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Schizophrenia Bulletin 2003 29(3):595-605;
© 2003 by Oxford University Press and the Maryland Psychiatric Research Center (MPRC)
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© Oxford University Press

Neurodevelopmental Interactions Conferring Risk for Schizophrenia: A Study of Dermatoglyphic Markers in Patients and Relatives

Matthew T. Avila, M.A., Jay Sherr, PharmD, Leanne E. Valentine, B.S., Teresa A. Blaxton, Ph.D. and Gunvant K. Thaker, M.D.
Predoctoral Research Fellow; Schizophrenia-Related Disorders Clinic, Maryland Psychiatric Research Center Baltimore, MD
Assistant Professor; Schizophrenia-Related Disorders Clinic, Maryland Psychiatric Research Center Baltimore, MD
Undergraduate Research Assistant; Schizophrenia-Related Disorders Clinic, Maryland Psychiatric Research Center Baltimore, MD
Associate Professor; Schizophrenia-Related Disorders Clinic, Maryland Psychiatric Research Center Baltimore, MD
Chief, Schizophrenia-Related Disorders Clinic, Maryland Psychiatric Research Center Baltimore, MD

Send reprint requests to M. Avila, Maryland Psychiatric Research Center, P.O. Box 21247, Baltimore, MD 21228; e-mail: mavila{at}mprc.umaryland.edu

Schizophrenia is hypothesized to be the result of an interaction between specific genetic factors and nonspecific insults during embryonic development. Dermatoglyphic abnormalities appear to mark these putative insults—providing information about the temporal sequence of aberrant developmental events as well as the organism's vulnerability to their adverse effects. In the present study, dermatoglyphic measures thought to mark first and second trimester development were examined in patients with schizophrenia and first degree relatives and compared with those of healthy controls to examine whether genetic factors may mediate this vulnerability. Both patients with schizophrenia and relatives exhibited dermatoglyphic abnormalities compared with controls. Patients were more likely to exhibit dermatoglyphic abnormalities indicative of early second trimester development, which suggests that vulnerability interacts with the timing of insults to produce overt disease. These findings indicate that the two-hit model, in which schizophrenia-specific genetic factors combine in an additive fashion with environmental insults to produce the illness, may be oversimplified. Rather, the data are consistent with a more complex model in which nonspecific genetic factors that increase susceptibility to developmental abnormalities interact with insults and specific genetic factors.

Keywords: Dermatoglyphics / developmental instability / schizophrenia / phenotypic markers / genetic risk


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S. H. Fatemi and T. D. Folsom
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Schizophr Bull, May 1, 2009; 35(3): 528 - 548.
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