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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, 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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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


Prof. Dr. Ludwig Aigner

Latest News

Modelling the L-DOPA Priming Effect in Rats

Parkinson’s disease (PD) is characterized by reduced dopamine levels in the striatum causing severe motor deficits. Patients are thus often treated with L-DOPA, the precursor of catecholamines, including dopamine, but positive effects of this treatment fade with prolonged treatment resulting in dyskinesia. To model this priming effect of L-DOPA treatment in vivo, Wistar Han rats can be utilized. Animals are unilaterally lesioned by injecting 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle to induce typical PD symptoms.

For L-DOPA priming, rats are treated intraperitoneally with L-DOPA for 21 days starting 3 weeks after lesioning.

For the evaluation of L-DOPA-induced dyskinesia (LID) rats are treated once with vehicle, 3 mg/kg, or 6 mg/kg L-DOPA about 2 weeks after the priming phase and afterwards analyzed in the ALO test to evaluate axial, limb and orolingual abnormal involuntary movements. Furthermore, rats are tested in the Rotometer bowl to evaluate contralateral rotations. The results show that L-DOPA induces a strong increase in the ALO score (A), and contralateral rotations (B) compared to vehicle-treated rats. Additionally, this effect was strongly dependent on the concentration of L-DOPA.

Priming Effect in Rats

Figure: ALO and rotation test after ICV 6-OHDA injection and L-DOPA priming. The ALO score (A) and the percentage of contralateral rotations (B) after acute L-DOPA treatment. n = 6 per group; mean + SEM; two-way ANOVA followed by Tukey’s multiple comparison post hoc test (A) and one way ANOVA followed by Tukey’s multiple comparison post hoc test; *p<0.05, ***p<0.001.

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