Guo-Li Ming MD, PhD
The intricate neural network formation during embryonic and perinatal development is fundamental for proper brain functions and recent aggregate data also implicates adult neuronal development in specific brain functions through adult neurogenesis. Aberrant neural network formation has been suggested to be the cellular basis for many mental disorders. My laboratory is interested in understanding the molecular and cellular mechanisms underlying neuronal navigation during early neural development and in adulthood. We are also interested in understanding the function of risk genes of mental disorders in neural development. (1). Neuronal migration and nerve guidance of newborn neurons from neural stem cells in the embryonic and adult brain: Although the environment in the developing brain and in the mature central nervous system (CNS) are quite different, adult neurogenesis in the hippocampus and in the olfactory bulb exhibit strikingly similar neural developmental processes to early embryonic neurogenesis, including neuronal morphogenesis and migration, axon/dendritic development and targeting, and finally synapse formation. We are particularly interested in understanding the intrinsic and extrinsic mechanisms regulating navigation of newborn neurons, including neuronal migration and axon/dendritic development in the embryonic and adult brain. In contrast to active and rapid axonal and dendritic growth of newborn neurons during adult neurogenesis, regenerative capability of mature neurons in the adult brain is extremely limited. We are interested in mechanisms promoting axon regeneration in the adult nervous system a focus on epigenetic regulation of intrinsic growth ability. (2). Understanding mechanisms of neurological diseases and mental disorders with neural developmental origins. We are currently focusing on investigating roles of several susceptibility genes for mental disorders in regulating different phases of embryonic and adult neurogenesis, including MeCP2 (Rett Syndrome), PTEN (autism), NF1 (neurofibromatosis type 1) and DISC1 (Schizophrenia and autism) using mouse as a model system. In parallel, we are using patient-specific, induced pluripotent stem cells (iPSCs) from fibroblasts of human patients with MeCP2, DISC1 mutations as human models to study the function of these risk genes in neural development and their contribution to the pathogenesis of diseases.