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Schizophrenia Research Forum: Researcher Profile - Paul Patterson
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Researcher Profile - Paul Patterson

RESEARCHER INFORMATION
First Name:Paul
Last Name:Patterson
Title:Professor
Advanced Degrees:PhD
Affiliation:California Institute of Technology
Department:Biology
Street Address 1:216-76
City:Pasadena
State/Province:CA
Zip/Postal Code:91125
Country/Territory:U.S.A.
Phone:626-395-6826
Fax:626-585-8743
Email Address:php@caltech.edu
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 20 October 2005]
View all comments by Paul Patterson
Clinical Interests:
Autism spectrum disorders (pervasive developmental disorders), Depression, Neurodevelopmental disorders (e.g., 22q11 deletion syndromes), Schizophrenia
Research Focus:
Neuropathology, Epidemiology, Glia/myelin, Immunology, Neurodevelopment, DNA microrrays, Stem cells, Animal models, Molecular and Cell biology
Work Sector(s):
University
Web Sites:
Personal: http://www.cco.caltech.edu/~phplab/phplab.html
Lab: http://www.cco.caltech.edu/~phplab/phplab.html
Top Papers
Shi, L, Fatemi, SH, Sidwell, RW and Patterson, PH (2003) A mouse model of mental illness: maternal influenza infection causes behavioral and pharmacological abnormalities in the offspring. J. Neurosci. 23: 297-302.

Patterson, PH (2004) Maternal infection causes altered behavior in the offspring. In “Neuropsychiatric Disorders and Infection”, SH Fatemi ed., Taylor & Francis, London, pp. 83-90.

Shi, L, Tu, N and Patterson, PH (2005) Maternal influenza infection is likely to alter fetal brain development indirectly: the virus is not detected in the fetus. Internl. J. Develop. Neurosci. 23: 299-305.

Patterson, PH (2005) Modeling features of autism in animals, In “Understanding Autism: From basic Neuroscience to Treatment”, Moldin, SO and Rubenstein, ,JLR, Eds., Taylor & Francis, Boca Raton, FL, in press.
What are the top three papers (not yours) you have read recently?
Brown, A.S., et al., Serologic evidence of prenatal influenza in the etiology of schizophrenia, Arch. Gen. Psychiatry, 61, 774, 2004

Meyer, U., Feldon, J., Schedlowski, M. and Yee, B.K., Towards an immuno-precipitated neurodevelopmental animal model of schizophrenia, Neurosci. Biobehav. Rev., 29, 913, 2005

Vargas, D.L., et al., Neuroglial activation and neuroinflammation in the brain of patients with autism, Ann. Neurol., 57, 67, 2005
What is your leading hypothesis?
Maternal infection interacts with genetic susceptibility to increase the risk for schizophrenia in the offspring. We hypothesize that infection-induced maternal cytokines mediate changes in fetal brain development, which leads to behavioral abnormalities and neuropathology in the offspring.
What piece of missing evidence would help prove it?
In a mouse model of maternal influenza infection, we are perturbing cytokines in the maternal circulation and observing changes in the behavior of the offspring.
What is your fallback position?
The maternal cellular immune response may play a role.



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