Jaekyoon Kim is a postdoctoral research scholar in the Department of Neuroscience and Pharmacology atCarver College of Medicine andIowa Neuroscience Institute at the University of Iowa. He received his bachelor’s degree in biochemistry from Yonsei University in Seoul, South Korea, and his master’s degree in biotechnology from Seoul National University. Hee received a Ph.D. in psychology, along with another master’s degree, at the University of Wisconsin, Milwaukee, where he worked with Karyn Frick, widely considered to be a world expert on the effects of estrogens on the brain and cognition. This background has given Kim the important ability to assess neuroscience from both a biomedical science perspective and a psychology perspective. Throughout his Ph.D., his work focused on the effects of sex steroid hormones, especially estrogen, on memory consolidation and he has become interested in sex differences in neurological disorders. Autism is a neurodevelopment condition with known sex differences. One of the most common genetic variations associated with autism is the deletion of the 16p11.2 chromosomal region, which can be faithfully modeled in mice. Using the 16p11.2 hemi-deletion mouse model, the Abel Lab at the University of Iowa revealed male-specific impairments in the acquisition of reward-dependent goal-directed behaviors. As a postdoctoral research scholar, Kim is working on elucidating the underlying mechanisms driving sex-dependent behavioral alterations in the 16p11.2 hemi-deletion mice.
Principal Investigator: Edwin Abel
Fellow: Luke Zaabel
Undergraduate Fellow Project:
The 16p11.2 hemi-deletion (16p11.2 del) is one of the most common genetic changes associated with autism. Because the human 16p11.2 region is highly conserved in mice, we can model and study this genetic risk factor. Using this mouse model, we previously reported alterations in the structure and function of striatal circuits, which is consistent with recent studies reporting changes in striatal structure and function in people with autism. The striatum is the input structure of the basal ganglia, the key neural substrate for reward processing and motor control and these functions are often disrupted in individuals with autism. In this project, we will investigate the molecular mechanisms, cell-type specific effects and specific neuronal circuits that lead to distinct behavioral phenotypes in 16p11.2 del mice, applying a combination of genetically modified mouse models and targeted intra-striatal virus injections with complementary behavioral and biochemical techniques. We will also examine the biological basis for the sex differences in autism, which is more prevalent in males, using 16p11.2 del mice. Together, these findings will identify molecular mechanisms specific to the striatal dysfunction in autism. We hope that our research will help to develop novel therapeutic approaches for autism.