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Schizophrenia Research Forum: Researcher Profile - Christine Konradi
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Researcher Profile - Christine Konradi

RESEARCHER INFORMATION
First Name:Christine
Last Name:Konradi
Affiliation:Vanderbilt University
Department:Psychiatry
Street Address 1:MRB3-Room 8160
Street Address 2:465 21st Ave S
City:Nashville
State/Province:TN
Zip/Postal Code:37323
Country/Territory:U.S.A.
Email Address:christine.konradi@vanderbilt.edu
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 28 September 2010]
View all comments by Christine Konradi
Clinical Interests:
Drug abuse, Bipolar disorder , Neurodevelopmental disorders (e.g., 22q11 deletion syndromes), Schizophrenia
Research Focus:
Animal models, Neurodevelopment, GABAergic transmission, Glia/myelin, Molecular and Cell biology, DNA microrrays, Signal transduction, Glutamatergic transmission
Work Sector(s):
University
Web Sites:
Lab: http://www.mc.vanderbilt.edu/root/vumc.php?site=konradi&doc=8954
Reasearcher Bio
1984 – 1986 Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Vienna, AUT
1986 – 1988 Postdoctoral Fellow at the University of Würzburg, Department of Psychiatry, Clinical Neurochemistry Group, GER
1989 Postdoctoral Fellow at the University of Medicine and Dentistry of New Jersey, Department of Neurology
1989 – 1990 Postdoctoral Fellow at Harvard Medical School and Massachusetts General Hospital, Department of Neurogenetics
1991 – 1992 Postdoctoral Fellow at Harvard Medical School and Massachusetts General Hospital, Department of Neurology
1992 – 1994 Instructor, Department of Psychiatry, Harvard Medical School, and Assistant, Department of Psychiatry, Massachusetts General Hospital
1994 – 2002 Assistant Research Scientist, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School
1994 – 2001 Assistant Professor, Department of Psychiatry, Harvard Medical School
2000 – 2006 Associate Molecular Neurobiologist, McLean Hospital and Harvard Medical School
2000 – 2006 Member, Department of Neurobiology, Harvard Medical School
2001 – 2006 Associate Professor, Department of Psychiatry, Harvard Medical School
2006 – present Professor, Department of Psychiatry, Vanderbilt University

Top Papers
1. Naydenov AV, MacDonald ML, Ongur D, Konradi C. Differences in lymphocyte electron transport gene expression levels between subjects with bipolar disorder and normal controls in response to glucose deprivation stress. Arch Gen Psychiatry. 2007 May;64(5):555-64. PMID: 17485607

2. Black YD, Maclaren FR, Naydenov AV, Carlezon WA Jr, Baxter MG, Konradi C. Altered attention and prefrontal cortex gene expression in rats after binge-like exposure to cocaine during adolescence. J Neurosci. 2006 Sep 20;26(38):9656-65. PMID: 16988036

3. Youngs RM, Chu MS, Meloni EG, Naydenov A, Carlezon WA Jr, Konradi C.Lithium administration to preadolescent rats causes long-lasting increases in anxiety-like behavior and has molecular consequences. J Neurosci. 2006 May 31;26(22):6031-9. PMID: 16738246

4. MacDonald ML, Naydenov A, Chu M, Matzilevich D, Konradi C. Decrease in creatine kinase messenger RNA expression in the hippocampus and dorsolateral prefrontal cortex in bipolar disorder. Bipolar Disord. 2006 Jun;8(3):255-64. PMID: 16696827

5. MacDonald ML, Eaton ME, Dudman JT, Konradi C.Antipsychotic drugs elevate mRNA levels of presynaptic proteins in the frontal cortex of the rat. Biol Psychiatry. 2005 May 1;57(9):1041-51. PMID: 15860345

6. Konradi C, Eaton M, MacDonald ML, Walsh J, Benes FM, Heckers S. Molecular evidence for mitochondrial dysfunction in bipolar disorder.
Arch Gen Psychiatry. 2004 Mar;61(3):300-8. PMID: 14993118
What is your leading hypothesis?
I believe in some form of mitochondrial involvement in bipolar disorder and schizophrenia, although I do not know if this is the primary cause or a secondary consequence. If mitochondrial dysfunction contributes to the clinical pathology it could be targeted for treatment. If the symptoms can be alleviated by targeting mitochondrial function it would be almost irrelevant if the dysfunction is a primary cause or secondary/tertiary consequence of the primary cause.
What is your fallback position?
That the reduction in nuclear genes coding for mitochondrial proteins is a consequence of reduced neuronal activity and/or of cell loss.



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