000238624 001__ 238624
000238624 005__ 20210924173038.0
000238624 0247_ $$2GEPRIS$$aG:(GEPRIS)5433545$$d5433545
000238624 0247_ $$2I:(DE-588)1065079516$$aG:(Dimensions)grant.4787308$$dgrant.4787308
000238624 035__ $$aG:(GEPRIS)5433545
000238624 150__ $$aRolle des Neurofibromin bei hippokampaler Funktion und Plastizität$$y2004-01-01 - 2008-12-31
000238624 5101_ $$0I:(DE-588b)2007744-0$$aGerman Research Foundation$$bDFG
000238624 680__ $$aI neurofibromatosis (NF1) is a common hereditary disease which is associated with learning and memory disorders. Decisive insights into the relationships of the NF1-associated learning and memory impairments underlying molecular and cellular mechanisms have been developed in mouse models of the disease. Remains unclear which central nervous system cell types are responsible for the formation of NF1-associated learning deficits. In the project proposed here transgenic mice with a cell-type specific deletion of the NF1 gene is to be determined (in inhibitory neurons, excitatory neurons or astrocytes) by investigating what is the critical cellular localization of the genetic lesion for training NF1-associated learning deficits. By studying potential structural correlates of learning and memory in the hippocampus (synaptic plasticity, hippocampal neurogenesis) in these transgenic mice are insights are obtained, how changes at the molecular level lead to disturbances of cellular functions, resulting in impairment of cognitive functions. Ultimately, should a based on these findings, pharmacological treatment of NF1-associated learning deficits are being tested in an animal model. About the Insights into the Pathogenesis of NF1-associated learning deficits, this project could provide valuable insights into normal learning and memory functions underlying biological mechanisms.
000238624 909CO $$ooai:juser.fz-juelich.de:893647$$pauthority$$pauthority:GRANT
000238624 909CO $$ooai:juser.fz-juelich.de:893647
000238624 980__ $$aG
000238624 980__ $$aAUTHORITY