PsychoGenics, a leading provider of preclinical CNS service,  has obtained a license from University of California, San Diego to its Line-41 mouse model of Alzheimer’s disease, expressing human APP with the Swedish (K670N/M671L) and London (V717I) mutations under the control of the murine-Thy-1 promoter.

This mouse model, developed by Prof. Eliezer Masliah and Edward Rockenstein at UCSD, (Rockenstein et al., 20011) overexpresses human APP with the Swedish double mutation and London mutation under the control of a neuron-specific Thy1 promoter. This mouse model shows early onset and progressive plaque deposition - in cerebral cortex and hippocampus as early as 3-4 months. Other hallmarks of human Alzheimer’s disease recapitulated in the Line 41 mice include: dystrophic neurites containing hyperphosphorylated tau protein in the vicinity of mature plaques and cognitive impairment coinciding with appearance of neuro-inflammation, characterized by astroglioses and increased micro-glia activation, starting at 6 months of age and progressively worsening as the amyloid load increases. This unique mouse model of Alzheimer’s disease will now be broadly available to Pharma and Biotech, providing an important tool in the development of novel treatments for this devastating neurodegenerative disease.

“We are very excited to add this mouse model to our portfolio of Alzheimer’s models which include: both mice (the Tg2576 and APP/PS1 from the University of South Florida) and rat (the McGill-R-Thy1-APP) models of amyloidosis, and, a Tauopathy mouse model, the rTg4510, from the Mayo Clinic. The Line-41 model displays key features of human Alzheimer’s disease and together with some of our other models offers a valuable tool to assess anti-neuroinflammatory and A-beta lowering strategies as treatments for Alzheimer’s disease,” remarked Emer Leahy, Ph.D., president and CEO of PsychoGenics. “Using our extensive array of behavioral tests including our Cube technology platforms and our full range of services in electrophysiology, biochemistry, neurochemistry, and quantitative immunohistochemistry, we expect to be able to identify an even earlier Alzheimer’s disease associated phenotype in Line-41 which will enable companies not only to assess treatment strategies but also to explore prevention and early intervention approaches.”