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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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  • Customer satisfaction is our absolute priority
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  • 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
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Latest News

Robust neuroinflammation in the Amyotrophic Lateral Sclerosis disease mouse model SOD1-G93A/low

Amyotrophic Lateral Sclerosis (ALS) as progressive motor neuron disease is characterized by quickly progressing muscle atrophy and correlating motor symptoms. Degeneration of the upper and lower motor neurons of the spinal cord is the main cause for the observed motor decline and paralleled by strong neuroinflammation as observed by occurrence of astrocytosis and many activated microglia. The SOD1-G93A/low transgenic mouse as preclinical model of ALS expresses SOD1 with G93A mutation with a lower gene copy number compared to the commonly used SOD1-G93A model, causing a delayed symptom onset and extended survival and thus providing a longer window for drug treatment studies. Here we show, that male SOD1-G93A/low mice develop astrocytosis in the cervical, thoracic and lumbar ventral horn of the spinal cord as early as 27 weeks of age (GFAP; Fig.1A-C). Changes in microgliosis levels, as determined by an increased number of activated microglia, are even more pronounced than changes in astrogliosis in the same spinal cord regions. Additionally, activated microglia show a strong progression compared to non-transgenic (ntg) littermates (Iba1; Fig.1D-F).

Robust neuroinflammation

Figure 1. Neuroinflammation in the spinal cord of male SOD1-G93A/low mice. Astrocytosis as analyzed by percent of cervical, thoracic and lumbar ventral horn immunoreactive (IR) area covered by GFAP (A-C) and activated microglia as analyzed by Iba1 IR area in the same spinal cord regions (D-F) in 24, 27 and 30 week old male SOD1-G93A/low mice. G: Representative images of Iba1 labeling in the cervical spinal cord of a 30 week old male SOD1-G93A/low mice compared to a ntg littermate. Two way ANOVA with Tukey’s and Sidak’s multiple comparison post hoc test. Mean + SEM. *p<0.05, **p<0.01, ***p<0.001. *differences between genotypes; # differences between age groups. DH: dorsal horn; VH: ventral horn.

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