NIMH Genetics Initiative Millennium Schizophrenia Consortium: Linkage Analysis of African-American Pedigrees Charles A. Kaufmann, 1 * Brian Suarez, 2 Dolores Malaspina, 1 John Pepple, 3 Dragan Svrakic, 2 Paul D. Markel, 4 Joanne Meyer, 4 Christopher T. Zambuto, 4 Karin Schmitt, 4 Tara Cox Matise, 5 Jill M. Harkavy Friedman, 1 Carol Hampe, 2 Hang Lee, 3 David Shore, 6 Debra Wynne, 6 Stephen V. Faraone, 3 Ming T. Tsuang, 3 and C. Robert Cloninger 2 1 College of Physicians and Surgeons, Columbia University, New York, New York 2 Washington University School of Medicine, St. Louis, Missouri 3 Harvard University School of Medicine, Boston, Massachusetts 4 Millennium Pharmaceuticals, Inc., Cambridge, Massachusetts 5 Rockefeller University, New York, New York 6 National Institute of Mental Health, Rockville, Maryland The NIMH Genetics Initiative is a multi-site collaborative study designed to create a na- tional resource for genetic studies of com- plex neuropsychiatric disorders. Schizo- phrenia pedigrees have been collected at three sites: Washington University, Colum- bia University, and Harvard University. This article—one in a series that describes the results of a genome-wide scan with 459 short-tandem repeat (STR) markers for sus- ceptibility loci in the NIMH Genetics Initia- tive schizophrenia sample—presents results for African-American pedigrees. The Afri- can-American sample comprises 30 nuclear families and 98 subjects. Seventy-nine of the family members were considered affected by virtue of having received a DSMIII-R di- agnosis of schizophrenia (n = 71) or schizoaf- fective disorder, depressed (n = 8). The fami- lies contained a total of 42 independent sib pairs. While no region demonstrated evi- dence of significant linkage using the crite- ria suggested by Lander and Kruglyak, sev- eral regions, including chromosomes 6q16- 6q24, 8pter-8q12, 9q32-9q34, and 15p13- 15q12, showed evidence consistent with linkage (P = 0.01–0.05), providing indepen- dent support of findings reported in other studies. Moreover, the fact that different ge- netic loci were identified in this and in the European-American samples, lends cre- dence to the notion that these genetic differ- ences together with differences in environ- mental exposures may contribute to the re- ported differences in disease prevalence, severity, comorbidity, and course that has been observed in different racial groups in the United States and elsewhere. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 81: 282–289, 1998. © 1998 Wiley-Liss, Inc. KEY WORDS: schizophrenia; linkage analy- sis; African-American; NIMH Genetics Initiative INTRODUCTION This is the third of 3 articles reporting the results of genome-wide nonparametric linkage analyses per- formed on nuclear families segregating schizophrenia derived from the NIMH Genetics Initiative, a multi- site collaborative study designed to create a national resource for genetic studies of complex neuropsychiat- ric disorders. In the first article of this series, Clon- inger et al. [1998] describe the background of the proj- ect and associated strategies for pedigree ascertain- ment and extension, diagnosis and data acquisition, and data analyses. The companion article by Faraone et al. [1998] presents the results of linkage analyses performed on European-American pedigrees within the NIMH Genetics Initiative sample. Here, we present the results of analyses performed on African-American pedigrees. Different genes may influence susceptibility to com- plex disorders in individuals of different racial back- grounds. For example, a recent genome-wide search for Contract grant sponsor: NIMH; Contract grant numbers: K02 MH00682, U01 MH46289, P20 MH50727, R01 MH44292, U01 MH46276, U01 MH46318. *Correspondence to: Charles A. Kaufmann, M.D., Department of Psychiatry, Columbia University College of Physicians & Sur- geons, 722 West 168th Street, Unit #58, New York, New York 10032. E-mail: cak2@columbia.edu Received 26 September 1997; Revised 24 March 1998 American Journal of Medical Genetics (Neuropsychiatric Genetics) 81:282–289 (1998) © 1998 Wiley-Liss, Inc.