American Journal of Psychiatry (AM J PSYCHIAT )

Publisher: American Psychiatric Association, American Psychiatric Publishing

Description

The American Journal of Psychiatry is the most widely read psychiatric journal in the world. Published monthly, it is indispensable for all psychiatrists and other mental health professionals who need to keep up-to-date with all aspects of psychiatry. Peer-reviewed articles focus on developments in biological psychiatry as well as on treatment innovations and forensic, ethical, economic, and social topics. Letters to the editor and book reviews also appear in each issue; official American Psychiatric Association reports appear from time to time. Of special interest are the overview and other special lead articles, which treat major psychiatric syndromes and issues in depth.

  • Impact factor
    14.72
    Show impact factor history
     
    Impact factor
  • 5-year impact
    14.40
  • Cited half-life
    0.00
  • Immediacy index
    2.57
  • Eigenfactor
    0.06
  • Article influence
    5.54
  • Website
    American Journal of Psychiatry website
  • Other titles
    The American journal of psychiatry
  • ISSN
    0002-953X
  • OCLC
    1480183
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

American Psychiatric Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo for author's post-print version
  • Conditions
    • Authors final version of accepted manuscript
    • Any repository
    • Non-commercial
    • Publisher's version/PDF cannot be used
    • Publisher copyright and source including DOI must be acknowledged
    • Must link to publisher version on publisher's website at journals.psychiatryonline.org with the phrase: "The official published article is available online at ."l
  • Classification
    ​ yellow

Publications in this journal

  • American Journal of Psychiatry 09/2014; 171(9):1003-4.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Schizophrenia affects approximately 3 million people in the United States. Individuals with this illness often ex- perience hallucinations, delusions, disorganized speech, disorganized behav- ior, and decreased emotional expression. African American patients tend to be overdiagnosed with schizophrenia and underdiagnosed with mood disorders (e.g., depression and bipolar disorder) compared with non-Hispanic white patients (1). African Americans are di- agnosed with schizophrenia 4–5 times more frequently than non-Hispanic whites (2). The frequency of this diagno- sis in this population is seen in juvenile, Veterans Administration, and public and private facilities that use DSM criteria. Between 1970 and 1986, the percent- age of African Americans hospitalized with schizophrenia increased from 33% to 50%
    American Journal of Psychiatry 03/2014; 9(3).
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Differential effects of maternal and paternal posttraumatic stress disorder (PTSD) have been observed in adult offspring of Holocaust survivors in both glucocorticoid receptor sensitivity and vulnerability to psychiatric disorder. The authors examined the relative influences of maternal and paternal PTSD on DNA methylation of the exon 1F promoter of the glucocorticoid receptor (GR-1F) gene (NR3C1) in peripheral blood mononuclear cells and its relationship to glucocorticoid receptor sensitivity in Holocaust offspring. Method: Adult offspring with at least one Holocaust survivor parent (N=80) and demographically similar participants without parental Holocaust exposure or parental PTSD (N=15) completed clinical interviews, self-report measures, and biological procedures. Blood samples were collected for analysis of GR-1F promoter methylation and of cortisol levels in response to lowdose dexamethasone, and two-way analysis of covariance was performed using maternal and paternal PTSD as main effects. Hierarchical clustering analysis was used to permit visualization of maternal compared with paternal PTSD effects on clinical variables and GR-1F promoter methylation. Results: A significant interaction demonstrated that in the absence of maternal PTSD, offspring with paternal PTSD showed higher GR-1F promoter methylation, whereas offspring with both maternal and paternal PTSD showed lower methylation. Lower GR-1F promoter methylation was significantly associated with greater postdexamethasone cortisol suppression. The clustering analysis revealed that maternal and paternal PTSD effects were differentially associated with clinical indicators and GR-1F promoter methylation. Conclusions: This is the first study to demonstrate alterations of GR-1F promoter methylation in relation to parental PTSD and neuroendocrine outcomes. The moderation of paternal PTSD effects by maternal PTSD suggests different mechanisms for the intergenerational transmission of trauma-related vulnerabilities.
    American Journal of Psychiatry 01/2014; AiA:1-9.
  • [Show abstract] [Hide abstract]
    ABSTRACT: O b je c t iv e : Antidopaminergic drugs bind to hERG1 potassium channels encoded by the gene KCNH2, which accounts for the side effect of QT interval prolongation. KCNH2 has also been associated with schizophrenia risk, and risk alleles predict increased expression of a brain-selective isoform, KCNH2 3.1, that has unique physiological properties. The authors assessed whether genetic variation associated with KCNH2 3.1 expression influences the therapeutic effects of antipsychotic drugs. M e th o d : The authors performed a pharmacogenetic analysis of antipsychotic treatment response in patients with schizophrenia using data from two independent studies: a National Institute of Mental Health (NIMH) double-blind, placebo-controlled inpatient crossover trial (N=54) and the multicenter outpatient Clinical Antipsychotic Trials in Intervention Effectiveness (CATIE) study (N=364). The KCNH2 genotype that was previously associated with increased expression of KCNH2 3.1 in the brain was treated as a predictor variable. Treatment-associated changes in symptoms were evaluated in both groups with the Positive and Negative Syndrome Scale. The authors also analyzed time to discontinuation in the olanzapine arm of the CATIE study. R e su lt s : In the NIMH study, individuals who were homozygous for the KCNH2 3.1 increased expression-associated T allele of rs1036145 showed significant improvement in positive symptoms, general psychopathology, and thought disturbance, while patients with other genotypes showed little change. In the CATIE study, analogous significant genotypic effects were observed. Moreover, individuals who were homozygous for the T allele at rs1036145 were one-fifth as likely to discontinue olanzapine. C o n c lu s io n s : These consistent findings in two markedly different treatment studies support the hypothesis that hERG1-mediated effects of antipsychotics may not be limited to their potential cardiovascular side effects but may also involve therapeutic actions related to the brainspecific 3.1 isoform of KCNH2.
    American Journal of Psychiatry 01/2012; 169:1-10.
  • American Journal of Psychiatry 01/2011; 168(1):97-98.