Professor of Biochemistry and Biophysics
(PhD – University of Texas)
HONORS & AWARDS
- Hilton Distinguished Investigator Award from the National Alliance for Research on Schizophrenia and Depression (NARSAD)
- Pogue Fellowship for Scholarly Research
- Member NIH Neurodifferentiation, Plasticity, and Regeneration (NDPR) Study Section
- NIH Research Career Development Award
- Jefferson-Pilot Award in Academic Research
BIO
Patricia F. Maness, Ph.D., received her doctorate in Biochemistry in 1975 from the University of Texas.聽 She was an Anna Fuller Fund Postdoctoral Fellow from 1978-1980 at the Rockefeller University in the laboratory of Nobel Laureate Dr. Gerald M. Edelman, and Assistant Professor. Since 1980 聽Dr. Maness has served on the faculty of the University of North Carolina School of Medicine-Chapel Hill, where she is currently Professor in the Department of Biochemistry and Biophysics.聽 She is a member of the 黑料网 Neuroscience Center, 黑料网 Carolina Institute for Developmental Disabilities, and 黑料网 Curriculum in Neurobiology.聽 Dr. Maness’s research focuses on understanding the molecular mechanisms governing development of the mammalian nervous system; specifically, mechanisms of axon guidance and synaptogenesis and their disruption in neuropsychiatric disorders such as autism, schizophrenia, and intellectual disability. As of April 2025, Dr. Maness has published 113 scientific papers, and trained 13 graduate students, 30 postdoctoral fellows, and 32 undergraduate and medical students.
RESEARCH
How neuronal circuitry in the brain is established during development and refined in the adult is a central unanswered question in neuroscience. Neural recognition molecules expressed on the neuronal surface are pivotal players in developing cortical circuits. Among the most relevant of these molecules to human disease are members of the NCAM and L1 family (L1, CHL1, NrCAM, Neurofascin). Each of these cell recognition molecules has established functions in axon guidance that mediate correct topographic synaptic targeting of axons, while exciting new findings reveal that they also have vital functions in regulating synaptogenesis and plasticity of cortical networks. Importantly, mutations in neural adhesion molecule genes may contribute to susceptibility to human neuropsychiatric diseases such as schizophrenia, autism spectrum disorders, and intellectual disability. To study the normal and abnormal function of neural cell adhesion molecules in brain development and function, our laboratory uses a multidisciplinary approach to generate and analyze novel mouse genetic models of neurodevelopmental disorders. Neural adhesion molecules of the immunoglobulin superfamily (Ig-CAMs) are risk factors for neurodevelopmental disorders such as autism, schizophrenia, and intellectual disability. Maness transformed our understanding of how IgCAMs function by discovering that they are not molecular 鈥済lue鈥� but are signaling receptors that establish and refine neuronal connectivity in the mammalian brain. Using novel mouse models she demonstrated that IgCAMs mediate topographic axon targeting and synaptogenesis, and identified their signaling pathways through Src, RhoA and MAP kinases. She was first to determine that a normal proto-oncogene product, c-Src, functions to regulate neuronal axon guidance, rather than proliferation, distinguishing it from its oncogenic counterpart. This finding had widespread implications for our understanding that proto-oncogenes play normal roles in cell differentiation.
