Family, twin, adoption, and molecular genetic studies of juvenile bipolar disorder

被引:49
作者
Althoff, RR
Faraone, SV
Rettew, DC
Morley, CP
Hudziak, JJ
机构
[1] Univ Vermont, Dept Psychiat, Div Behav Genet, Burlington, VT 05405 USA
[2] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA
[4] SUNY Upstate Med Univ, Dept Psychiat & Behav Sci, Syracuse, NY USA
[5] SUNY Upstate Med Univ, Med Genet Res Program, Syracuse, NY USA
关键词
bipolar affective disorder; child; genetics;
D O I
10.1111/j.1399-5618.2005.00268.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Juvenile bipolar disorder (JBD) has been a subject of significant research and debate. Phenotypic differences between JBD and adult-onset bipolar disorder have led researchers to question whether or not similar neuropathologic mechanisms will be found. While much is known about the genetic and environmental contributions to the adult-onset phenotype, less is known about their contributions to JBD. Here, we review family, twin, adoption, and molecular genetic studies of JBD. Behavioral genetic data suggest both genetic and environmental contributions to JBD, while molecular genetic studies find linkage to age of onset of bipolar disorder to chromosomes 12p, 14q, and 15q. Additionally, changes associated with symptom age of onset have been recently reported in the brain-derived neurotrophic factor (BDNF) and glycogen synthase kinase 3-beta (GSK3-beta) genes. We contend that further progress in discovering the precise genetic and environmental contributions to JBD may depend on advances in phenotypic refinement, an increased appreciation of comorbid conditions, and more investigation of the longitudinal course of the disorder.
引用
收藏
页码:598 / 609
页数:12
相关论文
共 132 条
  • [1] Methylomics in psychiatry: Modulation of gene-environment interactions may be through DNA methylation
    Abdolmaleky, HM
    Smith, CL
    Faraone, SV
    Shafa, R
    Stone, W
    Glatt, SJ
    Tsuang, MT
    [J]. AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS, 2004, 127B (01): : 51 - 59
  • [2] ACHENBACH TM, 1991, MANUAL CHILD BEHA VC
  • [3] ALTHOFF RR, 2004, P 51 ANN M AM AC CHI
  • [4] ANDREASEN NC, 1987, ARCH GEN PSYCHIAT, V44, P461
  • [5] Meta-analysis of whole-genome linkage scans of bipolar disorder and schizophrenia
    Badner, JA
    Gershon, ES
    [J]. MOLECULAR PSYCHIATRY, 2002, 7 (04) : 405 - 411
  • [6] Manic-depression genes and the new millennium: poised for discovery
    Baron, M
    [J]. MOLECULAR PSYCHIATRY, 2002, 7 (04) : 342 - 358
  • [7] A single nucleotide polymorphism in glycogen synthase kinase 3-β promoter gene influences onset of illness in patients affected by bipolar disorder
    Benedetti, F
    Bernasconi, A
    Lorenzi, C
    Pontiggia, A
    Serretti, A
    Colombo, C
    Smeraldi, E
    [J]. NEUROSCIENCE LETTERS, 2004, 355 (1-2) : 37 - 40
  • [8] Molecular linkage studies of bipolar disorders
    Berrettini, WH
    [J]. BIPOLAR DISORDERS, 2001, 3 (06) : 276 - 283
  • [9] DANISH TWIN STUDY OF MANIC-DEPRESSIVE DISORDERS
    BERTELSEN, A
    HARVALD, B
    HAUGE, M
    [J]. BRITISH JOURNAL OF PSYCHIATRY, 1977, 130 (APR) : 330 - 351
  • [10] Pediatric mania: A developmental subtype of bipolar disorder?
    Biederman, J
    Mick, E
    Faraone, SV
    Spencer, T
    Wilens, TE
    Wozniak, J
    [J]. BIOLOGICAL PSYCHIATRY, 2000, 48 (06) : 458 - 466