Fróðskaparrit - 31.12.2000, Page 54

Fróðskaparrit - 31.12.2000, Page 54
58 SEARCH FOR SUSCEPTIBILITY LOCION SELECTED CHROMOSOMES IN PATIENTS WITH PANIC DISORDER FROM THE FAROE ISLANDS firm an interesting area, related to the Di- George syndrome and Velocardiofacial syndrome, but did show an interesting area more distally on 22ql3 (Mors et al., 1999; 2000), Table 1. Panic Disorder For panic disorder, results have been de- scribed in 1998, 1999, and 2000 (Degn et ai, 1998; Wang et al., 1999; 2000). Our data could not support the previously re- ported association between panic disorder and the cholecystokinin genes on chromo- somal regions 3pter-p21 and llpl5,4 (Degn et al., 1998). Instead, our prelimi- nary data point towards an interesting area on chromosome 21 q22 (Wang et al., 2000), Table 1. Discussion When mapping complex diseases, the choice of population is a critical factor. A genetically simplified isolate is probably more useful than a diverse continental pop- ulation (Editorial, 1998; Wright et al., 1999). A basic requirement for LD map- ping is a homogenous population, thus, iso- lated population regions were sought. The suitability of some of these isolated popula- tions is at present being questioned (Arna- son et al., 2000; Eaves et al., 2000) and, more theoretically, the whole idea has been disputed on the grounds that the study mod- els are inadequate for diseases that are probably multifactoral (Edwards, 1999). However, the findings of a high degree of homogeneity for cystic fibrosis and benign, recurrent intrahepatic cholestasis in the Faroe Islands (Tygstrup et al., 1999; á Table 1. Areas ofpossible inlerest, sofar identified. Øki higartil funnin, sum kunnu hava týdning. Disorder Chromosome area Bipolar affective disorder 18q23 10q26 Schizophrenia 22ql3 Panic disorder 21q22 Steig, 1999) could be taken as an indication that the Faroe Islands might meet the crite- ria of homogeneity. In our genome screening, although not fínished, we do see moderate numbers of candidate regions. In a totally out-bred population, the useful levels of LD will rarely extend beyond 3 kb (Kruglyak, 1999) and no regions of LD would be ex- pected with the marker density used in the present study. On the other hand, a small population size may tend to increase LD by genetic drift and, in addition, the process might be enhanced by population stratifica- tion into small, inbred communities (Wright et al., 1999). The result would be many regions with LD. Whether the re- gions detected in this study are false posi- tives caused by stratification, or true, dis- ease-bearing, identical-by-descent seg- ments is not yet clear, but the small amount of detected regions does signal a low de- gree of stratification. With a common forefather 10-12 genera- tions ago, the possible size of a common haplotype among persons with a disease would require about 500 markers to ensure its capture. However, the availability and order of the markers could make some ar- eas too long, with the result of missing the
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