Rebecca R. Knickmeyer, PhD

Associate Professor, Institute for Quantitative Health Sciences
Associate Professor, Department of Pediatrics and Human Development
Co-Director, Center for Research in Autism, Intellectual, and Other Neurodevelopmental Disabilities (C-RAIND)  B240 Life Science
Adjunct Associate Professor,
Department of Epidemiology and Biostatistics
Michigan State University

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The long-term goal of the Knickmeyer lab is to develop therapeutic interventions which could normalize adverse neurodevelopmental trajectories in infancy and early childhood, thereby preventing the onset of psychiatric disorders or reducing their severity. Our immediate goal is to identify genes and molecular pathways associated with altered brain development in infancy and early childhood through the integration of pediatric neuroimaging with cutting-edge techniques in genomics, metagenomics, and analytical chemistry.

Major areas of research in the lab include:

  • Influence of the Gut Microbiota on Infant Brain Development. The gut microbiome is a complex microbial ecosystem which varies between individuals and may be a key modulator of neurodevelopment. Projects in this area will utilize gnotobiotic mice, human clinical samples, neuroimaging, and neurobehavioral techniques to understand how microbes contribute to risk for anxiety, depression, and autism spectrum conditions.
  • Genetic Influences on Infant Brain Development. Imaging-genetics represents a powerful strategy for understanding how genetic variants impact neural structure and function. Projects in this area will utilize large imaging-genetics datasets to identify genes influencing neurodevelopmental trajectories from birth to age 6, develop predictive models for cognitive ability and emotional functioning using genetic variation, environmental risk factors, and neuroimaging phenotypes, and clarify how genetic risk for psychiatric disease manifests in infancy and early childhood.
  • Sexual Differentiation of the Human Brain: Relative risk levels for many psychiatric disorders are dramatically different in males and females. X-chromosome effects and early exposure to gonadal hormones are strong candidates for a causal role. Projects in this area include neuroimaging studies of typical children and individuals with Turner syndrome (TS), a well-defined genetic disorder resulting from partial or complete loss of one of the sex chromosomes.