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Schizophrenia Research Forum: Researcher Profile - Robert Beech
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Researcher Profile - Robert Beech

First Name:Robert
Last Name:Beech
Title:Assistant Professor
Advanced Degrees:MD, PhD
Affiliation:Yale University
Street Address 1:300 George St., Room 8304
City:New Haven
Zip/Postal Code:06515
Phone:(203) 737-1375
Fax:(203) 737-1031
Email Address:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 20 October 2005]
Clinical Interests:
Drug abuse, Bipolar disorder , Borderline personality disorder, Neurodevelopmental disorders (e.g., 22q11 deletion syndromes), Schizophrenia, Depression
Research Focus:
Animal models, Microscopy, Neurodevelopment, Neuropathology, DNA microrrays, Signal transduction, Genetics, Stem cells, Glia/myelin, Bioinformatics/Statistics, Molecular and Cell biology, Chemistry/pharmacology, Clinical trials, Pharamacology
Work Sector(s):
Medical hospital, University
Web Sites:
Reasearcher Bio
B.A., 1987, Harvard College
Ph.D., 1994, University of Illinois at Chicago
MD, 1997 University of Illinois at Chicago
Professional Experience:
Residency Training: 1997-2001 Yale University
Postdoctoral Fellowship in Biological Psychiatry,
Yale University 2001-2004
Assistant Professor in Psychiatry,
Yale University 2004-present
Top Papers
Beech, R.D., and Duman, R.S. (2005) "The role of transcription factors in the biology of depression" in Biology of Depression: Towards a Novel Understanding and Therapeutic Strategies, Licinio, J., and Wong, M.-L. eds. (Wiley-VCH, Weinheim) pp. 823-854.

Beech, R.D., Cleary, M.A., Treloar, H.B., Eisch, A.J., Harist, A.V., Zhong, W., Greer, C.A., Duman, R.S., and Picciotto,M.R. (2004) "The nestin promoter/enhancer direct transgene expression to precursors of adult generated periglomerular neurons." Journal of Comparative Neurology 475:128-141.

Caldarone, B.J., Harrist, A.V., Cleary, M.A., Beech, R.D., King, S.L., and Picciotto, M.R. (2004) "High affinity nicotinic acetylcholine receptors are required for antidepressant effects of amitriptyline cell proliferation." Biological Psychiatry 9: 657-664.

Harrist, A., Beech, R.D., King, S.L., Zanardi, A., Cleary, M.A., Caldarone, B.J., Eisch, A.J., Zoli, M., and Picciotto, M.R. (2004) "Alteration of hippocampal cell proliferation in mice lacking the ?2 subunit of the neuronal nicotinic acetylcholine receptor" Synapse 54: 200-206.

Hsu, L.-C., Liu, S., Abedinpour, F., Beech, R.D., Lahti, J.M., Kidd, V.J., Greenspan, J.A., and Yeung, C.-Y. (2003) "The Murine G+C-rich promoter binding protein mGPBP is required for promoter-specific transcription" Molecular and Cellular Biology Molecular & Cellular Biology. 23(23):8773-85.

Beech, R.D. (1997) "Thyroid hormones, affective disorders, and gene regulation: a re-examination" Psychiatric Annals 27: 773-778.
What are the top three papers (not yours) you have read recently?
Mayberg HS, Lozano AM, Voon V, McNeely HE, Seminowicz D, Hamani C, Schwalb JM,Kennedy SH. (2005) "Deep brain stimulation for treatment-resistant depression." Neuron 45(5):651-60.

Pezawas L, Meyer-Lindenberg A, Drabant EM, Verchinski BA, Munoz KE, Kolachana BS, Egan MF, Mattay VS, Hariri AR, Weinberger DR. (2005) "5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: a genetic susceptibility mechanism for depression."
Nat Neurosci. 8(6):828-34.

Lieberman JA, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DO, Keefe RS, Davis SM, Davis CE, Lebowitz BD, Severe J, Hsiao JK; Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators. (2005)
"Effectiveness of antipsychotic drugs in patients with chronic schizophrenia." N Engl J Med. 353(12):1209-23.
If resources were not limited, what research projects would you pursue?
I am particularly interested in the cellular changes associated with psychiatric illness and the relationship of these changes to events that occur during both embryonic and post-natal development of the CNS. Developing new methods for studying the generation and migration of cells in vivo is an important area that we would like to explore. In particular the development of new PET ligands that might permit neurogenesis and related processes to be studied in human patients with schizophrenia and other psychiatric illnesses is an exciting goal.
What is your leading hypothesis?
Schizophrenia is now generally accepted to be a neurodevelopmental disorder. However, when and where in the brain the relevant neurodevelopmental abnormalities occur is still the subject on ongoing research and debate. The fact that susceptiblity genes for schizophrenia are also involved in neuronal migration suggests that this may be one of the important processes involved in the pathogenesis of schizophrenia.
What piece of missing evidence would help prove it?
Currently there are no methods for studying neuronal development at the cellular level in live human beings. New imaging modalities that would permit the generation and and migration of cells to be studied in vivo, combined with longitudinal studies of patients with known genetic risk factors would allow these factors to be studied in the most relevant model system: the human brain.
What is your fallback position?
Since there are no currently available methods to carry out such studies in humans we will continue to use animal models of neurodevelopmental abnormalities and try to correlate effects of such abnormalities on rodent neuoanatomy and behavior with what is known about neuodevelopmental abnormalities in patients with schizophrenia.

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