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Matthew State
Matthew W. State, MD PhD
Harris Associate Professor of Child Psychiatry and Genetics
* B.A. Stanford 1984
* M.D. Stanford 1991
* Ph.D. Yale 2001
Research Interests:
Identifying and characterizing genes and genetic mechanisms involved in neuropsychiatric disorders of childhood.
Current Research:
Our lab is interested in identifying and characterizing genes and genetic mechanisms involved in neuropsychiatric disorders of childhood. Currently we are focused on Tourette syndrome (TS) and Obsessive Compulsive disorder (OCD), Autism and related pervasive developmental disorders, and mental retardation. Several decades of effort aimed at elucidating the genetic contributors to these conditions has been hampered by marked genetic and clinical heterogeneity. Our lab is tackling these obstacles through the identification and study of rare individuals and families. We are particularly interested in two populations that present the opportunity for the identification of genes of major effect: (1) children who possess both chromosomal abnormalities and psychiatric syndromes; and (2) families that demonstrate Mendelian transmission of some aspect of a neuropsychiatric phenotype. As a complement to this line of research, the lab is leveraging newer high-throughput, high-resolution methods for identifying chromosomal rearrangements. The lab works closely with clinical collaborators in Venezuela, Saudi Arabia, Iran, Turkey and Brazil as well as with the Autism and TS groups at the Yale Child Study Center that serve as an invaluable resource for our research.
Representative Publications:
Abelson JF, Kwan KY, O'Roak BJ, Baek DY, Stillman AA, Morgan TM, Mathews CA, Pauls DL, Rasin MR, Gunel M, Davis NR, Ercan-Sencicek AG, Guez DH, Spertus JA, Leckman JF, Dure LS 4th, Kurlan R, Singer HS, Gilbert DL, Farhi A, Louvi A, Lifton RP, Sestan N, State MW (2005). Sequence variants in SLITRK1 are associated with Tourette's syndrome. Science 310(5746):317-20
Fernandez T, Morgan T, Davis N, Klin A, Morris A, Farhi A, Lifton RP, State MW (2004) Disruption of contactin 4 (CNTN4) results in developmental delay and other features of 3p deletion syndrome. Am J Hum Genet. 74(6): 1286-93.
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