A linkage study of schizophrenia to markers within Xp11 near the MAOB gene

Dann, Janine; DeLisi, Lynn E.; Devoto, Marcella; Laval, Steven H.; Nancarrow, Derek J.; Shields, Gail; Smith, Amanda M.; Loftus, J.; Peterson, Paula; Vita, Antonio; Comazzi, Margherita; Invernizzi, G; Levinson, Douglas F.; Wildenauer, Dieter B.; Mowry, Bryan; Collier, David; Powell, John; Crowe, Raymond R.; Andreasen, Nancy C.; Silverman, Jeremy M.; Mohs, Richard C.; Murray, Robin M.; Walters, Marilyn K.; Lennon, David P.; Hayward, Nicholas K.; Albus, Margot; Lerer, Bernard; Maier, Wolfgang; Crow, Timothy J.

doi:10.1016/s0165-1781(97)03138-7

Cited by 63 publications

(43 citation statements)

References 35 publications

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“…It is possible that a variation on a locus closely related to MAO genes might exist. In our present study, the DXS7 locus, which is closely linked to monoamine oxidase genes and shows contradictory evidences of linkage to schizophrenia [Okoro et al, 1995;Dan et al, 1997], was selected to study the possible association between this locus and unipolar depression. In a Chinese sample containing 66 patients and 85 normal controls, no association was found in the total population set.…”

Section: Discussionmentioning

confidence: 99%

Studies of the DXS7 polymorphism at the MAO loci in unipolar depression

et al. 1999

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From the fact that DXS7 polymorphism is closely related to monoamine oxidase (MAO) genes and MAO inhibitors are widely used in the treatment of unipolar depression, it is of particular interest to study the relationship between the DXS7 polymorphism and unipolar depression. Thus, this study examined the possible association between DXS7 polymorphism and unipolar depression in 66 cases versus 85 controls from Shanghai. Polymerase chain reaction and amplification fragment length polymorphism techniques were used for genotyping of the DXS7 locus in this study. Four alleles at the DXS7 locus were detected with length generated by polymerase chain reaction amplification ranging from 157 to 167 bp. Comparison of allele frequency in the DXS7 locus showed no difference between unipolar depression cases and normal controls in the total population set. When subclassified by age, a significant difference of allele frequency distribution was observed between early onset (before age 40) and late onset (after age 40) patients. The frequency of the 157-bp allele was decreased, whereas the frequency of the 165 allele was increased in late onset patients (0.3810 for the 157-bp allele and 0.5238 for the 165-bp allele) compared with that of early onset patients (0.6304 for the 157-bp allele and 0. 3261 for the 165-bp allele). There was also a difference of allele frequency between patients and normal controls with age over 40 years. The frequency of 165-bp allele increased significantly in late onset patients (0.5238) compared with that of controls within the same age range (0.3454). Association studies suggested that in the population with age over 40 years, presence of the 165-bp allele of DXS7 locus was significantly associated with unipolar depression (relative risk = 2.08, P < 0.05), whereas in the total population set, this association did not exist. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:598-600, 1999.

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Section: Discussionmentioning

confidence: 99%

Studies of the DXS7 polymorphism at the MAO loci in unipolar depression

et al. 1999

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“…A large collaborative study examining markers within band Xp11 near the MAO loci found a LOD of 1.97 under a dominant model for DXS7 in a set of 92 sib pairs selected for maternal inheritance. In a second analysis, 34 families not selected for inheritance pattern gave a LOD of 2.16 at MAOB under a dominant model [Dann et al, 1997]. Results from a number of recent genome screens have suggested a possible X chromosome locus, but these results are of weaker magnitude than the most positive loci in these studies [Paterson et al, 1999].…”

Section: Chromosomementioning

confidence: 93%

Linkage and associated studies of schizophrenia

2000

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Genetic epidemiology has provided consistent evidence over many years that schizophrenia has a genetic component, and that this genetic component is complex, polygenic, and involves epistatic interaction between loci. Molecular genetics studies have, however, so far failed to identify any DNA variant that can be demonstrated to contribute to either liability to schizophrenia or to any identifiable part of the underlying pathology. Replication studies of positive findings have been difficult to interpret for a variety of reasons. First, few have reproduced the initial findings, which may be due either to random variation between two samples in the genetic inputs involved, or to a lack of power to replicate an effect at a given alpha level. Where positive data have been found in replication studies, the positioning of the locus has been unreliable, leading no closer to positional cloning of genes involved. However, an assessment of all the linkage studies performed over the past ten years does suggest a number of regions where positive results are found numerous times. These include regions on chromosomes 1, 2, 4, 5, 6, 7, 8, 9, 10, 13, 15, 18, 22 and the X. All of these data are critically reviewed and their locations compared. Reasons for the difficulty in obtaining consistent results and possible strategies for overcoming them are discussed. Am. J. Med. Genet. (Semin. Med. Genet.) 97:23-44, 2000.

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“…At the moment, the following ten regions are, arguably, those most deserving of higher density mapping and follow-up studies: 1q21-22, 19 67 and Xp11. 64,[68][69][70][71] The Irish Study of High Density Schizophrenia Families (ISHDSF) contains 1425 individuals with DNA available in 270 families systematically ascertained from psychiatric facilities in Ireland and Northern Ireland. In previous studies with these families we have, in conjunction with other research groups, generated support for the presence of four loci influencing the vulnerability to schizophrenia, on chromosomes 5q21-31, 29 6p24-p21, 34 8p22-21, 42 and 10p15-11.…”

Section: Introductionmentioning

confidence: 99%

Genome-wide scans of three independent sets of 90 Irish multiplex schizophrenia families and follow-up of selected regions in all families provides evidence for multiple susceptibility genes

et al. 2002

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From our linkage study of Irish families with a high density of schizophrenia, we have previously reported evidence for susceptibility genes in regions 5q21-31, 6p24-21, 8p22-21, and 10p15-p11. In this report, we describe the cumulative results from independent genome scans of three a priori random subsets of 90 families each, and from multipoint analysis of all 270 families in ten regions. Of these ten regions, three (13q32, 18p11-q11, and 18q22-23) did not generate scores above the empirical baseline pairwise scan results, and one (6q13-26) generated a weak signal. Six other regions produced more positive pairwise and multipoint results. They showed the following maximum multipoint H-LOD (heterogeneity LOD) and NPL scores: 2p14-13: 0.89 (P = 0.06) and 2.08 (P = 0.02), 4q24-32: 1.84 (P = 0.007) and 1.67 (P = 0.03), 5q21-31: 2.88 (P = 0.0007), and 2.65 (P = 0.002), 6p25-24: 2.13 (P = 0.005) and 3.59 (P = 0.0005), 6p23: 2.42 (P = 0.001) and 3.07 (P = 0.001), 8p22-21: 1.57 (P = 0.01) and 2.56 (P = 0.005), 10p15-11: 2.04 (P = 0.005) and 1.78 (P = 0.03). The degree of 'internal replication' across subsets differed, with 5q, 6p, and 8p being most consistent and 2p and 10p being least consistent. On 6p, the data suggested the presence of two susceptibility genes, in 6p25-24 and 6p23-22. Very few families were positive on more than one region, and little correlation between regions was evident, suggesting substantial locus heterogeneity. The levels of statistical significance were modest, as expected from loci contributing to complex traits. However, our internal replications, when considered along with the positive results obtained in multiple other samples, suggests that most of these six regions are likely to contain genes that influence liability to schizophrenia.

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A linkage study of schizophrenia to markers within Xp11 near the MAOB gene

Cited by 63 publications

References 35 publications

Studies of the DXS7 polymorphism at the MAO loci in unipolar depression

Studies of the DXS7 polymorphism at the MAO loci in unipolar depression

Linkage and associated studies of schizophrenia

Genome-wide scans of three independent sets of 90 Irish multiplex schizophrenia families and follow-up of selected regions in all families provides evidence for multiple susceptibility genes

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