The Division of Translational Neuroscience of Schizophrenia is a research group, which focuses on developing, supporting, and administering programs of research, research training and resource development aimed at understanding the pathophysiology of schizophrenia and related disorders, and hastening the translation of behavioral and neuroscience advances into innovations in clinical care.
The division supports a broad research portfolio, which includes studies of the phenotypic characterization and risk factors for schizophrenia and related disorders; clinical neuroscience to elucidate etiology and pathophysiology of these disorders; and psychopharmacologic and somatic treatment development.
One of the main focuses our group is to investigate the nature and treatment of cognitive deficits commonly seen in schizophrenia and related disorders. It is now widely accepted that cognitive deficits are a core feature of schizophrenia and are highly implicated in the occupational and social deficits seen in this patient population. Another important focus of our research group is to conduct phenotyping to understand the genetic inheritance patterns of schizophrenia and related disorders. This research is being conducted by using molecular biological techniques in post-mortem brain tissue, as well as, a variety of physiological and genetic assessments in probands and their family members.
Hence, our primary focus is to conduct research on the etiology and pathophysiology of schizophrenia and related disorders in an order to: * Define predictors and understand the mechanism of treatment response * Create and refine biomarkers, behavioral assessments, and phenotypic characterizations of psychotic disorders * Evaluate existing therapies for new indications, and, in collaboration, with academic, industry and regulatory agencies, hasten the development of more effective new treatments for psychotic disorders with an emphasis on schizophrenia.
Thus, our group supports an integrated research program in an effort to clarify psychopathology and neurocognitive deficits to better understand the underlying pathophysiology in an effort to develop new treatments to enhance neurocognition in schizophrenia and related disorders.
To achieve the stated goals, we propose to study (1) human volunteers with schizophrenia and related disorders using in vivo brain imaging, novel pharmacological interventions, and postmortem tissue analysis, and (2) laboratory mice with and without genetic manipulations using behavior, electrophysiology, and pharmacology.
Isohanni, M., Miettunen, J., Maki, P., Murray, G. K., Ridler, K., Lauronen, E., Moilanen, K., Alaraisanen, A., Haapea, M., Isohanni, I., Ivleva, E., Tamminga, C., McGrath, J., and Koponen, H., "Risk factors for schizophrenia. Follow-up data from the Northern Finland 1966 Birth Cohort Study" World Psychiatry, 2006
Hayashi, K., Pan, Y., Shu, H., Ohshima, T., Kansy, J.W., White, C.L., III, Tamminga, C.A., Sobel, A., Curmi, P.A., Mikoshiba, K., Bibb, J.A., "Phosphorylation of the tubulin binding protein, stathmin by Cdk5 and MAP kinases in the brain" J Neurochem, 2006
Tamminga, C.A., "Explaining side effects and therapeutic effects of drugs by actions upon neurotransmitter receptors" Solomon Snyder, Research Career, APPI, 2006
SIGNIFICANT PUBLICATIONS
Tamminga, C.A., Smith, R.C., Ericksen, S.E., Chang, S., Davis, J.M., "Cholinergic influences in tardive dyskinesia" Am J Psychiatry, 134:769-774, 1977
Thaker, G.K., Nguyen J.A., Strauss, M.E., Jacobson, R., Kaup, B.A., Tamminga, C.A., "Clonazepam treatment of tardive dyskinesia: A practical GABAmimetic strategy" Am J Psychiatry, 147(4):445-451, 1990
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