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            <funder>Grant sponsor: INSERM; Grant sponsor: Assistance Publique des Hôpitaux de Paris; Grant sponsor: Agence Nationale pour la Recherche (ANR-Project Manage-BP); Grant sponsor: National Alliance for Research on Schizophrenia and Depression (NARSAD); Grant sponsor: Fondation pour la Recherche sur le Cerveau (FRC); Grant sponsor: RTRS Santé Mentale (FondaMental); Grant sponsor: National Genomic Network (NGFN) of the German Ministry of Education and Research; Grant sponsor: Deutsche Forschungsgemeinschaft (SFB 400 Subprojects D1 and D3, Graduiertenkolleg GRK 246, FOR 423 Subproject D1); Grant sponsor: Alfried Krupp von Bohlen und Halbach-Stiftung; Grant sponsor: Interuniversity Attraction Poles program P5/19 of the Belgian Federal Science Policy Office; Grant sponsor: German Research Society (Grant Numbers: AL 230-1/2/3-230-5/1/2, SFB 400); Grant sponsor: Aware; Grant sponsor: Health Research Board (Grant Number: H01069 HRB RP153/2000); Grant sponsor: Friends of St. Patrick‟s Hospital; Grant sponsor: Swiss National Foundation ( Grant Numbers: 32-40677.94, 32-47315.96, 32-061974.00, 32-66793.01, 32-102168.03).</funder>
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                <title level="j">American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title>
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                  <publisher>Wiley</publisher>
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                <term xml:lang="nl">Bipolar disorder</term>
                <term xml:lang="nl">genetic heterogeneity</term>
                <term xml:lang="nl">age at onset</term>
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              <classCode scheme="mesh">Adolescent</classCode>
              <classCode scheme="mesh">Age of Onset</classCode>
              <classCode scheme="mesh">Genetic Linkage</classCode>
              <classCode scheme="mesh">Genetic Markers</classCode>
              <classCode scheme="mesh">Genetic Predisposition to Disease</classCode>
              <classCode scheme="mesh">Genotype</classCode>
              <classCode scheme="mesh">Humans</classCode>
              <classCode scheme="mesh">Male</classCode>
              <classCode scheme="mesh">Young Adult</classCode>
              <classCode scheme="mesh">Bipolar Disorder</classCode>
              <classCode scheme="mesh">Chromosome Mapping</classCode>
              <classCode scheme="mesh">Chromosomes, Human, Pair 2</classCode>
              <classCode scheme="mesh">Data Interpretation, Statistical</classCode>
              <classCode scheme="mesh">Europe</classCode>
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              <classCode scheme="halDomain" n="sdv.spee">Life Sciences [q-bio]/Santé publique et épidémiologie</classCode>
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              <p>Bipolar disorder has a genetic component, but the mode of inheritance remains unclear. A previous genome scan conducted in 70 European families led to detect eight regions linked to bipolar disease. Here, we present an investigation of whether the phenotypic heterogeneity of the disorder corresponds to genetic heterogeneity in these regions using additional markers and an extended sample of families. The MLS statistic was used for linkage analyses. The predivided sample test and the maximum likelihood binomial methods were used to test genetic homogeneity between early-onset bipolar type I (cut-off of 22 years) and other types of the disorder (later onset of bipolar type I and early-onset bipolar type II), using a total of 138 independent bipolar-affected sib-pairs. Analysis of the extended sample of families supports linkage in four regions (2q14, 3p14, 16p23, and 20p12) of the eight regions of linkage suggested by our previous genome scan. Heterogeneity testing revealed genetic heterogeneity between early and late-onset bipolar type I in the 2q14 region (P = 0.0001). Only the early form of the bipolar disorder but not the late form appeared to be linked to this region. This region may therefore include a genetic factor either specifically involved in the early-onset bipolar type I or only influencing the age at onset (AAO). Our findings illustrate that stratification according to AAO may be valuable for the identification of genetic vulnerability polymorphisms. © 2010 Wiley-Liss, Inc.</p>
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