Severe motor deficits of the murine Parkinson’s disease model hA53Ttg
QPS Neuropharmacology
Newest results of our R&D team at QPS Neuropharmacology validate severe and very early motor deficits in hA53Ttg mice, making this model well-suited for preclinical Parkinson’s disease (PD) research. PD belongs to the most devastating neurodegenerative diseases of the 21st century. The development of new drugs halting disease progression is therefore the main focus of …
Automated quantitative analysis of spine density in Golgi-Cox-stained brain sections
QPS Neuropharmacology
To simplify dendritic spine analysis, our histology and IT team joined forces and developed a macro-based image analysis for rater-independent, unbiased, fast, and efficient automated dendritic spine quantification. Brain sections are stained by the Golgi-Cox method. For spine density analysis, Z-stack images are taken using 63x oil lens, and stacks are collapsed using Zeiss ZEN …
Fmr1-knockout Mice Present Main Phenotypic Traits of Fragile X Syndrome
QPS Neuropharmacology
Newest results of our student’s FFG-funded PhD thesis at QPS Neuropharmacology in cooperation with Prof. Marcello Leopoldo from the University of Bari, Italy, confirms the value of Fmr1-knockout (KO) mice to model neurobehavioral deficits manifested in fragile X syndrome. Fragile X syndrome is the most commonly inherited form of intellectual disability and a monogenic cause …
BTBR T+ Itpr3tf/J (BTBR) mice, a suitable animal model to study anxiety and repetitive behavior in Autism Spectrum Disorders (ASD)
QPS Neuropharmacology
In her FFG-funded PhD thesis at QPS Neuropharmacology in cooperation with Prof. Marcello Leopoldo from the University of Bari, Italy, Shirin Sharghi behaviorally characterized the BTBR T+ Itpr3tf/J mouse model of Autism Spectrum Disorders (ASD). BTBR T+ Itpr3tf/J mice were allocated to three different treatment groups of either LP-211 (a serotonergic compound), R-Baclofen (a GABAergic …
6neo mice closely mimic Pompe disease muscle pathology
QPS Neuropharmacology
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 …