McLean Hospital 115 Mill Street Belmont, MA 02478
Dr. Woo’s research interest is in defining the nature of cortical circuitry disturbances in schizophrenia and other psychotic disorders, and in understanding the developmental neurobiological pathways that lead to these disturbances.
In addition to his research, Dr. Woo maintains an active clinical practice. His ultimate goal is to translate research findings from the laboratory into fundamentally novel, rational, and truly effective treatment and prevention strategies.
In addition to his role as medical director of the Harvard Brain Tissue Resource Center, Dr. Woo is also interested in determining how specific neural circuitry elements in the brain, specifically the cerebral cortex, are altered in schizophrenia in order to understand how, collectively, neural circuits become functionally disturbed. Dr. Woo’s Laboratory for Cellular Neuropathology, founded in 2004, also focuses on how these abnormalities may arise during development.
Altogether, findings of Dr. Woo’s research have implications for the development of rational strategies for the diagnosis, treatment, early intervention, and prevention of schizophrenia.
The clinical symptoms and cognitive and functional deficits of schizophrenia typically begin to emerge during late adolescence and early adulthood. Recent findings suggest that disturbances of a specific subset of inhibitory neurons that contain the calcium-binding protein parvalbumin (PV) may be involved in the pathogenesis of the onset of this illness. Specifically, converging lines of evidence suggest that mechanisms such as oxidative stress and extracellular matrix (ECM) deficit may contribute to the functional impairment of PV neurons, leading to aberrant developmental synaptic pruning of prefrontal cortex neural circuitry and hence a failure in the maintenance of synaptic stability. In addition to promoting the functional integrity of PV neurons, maturation of ECM may also play an instrumental role in the termination of developmental synaptic pruning; thus, ECM deficit can lead to excessive loss of synapses by prolonging the course of pruning.
Together, these mechanisms may contribute to the onset of schizophrenia by compromising the synaptic integrity of PFC connectional architecture and may also lead to persistent and unwanted plasticity of cortical circuits, providing a pathophysiological pathway that sustains the chronicity of the illness. In this context, Dr. Woo’s work focuses on deepening the understanding of these mechanisms based on postmortem human brains and animal studies using a variety of protein and gene expression techniques, in addition to the utilization of differentiated human neurons.
Dr. Woo is also particularly interested in, and has expertise in, the translation of research findings from the laboratory into diagnostic and treatment strategies that are of potential clinical importance.
Mauney SA, Athanas KM, Pantazopoulos H, Shaskan N, Passeri E, S Berretta, Woo TUW. Developmental pattern of perineuronal nets in the human prefrontal cortex and their deficit in schizophrenia. Biological Psychiatry 2013;74:427-435.
Pietersen CY, Kim S, Lim MP, Chen J, Stephens R, Rooney R, Goldstein JM, Petryshen TL, Seidman LJ, Shenton M, McCarley RM, Sonntag, KS, Woo TUW. Molecular profiles of pyramidal neurons in schizophrenia. Journal of Neurogenetics 2014;28:70-85.
Woo TUW. Neurobiology of schizophrenia onset. Current Topics on Behavioral Neurosciences 2014;16:267-295.
Belmont campus - Mailman Research Center, Room 332A