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Genetic determinants of depression: recent findings and future directions.

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      Abstract

      After participating in this activity, learners should be better able to: 1. Evaluate current evidence regarding the genetic determinants of depression 2. Assess findings from studies of gene-environment interaction 3. Identify challenges to gene discovery in depression Depression is one of the most prevalent, disabling, and costly mental health conditions in the United States and also worldwide. One promising avenue for preventing depression and informing its clinical treatment lies in uncovering the genetic and environmental determinants of the disorder as well as their interaction (G × E). The overarching goal of this review article is to translate recent findings from studies of genetic association and G × E related to depression, particularly for readers without in-depth knowledge of genetics or genetic methods. The review is organized into three major sections. In the first, we summarize what is currently known about the genetic determinants of depression, focusing on findings from genome-wide association studies (GWAS). In the second section, we review findings from studies of G × E, which seek to simultaneously examine the role of genes and exposure to specific environments or experiences in the etiology of depression. In the third section, we describe the challenges to genetic discovery in depression and promising strategies for future progress.

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      Most cited references 150

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      Gene ontology: tool for the unification of biology. The Gene Ontology Consortium.

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        KEGG: kyoto encyclopedia of genes and genomes.

         S. Goto,  M Kanehisa (2000)
        KEGG (Kyoto Encyclopedia of Genes and Genomes) is a knowledge base for systematic analysis of gene functions, linking genomic information with higher order functional information. The genomic information is stored in the GENES database, which is a collection of gene catalogs for all the completely sequenced genomes and some partial genomes with up-to-date annotation of gene functions. The higher order functional information is stored in the PATHWAY database, which contains graphical representations of cellular processes, such as metabolism, membrane transport, signal transduction and cell cycle. The PATHWAY database is supplemented by a set of ortholog group tables for the information about conserved subpathways (pathway motifs), which are often encoded by positionally coupled genes on the chromosome and which are especially useful in predicting gene functions. A third database in KEGG is LIGAND for the information about chemical compounds, enzyme molecules and enzymatic reactions. KEGG provides Java graphics tools for browsing genome maps, comparing two genome maps and manipulating expression maps, as well as computational tools for sequence comparison, graph comparison and path computation. The KEGG databases are daily updated and made freely available (http://www. genome.ad.jp/kegg/).
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          Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication.

          Little is known about lifetime prevalence or age of onset of DSM-IV disorders. To estimate lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the recently completed National Comorbidity Survey Replication. Nationally representative face-to-face household survey conducted between February 2001 and April 2003 using the fully structured World Health Organization World Mental Health Survey version of the Composite International Diagnostic Interview. Nine thousand two hundred eighty-two English-speaking respondents aged 18 years and older. Lifetime DSM-IV anxiety, mood, impulse-control, and substance use disorders. Lifetime prevalence estimates are as follows: anxiety disorders, 28.8%; mood disorders, 20.8%; impulse-control disorders, 24.8%; substance use disorders, 14.6%; any disorder, 46.4%. Median age of onset is much earlier for anxiety (11 years) and impulse-control (11 years) disorders than for substance use (20 years) and mood (30 years) disorders. Half of all lifetime cases start by age 14 years and three fourths by age 24 years. Later onsets are mostly of comorbid conditions, with estimated lifetime risk of any disorder at age 75 years (50.8%) only slightly higher than observed lifetime prevalence (46.4%). Lifetime prevalence estimates are higher in recent cohorts than in earlier cohorts and have fairly stable intercohort differences across the life course that vary in substantively plausible ways among sociodemographic subgroups. About half of Americans will meet the criteria for a DSM-IV disorder sometime in their life, with first onset usually in childhood or adolescence. Interventions aimed at prevention or early treatment need to focus on youth.
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            Author and article information

            Affiliations
            [1 ] From the Department of Psychiatry, Harvard Medical School (Drs. Dunn and Smoller); Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA (Drs. Dunn, Rosand, and Smoller, and Ms. Dai); Stanley Center for Psychiatric Research (Drs. Dunn and Smoller) and Program in Medical and Population Genetics (Dr. Rosand), Broad Institute of Harvard and MIT, Cambridge, MA; Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University (Drs. Brown and Amstadter); Department of Neurology, Massachusetts General Hospital, Boston, MA (Dr. Rosand); Department of Psychiatry and Human Behavior, Alpert Brown Medical School (Dr. Nugent); Center on the Developing Child, Harvard University (Dr. Smoller).
            Journal
            Harv Rev Psychiatry
            Harvard review of psychiatry
            Ovid Technologies (Wolters Kluwer Health)
            1465-7309
            1067-3229
            January 8 2015
            : 23
            : 1
            25563565
            10.1097/HRP.0000000000000054
            00023727-201501000-00001
            4309382
            NIHMS645804

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