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Schizophrenia Research Forum: Researcher Profile - Michael Owen
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Researcher Profile - Michael Owen

First Name:Michael
Last Name:Owen
Advanced Degrees:PhD FRCPsych
Affiliation:Cardiff University
Department:Psychological Medicine
Street Address 1:Henry Wellcome Building
Street Address 2:Heath Park
Zip/Postal Code:CF14 4XN
Country/Territory:United Kingdom
Phone:44 2920 743248
Fax:44 2920 746554
Email Address:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 4 January 2006]
View all comments by Michael Owen
Clinical Interests:
Neurodevelopmental disorders (e.g., 22q11 deletion syndromes), Bipolar disorder , Depression, Attention-deficit hyperactivity disorder (ADHD, ADD) , Autism spectrum disorders (pervasive developmental disorders), Schizophrenia
Research Focus:
Bioinformatics/Statistics, DNA microrrays, Glia/myelin, Glutamatergic transmission, Animal models, Brain imaging, Genetics
Work Sector(s):
Web Sites:
Reasearcher Bio
Professor of Psychological Medicine, Head of Department of Psychological Medicine, Wales College of Medicine, Cardiff University. Honorary Consultant Psychiatrist, Cardiff and Vale NHS Trust.

Michael Owen qualified in Medicine in Birmingham in 1983 having previously taken a BSc in Anatomical Studies in 1979 and a PhD in Neuroscience in 1982. He studied Psychiatry at the Maudsley Hospital and was subsequently a Lecturer at the Institute of Psychiatry, London. In 1997 he became an MRC Training Fellow at the Department of Biochemistry and Molecular Genetics at Imperial College, London. In 1990 he was appointed Senior Lecturer in Neuropsychiatric Genetics at the University of Wales College of Medicine (UWCM), being promoted to Personal Chair in 1995. Since 1998 he has been Professor of Psychological Medicine and Head of Department of Psychological Medicine where he also heads the Cardiff Neuropsychiatric Genetics group, which is one of the largest such groups in the world. He was Pro Vice Chancellor for Research (PVCR) at UWCM from 2001-2005 and is currently Deputy PVCR at Cardiff University. His own research interests relate to genetic aspects of schizophrenia, Alzheimer’s disease and bipolar disorder, and in the relationship between 22q11 deletions and psychosis. In addition, he continues to work as a consultant in General Adult Psychiatry. He was President of the International Society of Psychiatric Genetics (2000-2005) and was a member of the council of the Academy of Medical Sciences (2001-2004).
Top Papers
Goate A, Chartier-Harlin M-C, Mullan M, Brown J, Crawford F, Fidani L, Giuffra L, Haynes A, Irving N, James L, Mant R, Newton P, Rooke K, Roques P, Talbot C, Pericak-Vance M, Roses A, Williamson R, Rossor M, Owen M, Hardy J. (1991). Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature 349: 704-706.

Murphy KC, Jones LA, Owen MJ. (1999) High rates of schizophrenia in adults with velo-cardio-facial syndrome. Archives of General Psychiatry 56:940-945.

Kehoe PG, Carsten R, McIlroy S, Williams H, Holmans P, Holmes C, Liolitsa D, Vahidassr D, Powell J, McGleenon B, Liddel M, Plomin R, Dynan K, Williams N, Neal J, Cairns NJ, Wilcock G, Passmore P, Lovestone S, Williams J, Owen MJ (1999). Variation in DCP1, encoding ACE, is associated with susceptibility to Alzheimer’s disease. Nature Genetics 21:71-72.

Kehoe P, Wavrant-De Vrieze F, Crook R, Wu WS, Holmans P, Fenton I, Spurlock G, Norton N, Williams H, Williams N,Lovestone S, Perez-Tur J, Hutton M, Chartier-Harlin M, Shears S, Roehi K, Booth J, Van Voorst W, Ramic D, Williams J, Goate A, Hardy J, Owen MJ. (1999). A Full Genome Scan for Late Onset Alzheimer’s Disease. Human Molecular Genetics 8: 237-245.

Myers A, Holmans P, Marshall H, Kwon J, Meyer D, Ramic D, Shears S, Booth J, Wavrant DeVrieze F, Crook R, Hamshere M, Abraham R, Tunstall N, Rice F, Carty S, Lillystone S, Kehoe P, Rudrasingham V, Jones L, Lovestone S, Perez-Tur J, Williams J, Owen MJ, Hardy J, Goate AM. (2000) Susceptibility locus for Alzheimer’s disease on chromosome 10. Science 290: 2304-05.

Williams NM, Preece A, Morris DW, Spurlock G, Bray NJ, Stephens M, Norton N, Williams H, Clement M, Dwyer S, Curran C, Wilkinson J, Moskvina V, Waddington JL, Gill M, Corvin AP, Zammit S, Kirov G, Owen MJ, O’Donovan MC (2004). Identification in two independent samples of a novel schizophrenia risk haplotype of the dystobrevin binding protein gene (DTNBP1). Archives of General Psychiatry 61: 336-344.

Williams NM, Norton N, Williams H, Ekholm B, Hamshere ML, Lindblom Y, Chowdare KV, Cardno AG, Zammit S, Jones LA, Murphy KC, Sanders RD, McCarthy G, Gray MY, Jones G, Holmans P, Nimgaonkar V, Adolfson R, Osby U, Terenius L, Sedvall G, O’Donovan MC, Owen MJ. (2003). A systematic genome-wide linkage study in 353 sib pairs with schizophrenia. American Journal of Human Genetics 73: 1355-1367.

Thapar A, Langley K, Fowler T, Rice F, Turic D, Whittinger N, Aggleton J, Van den Bree M, Owen M, O’Donovan M (2005) Catechol- O-methyltransferase gene variant and birth weight predict early onset antisocial behaviour. Archives of General Psychiatry 62:1275-1278.

Hamshere ML, Bennet P, Willimas N, Segurado R, Cardno A, Norton N, Lambert D, Williams H, Kirov G, Corvin A, Holmans P, Jones L, Jones I, Gill M, O’Donovan MC, Owen MJ, Craddock N (2005) Genome-wide linkage scan in schizoaffective disorder: Significant evidence for linkage (LOD = 3.54) at 1q42 close to DISC1, and suggestive evidence at 22q11 and 19q13. Archives of General Psychiatry 62: 1081-1088.

Peirce T, Bray N, Williams NM, Norton N, Moskivina V, Preece A, Haroutunian V, Buxbaum JD, Owen MJ, O’Donovan MC. (2005) Convergent evidence for 2’, 3’ – Cyclic Nucleotide 3’ – Phosphodiesterase (CNP) as a possible susceptibility gene for schizophrenia. Archives of General Psychiatry (in press).
If resources were not limited, what research projects would you pursue?
Whole genome searches for SNP association and CNV association.
What is your leading hypothesis?
That is has a strong genetic component and that identifying the nature of the genetic contribution will be crucial to understanding aetiology and pathogenesis.
What piece of missing evidence would help prove it?
This will take time but, as replicated genetic associations accumulate, research to develop new understandings of pathogenesis is beginning.
What is your fallback position?

Research Participants
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