Bipolar Disorders: Mixed States, Rapid-Cycling, and Atypical Forms

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292 K. Merikangas and K. YuMarkers in the candidate region identified by linkage analysis can be used tonarrow the location of the disease gene through linkage disequilibrium analysis.Linkage disequilibrium is a population association between two alleles at differentloci, and occurs when the same founder mutation exists in a large proportion ofaffected subjects in the population studied. Usually, the closer the marker is to thedisease locus, the greater the proportion of affected subjects who carry the identicalallele at the marker (Risch, 2000). However, in measuring the strength of linkagedisequilibrium for a given marker, it is also important to select unaffected controlsubjects from the same population, because an allele shared among affectedsubjects may also be common in the general population and thus shared by chancerather than due to proximity to the disease locus (Risch, 2000).Review of empirical evidenceThe initial enthusiasm generated by early claims of linkage between bipolardisorder and DNA markers including Xq (Baron et al., 1987; Mendlewicz et al.,1987; Lucotte et al., 1992) and 11p (Egeland et al., 1987) was diminished bysubsequent non-replications (Risch and Botstein, 1996). Numerous linkage studiesof bipolar disorder have subsequently been reported to regions on all but sixchromosomes (Straub et al., 1994; Pekkarinen et al., 1995; Stine et al., 1995;Blackwood et al., 1996; Detera-Wadleigh et al., 1996, 1999; Freimer et al., 1996;McMahon et al., 1997; Moldin, 1997; Smyth et al., 1997; Ewald et al., 1998a, b;Aita et al., 1999; Kelsoe, 1999; Morissette et al., 1999; Kelsoe et al., 2001).Table 13.3 presents a summary of genome-wide linkage studies of bipolar disorderupdated from a recent review by Prathikanti and McMahon (2001). Based on atotal of 3538 bipolar I disorder scans in affected subjects from 1119 pedigreesreported in 20 samples, the authors conclude that no two studies conclusivelyimplicate the same region. However, suggestive findings emerged for two loci(i.e., 4p12–13 and 13q31–33). The most striking conclusion was that no two studiesemployed identical ascertainment procedures and there was substantial diversityin sampling and methods. In conclusion, sufficient ambiguities exist to give pausein considering any of these linkage results as unambiguously replicated (Goldinet al., 1997; Reus and Freimer, 1997; Rice et al., 1997; DeLisi et al., 2000; Altmülleret al., 2001; Craddock and Jones, 2001). More recently, McMahon et al. (2001)reported replication of the suggestive finding reported earlier by Nöthen et al.(1999). The demonstration of the low power of existing linkage studies by Rischand Merikangas (1996) generated a spate of association studies of mood disorders,particularly those employing within-family controls (Merikangas et al., 2002b).Some other features of mood disorders that complicate genetic analyses aredescribed below.
Table 13.3 Summary of recent bipolar linkage studiesStudy Sample Pedigrees Affected subjects Genotyped pairs Pair type Number of markers Scanned what? Locus = LODStraubet al.(1994)Ewaldet al.(1995)Blackwoodet al.(1996)McMahonet al.(1997)Ginnset al.(1996)Adamset al.(1998)Ewaldet al.(1998b)Ewaldet al.(1998a)Columbia/HadassahUniversity47 490 443 ERP 5–153markers perchromosomeDanish 2 89 87 ERP 12 Chromosome16p13Edinburgh 1 27 26 ERP 135 (87 additionalmarkers on 4p)Clinic andinpatientfromBaltimoreand Iowa CityOlder-orderAmish23 251 228 ASP;ERPGenome-wide 21q22 = 3.416p13 = 2.5Genome-wide 4p12–13 = 4.813 Chromosome18 18q23 = 2.85 207 202 ERP 551 Genome-wide 6p25 = 2.5;13q13 = 1.4;15q21 = 1.1Australian 11 224 213 ERP 214 Genome-wide 4q35 = 3.2Danish 2 89 87 ERP 16 Chromosome12q22-q2412q24 = 3.4Danish 2 89 87 ERP 16 Chromosome 4 4p16 = 2.0
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Bipolar DisordersMixed States, Rapi
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ContentsList of contributorsPreface
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ContributorsValadeta Ajdacic PhDPsy
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ixList of contributorsAlexia E. Kou
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PrefaceBipolar disorders have a lon
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46 G. Perugi and H. S. AkiskalTable
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54 G. Perugi and H. S. Akiskal3020.
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59 Longitudinal perspective of mixe
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3Rapid-cycling bipolar disorder1 2O
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63 Rapid-cycling bipolar disorderPs
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89 Bipolar I and bipolar II: a dich
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101 Bipolar I and bipolar II: a dic
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5Recurrent brief depression as an i
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Chronic 4.8 18.2 9.1 10 NCRapid-cyc
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121 Recurrent brief depressionTable
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127 Recurrent brief depressionREFER
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129 Recurrent brief depressionMarne
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6Atypical depression and its relati
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133 Atypical depression and bipolar
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7Agitated depression: spontaneous a
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8Schizoaffective mixed statesAndrea
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9Acute and transient psychotic diso
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Table 9.10 (cont.)ATPD(n ¼ 39)Bipo
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Table 9.11 (cont.)Bipolar affective
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Table 9.14b Significant differences
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10Bipolar disorder in children and
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239 Bipolar disorder in children an
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Page 309 and 310: 13q32 = 3.321q22 = 3.6Liu, C.et al.
Page 325 and 326: 14Biological aspects of rapid cycli
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Page 339 and 340: 325 The treatment of bipolar mixed
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343 The treatment of bipolar mixed
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16The use of atypical antipsychotic
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17Investigational strategies: treat
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371 Investigational strategiesBIPOL
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381 Investigational strategiesTable
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383 Investigational strategies2. Th
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387 Indexclinical course and outcom
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389 Indexdepressive mixed states 51
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391 IndexLange, J. 163learning disa
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393 Indexpsychopharmacological revo
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395 Indexmania, acute 334mixed stat
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Bipolar Disorders: Mixed States, Rapid-Cycling, and Atypical Forms

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