Michigan State University

College of Social Science









Human Development Initiative

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The Human Development Initiative, begun in 2009, is a community of scholars throughout the university interested in development across the lifespan. The initiative creates venues where scholars involved in cutting-edge research in the social and health sciences (including genetics, neuroscience, and psychosocial development) can focus on the intersections between their own work and that of other researchers. We invite faculty and graduate students to join us at our bi-weekly brown bag speaker series and our fall and spring colloquia.


Friderici Karen Friderici
Professor
Ph.D. Michigan State University
frideric@msu.edu


Research Statement
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Research in the Friderici laboratory centers on the molecular pathology of genetic disease, primarily human disease. The understanding of normal function of organs or proteins can be better understood when we observe the effects of mutation. In collaboration with Dr. Rachel Fisher (MSU Department of Pediatrics & Human Development), the Friderici lab investigates the genetics of hearing, and have identified families from the Mid-Michigan area that have genetic hearing loss. Several of the families are now being studied in detail. In one of the families the lab has found the location of a gene that has not been previously described to be involved in the hearing process. They are using the resources of the Human Genome Project to identify the gene and intend to pursue studies of its function once the gene has been identified. In another very large family the Friderici lab is studying the genes for recessive hearing loss. One of the mutated genes has been identified but at least one other defective gene causes deafness in this family. Dr. Friderici also collaborates in studies that examine the role candidate genes may play in the etiology of multifactorial disease by correlating common polymorphisms in selected genes with disease risk. For example, her lab is examining genes potentially involved in Attention Deficit Hyperactivity Disorder (with Dr. Joel Nigg at the Department of Psychiatry at the University of Oregon Health Science Center) and in infant prematurity (with Dr. Claudia Holtzman at MSU Department of Epidemiology).


Research Publications    
 Title
2009Waldman ID, Nigg JT, Gizer IR, Park L, Rappley M, Friderici KH. The Adrenergic Receptor 2-alpha gene (ADRA2alpha) and neuropsychological executive functions as putative endophenotypes for childhood ADHD. Cognitive, Affective and Behavioral Neuroscience.6:18-30
2007Nigg J, Nikolas M, Friderici K, Park L, Zucker RA. (2007) Genotype and Neuropsychological Response Inhibition as Resilience Promoters for ADHD, ODD, and CD under Conditions of Psychosocial Adversity. Development & Psychopathology. Dev Psychopathol. 19(3):767-86.
2007Sheid JM, Holzman CB, Jones N, Friderici KH, Nummy KA, Symonds LL, Sikorskii A, Regier MK, Fisher RA. (2007). Elevated depressive symptoms in mid-pregnancy: associations with 5-HTTLPR geneotype and lifetime stressors. Genes, Brains and Behavior. 6(5):453-64.
2006Rendtorff ND, Zhu M, Fagerheim T, Antal TL, Jones P-P, Teslovish TM, Gillanders EM, Barmada M, Teig E, Trent JM, Friderici KH, Stephan DA, Tranebjaerg L. (2006). A novel missense mutation in ACTG1 causes dominant deafness in a Norwegian DFNA20/26 family, but ACTG1 mutations are not frequent among families with hereditary hearing impairment. Eur. J. Hum. Genet. Oct;14(10):1097-105