Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Searching high and low: a review of the genetics of bipolar disorder
Autore:
Potash, JB; DePaulo, JR;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 av Sci, Baltimore, MD 21205 USA
Titolo Testata:
BIPOLAR DISORDERS
fascicolo: 1, volume: 2, anno: 2000,
pagine: 8 - 26
SICI:
1398-5647(200003)2:1<8:SHALAR>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
MANIC-DEPRESSIVE ILLNESS; SEROTONIN TRANSPORTER GENE; O-METHYLTRANSFERASE GENE; OLD-ORDER AMISH; TYROSINE-HYDROXYLASE GENE; LOW-ACTIVITY ALLELE; UNIPOLAR AFFECTIVE-DISORDERS; CHROMOSOME-18 DNA MARKERS; EXPANDED CAG/CTG REPEATS; MAJOR AFFECTIVE-DISORDER;
Keywords:
bipolar disorder; comorbidity; genetics; human; methods; mood disorders; phenotype;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
199
Recensione:
Indirizzi per estratti:
Indirizzo: Potash, JB Johns Hopkins Hosp, Meyer 3-181,600 N Wolfe St, Baltimore, MD 21287 USA Johns Hopkins Hosp Meyer 3-181,600 N Wolfe St Baltimore MD USA 21287
Citazione:
J.B. Potash e J.R. DePaulo, "Searching high and low: a review of the genetics of bipolar disorder", BIPOL DIS, 2(1), 2000, pp. 8-26

Abstract

Objectives: To review the methodologies and findings in the genetics of bipolar disorder (BPD), and to suggest future directions for research. Methods: Reports of family, twin, adoption, linkage, association, cytogenetic, and animal model studies, and segregation analyses in English, were identified from multiple MEDLINE searches. Hand searches were carried out in bibliographies from review articles. Results: Family, twin, and adoption studies have provided strong evidence for a genetic etiology in BPD. Early reports of linkage of BPD to DNA markers at several chromosomal sites have not proven robust. perhaps because or the complex nature of BPD inheritance. However. linkage findings in the 1990s, on chromosomes 18, 21q, 12q, and 4p, have provided leads that are bringpursued through both genetic and physical mapping. No gene has yet been definitively implicated in BPD. Conclusions: Strategies for increasing the power to detect BPD genes include: (1) dividing the phenotype into genetically meaningful subtypes to decrease heterogeneity: and (2) ascertaining a very large family sample - a multicenter study now in progress will collect 700 bipolar I sibling pairs. BPD may result from several genes acting in concert so that new multilocus statistical methods could enhance the capacity to detect loci involved. Family-based association studies using a very large number of newly identified single nucleotide polymorphisms (SNPs) may allow for more efficient screening of the genome. As the Human Genome Project approaches its goal of isolating all genes by 2003, the data generated is likely to speed identification of candidate BPD genes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 00:44:28