Motor deficits in the Rota Rod test at 6 months (Chandra et al., 2005; Rothman et al., 2013)
  • Muscle weakness in the Wire Hanging test at ~ 8 weeks (Maki et al., 2019)
  • Reduced anxiety in the Open Field and Elevated Plus Maze test starting at 10 and 14 weeks, respectively (Rothman et al., 2013)
  • Mean survival of about 43 weeks (Chandra et al., 2005)

The phenotype described above closely reflects PD pathology making the hA53T-Sud mouse a perfect model for your drug testing.

Newsletter Archive