In our lab we study two cognitive disorders: Fragile X Mental Retardation and Alzheimer's disease. To study these disorders we utilize Drosophila models. These models are mutants of the Drosophila homologues of the humans genes associated with these disorders. With these models we are investigating the biochemical functions and biochemical pathways affected by the loss of the disease related proteins that cause phenotypes that are similar to symptoms display by patients of these diseases (see below). Our goals are to gain insight into the underlying causes of the respective disease symptoms as an approach to develop therapeutic strategies to treat these disease as well as to learn more about the basic mechanisms required for normal learning and memory.
This stock contains a deletion of the dfmr1 gene as described in, "Drosophila Lacking dfmr1 Activity Show Defects in Circadian Output and Fail to Maintain Courtship Interest." The mutants are viable but display defects in several neurons and behavioral test including naïve courtship, memory and circadian behavior.