The Bearden lab’s research aims to understand genetic, cognitive and neurobiological risk factors for the development of adolescent-onset neuropsychiatric disorders. We are examining these questions through two complementary lines of research: 1) The investigation of intermediate neuroanatomic and cognitive traits associated with the development of psychosis and mood disorder; and 2) The study of neurobehavioral manifestations of syndromes with an identified genetic origin
One of these studies focuses on the 22q11.2 Deletion Syndrome, a genetic disorder which results in a disruption of early neuronal migration and confers a particularly high risk for psychosis. Dr. Bearden’s research group has an ongoing, NIMH-funded longitudinal study of risk factors for psychiatric disorder in children and adolescents with this syndrome. This project involves comprehensive phenotyping (i.e., dimensional measures of psychopathology, neurocognition, and structural and functional neuroanatomy) which will be examined in relation to genetic variation at the 22q11.2 locus.
We are also investigating risk factors for psychosis in youth with subthreshold clinical symptoms indicating high risk for the development of psychotic illness, in the Center for Assessment and Prevention of Prodromal States (CAPPS) . The CAPPS program, directed by Dr. Bearden, is part of the NIMH-funded North American Prodromal Longitudinal Study (NAPLS) Consortium.
In collaboration with Alcino Silva , Dr. Bearden’s lab is also conducting two translational studies of the neural basis of cognitive and social difficulties in children with another genetic disorder, Neurofibromatosis I, one of the most common single-gene disorders affecting neurologic function in humans. We have just completed enrollment for an NIMH-funded exploratory intervention grant , which examines a potential pharmacologic treatment for cognitive disability in individuals with NF1, the HMG-CoA reductase inhibitor lovastatin, which acts as a potent inhibitor of Ras activity and is commonly used for the treatment of hypercholesterolemia. The rationale for this novel intervention is based on findings from the mouse model of the disorder, in which lovastatin treatment was able to reverse the biochemical, electrophysiological and cognitive deficits associated with NF1 (Li et al. Curr Biol. 2005 ). This study represents one of the first translational clinical trials for developmental learning disabilities.
The Bearden lab also has a new study funded by the Department of Defense NF1 Research Program. This study aims to investigate potential blood biochemical and brain biomarkers of cognitive control and social deficits, both cross-sectionally and longitudinally over a two-year period, in school-age children with NF1.