InfrafrontierGR/Phenotypos

These include: (i) the Davis tauopathy mouse, which models aspects of Alzheimer’s and Picks disease. These mice lack all endogenous Tau, but carry the entire human locus and develop progressively intensifying age-dependent cognitive deficits. (ii) models of Neurofibromatosis 1, an autosomal dominant human nervous system genetic disorder. Similar with patients, these conditional knock-outs exhibit deficient spatial learning and memory, attention and motor coordination. (iii) Mice lacking the anaplastic lymphoma kinase (Alk), which exhibit enhanced performance in certain cognitive tests. (iv) Mouse models of Fragile X syndrome, a genetic disease distinguished by mental retardation, learning deficits, decrease sociability and social interactions. (v) Alpha-synuclein mutants that model Parkinson’s disease, degeneration in the CNS, motor dysfunction and dopamine malfunction. Furthermore, given that many behavioral platforms have been established and characterized in the rat model, which lacks strong genetics, novel findings from the rat platform will be modeled and genetically analyzed in the mouse.