University of Minnesota
University Relations

Minnesota Supercomputing Institute

Log out of MyMSI

Research Abstracts Online
January 2009 - March 2010

Main TOC ....... College TOC ....... Next Abstract

University of Minnesota Twin Cities
Medical School
Department of Psychiatry

PI: S. Hossein Fatemi

Prenatal Virally Induced Brain Disorder

Schizophrenia, which affects 1% of the world's population, has been linked epidemiologically to prenatal exposure to human influenza virus. Experimental animal data supporting this linkage are lacking. The overall goal of this group’s research is to understand how prenatal human influenza viral infection affects brain development adversely, leading to the genesis of schizophrenia. The objective of the project at MSI is to determine how prenatal infection of mice with human influenza virus causes subsequent brain structural and behavioral abnormalities in adult animals. The central hypothesis is that prenatal viral infection at critical periods during embryogenesis causes permanent changes in brain structure and function, leading to the development of postnatal behavioral abnormalities. Once the pathogenesis of influenza virus-induced behavioral abnormalities is understood in mice, similar pathogenic mechanisms can be selectively sought for schizophrenia. These researchers have succeeded in performing pilot studies, indicating that infection of mice on day 9 of pregnancy with a sublethal dose of human influenza virus causes abnormal corticogenesis and changes in levels of several important brain markers in postnatal life. Additionally, infection on day 9 of pregnancy leads to development of abnormal behavioral responses on prepulse inhibition in the affected adult mice.

The central hypothesis will be tested and the project objective accomplished by pursuing two specific aims: to identify neuroanatomical molecular profiles for postnatal brain development that result from the effects of prenatal human influenza viral infection in mice; and to characterize morphometric abnormalities that are produced in the offspring following prenatal human influenza viral infection in mice. This work is innovative, because it capitalizes on a new animal model, which links a viral insult to abnormal brain development.

Group Members

Timothy Folsom, Research Associate
Rachel Kneeland, Research Associate
Stephanie Liesch, Research Associate
Teri Reutiman, Research Associate