Rebecca Knickmeyer

Contact

knickmey@msu.edu
Office:  517-355-3977
Lab:  517-355-3978
IQ DIVISION – Neuroengineering

Departmental AFFILIATIONS

• Pediatrics

About

Rebecca Knickmeyer is an associate professor in the Department of Pediatrics and Human Development within the College of Human Medicine. Her research focuses on understanding how genetic and environmental factors influence the development of brain morphometry, anatomical and functional connectivity, and cognitive and emotional function in infancy and early childhood. She has a particular interest in mechanisms underlying sexual differentiation of the brain and the microbiome-gut-brain axis. Dr. Knickmeyer received her Ph.D. in Experimental Psychology from the University of Cambridge (U.K.) and completed her postdoctoral training in the Neurodevelopmental Disorders Research Center at the University of North Carolina at Chapel Hill.

The Knickmeyer Lab

At present, treatments for psychiatric conditions such as autism and schizophrenia only ameliorate and manage symptoms, a cure is not possible. By the time clinical symptoms are recognized, the underlying pathological brain development has, in large part, already occurred and may be irreversible. Therefore, our best hope of making a major impact on these devastating disorders is through prevention and very early intervention. Infancy and early childhood represent a particularly promising period for intervention as this is the most plastic phase of postnatal human development, marked by explosive brain growth, the emergence of functional brain networks, and dramatic advances in cognitive ability and behavioral repertoire.

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

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, producing individual differences in psychiatric risk. Large-scale cross-sectional studies in adolescents and adults are demonstrating the power of this framework, but cannot fully address the reality that mental illnesses are unfolding developmental processes, which commence in prenatal life and have different consequences at different life stages. The Knickmeyer lab is addressing this challenge by assembling a large and well-characterized imaging-genomics dataset focused on infancy through collaborations with world-leaders in infant neuroimaging. This effort is called ORIGIN (Organization for Imaging Genomics of Infancy) and is a working group of the ENIGMA consortium (Enhancing Neuro Imaging Genetics through Meta-Analysis). Specific goals include:

• Identify genes influencing neurodevelopmental trajectories from birth to age 6 using univariate and multivariate GWAS approaches.
• 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. It has been hypothesized that the prevalence and expression of these disorders are related to sex differences in brain development and that X-chromosome effects and early exposure to gonadal hormones (especially androgens and estrogens) 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.