Development and Psychopathology Journal Impact Factor & Information

Publisher: Cambridge University Press (CUP)

Journal description

This multidisciplinary journal is devoted to the publication of original empirical theoretical and review papers which address the interrelationship of normal and pathological development in adults and children. It is intended to serve and integrate the emerging field of developmental psychopathology which strives to understand patterns of adaptation and maladaptation throughout the lifespan. This journal is of vital interest to psychologists psychiatrists social scientists neuroscientists paediatricians and researchers.

Current impact factor: 4.89

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2009 Impact Factor 4.949

Additional details

5-year impact 6.69
Cited half-life 9.10
Immediacy index 1.31
Eigenfactor 0.01
Article influence 2.41
Website Development and Psychopathology website
Other titles Development and psychopathology
ISSN 0954-5794
OCLC 19716359
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Cambridge University Press (CUP)

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's Pre-print on author's personal website, departmental website, social media websites, institutional repository, non-commercial subject-based repositories, such as PubMed Central, Europe PMC or arXiv
    • Author's post-print on author's personal website on acceptance of publication
    • Author's post-print on departmental website, institutional repository, non-commercial subject-based repositories, such as PubMed Central, Europe PMC or arXiv, after a 6 months embargo
    • Publisher's version/PDF cannot be used
    • Published abstract may be deposited
    • Pre-print to record acceptance for publication
    • Publisher copyright and source must be acknowledged with set statement, for deposit of Authors Post-print or Publisher's version/PDF
    • Must link to publisher version
    • Publisher last reviewed on 07/10/2014
    • This policy is an exception to the default policies of 'Cambridge University Press (CUP)'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The relationship between developmental exposure to adversity and affective disorders is reviewed. Adversity discussed herein includes physical and sexual abuse, neglect, or loss of a caregiver in humans. While these stressors can occur at any point during development, the unique temporal relationship to specific depressive symptoms was the focus of discussion. Further influences of stress exposure during sensitive periods can vary by gender and duration of abuse as well. Data from animal studies are presented to provide greater translational and causal understanding of how sensitive periods, different types of psychosocial stressors, and sex interact to produce depressive-like behaviors. Findings from maternal separation, isolation rearing, chronic variable stress, and peer–peer rearing paradigms clarify interpretation about how various depressive behaviors are influenced by age of exposure. Depressive behaviors are broken down into the following categories: mood and affect, anhedonia, energy, working memory, sleep–wake, appetite changes, suicide, and general malaise. Cross-species evidence from humans, nonhuman primates, rats, and mice within each of these categories is discussed. In conclusion, sensitive periods for affective-related behaviors (anxiety, mood, and controllability) occur earlier in life, while other aspects of depression are associated with adversity later during adolescence.
    Development and Psychopathology 05/2015; 27(02):477-491. DOI:10.1017/S0954579415000103
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    ABSTRACT: Research on neurobiological development is providing insight into the nature and mechanisms of human neural plasticity. These mechanisms appear to support two different forms of developmental learning. One form of learning could be described as externalizing , in which neural representations are highly responsive to environmental influences, as the child typically operates under a mode of hedonic approach. A second form of learning supports internalizing , in which motive control separates attention and self-regulation from the immediate influences of the context, particularly when the child faces conditions of avoidance and threat. The dorsal cortical networks of externalizing are organized around dorsal limbic (cingulate, septal, lateral hypothalamic, hippocampal, and ventral striatal) circuits. In contrast, the ventral cortical networks of internalizing are organized around ventral limbic (anterior temporal and orbital cortex, extended amygdala, dorsal striatal, and mediodorsal thalamic) circuits. These dual divisions of the limbic system in turn self-regulate their arousal levels through different brain stem and forebrain neuromodulator projection systems, with dorsal corticolimbic networks regulated strongly by locus coeruleus norepinephrine and brain stem raphe nucleus serotonin projection systems, and ventral corticolimbic networks regulated by ventral tegmental dopamine and forebrain acetylcholine projections. Because the arousal control systems appear to regulate specific properties of neural plasticity in development, an analysis of these systems explains differences between externalizing and internalizing at multiple levels of neural and psychological self-regulation. In neuroscience, the concept of critical periods has been applied to times when experience is essential for the maturation of sensory systems. In a more general neuropsychological analysis, certain periods of the child's development require successful self-regulation through the differential capacities for externalizing and internalizing.
    Development and Psychopathology 05/2015; 27(02):321-346. DOI:10.1017/S0954579415000024
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    ABSTRACT: The human brain undergoes a remarkable transformation during fetal life and the first postnatal years from a relatively undifferentiated but pluripotent organ to a highly specified and organized one. The outcome of this developmental maturation is highly dependent on a sequence of environmental exposures that can have either positive or negative influences on the ultimate plasticity of the adult brain. Many environmental exposures are beyond the control of the individual, but nutrition is not. An ever-increasing amount of research demonstrates not only that nutrition shapes the brain and affects its function during development but also that several nutrients early in life have profound and long-lasting effects on the brain. Nutrients have been shown to alter opening and closing of critical and sensitive periods of particular brain regions. This paper discusses the roles that various nutrients play in shaping the developing brain, concentrating specifically on recently explicated biological mechanisms by which particularly salient nutrients influence childhood and adult neural plasticity.
    Development and Psychopathology 05/2015; 27(02):411-423. DOI:10.1017/S0954579415000061
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    ABSTRACT: Prior research has found inconsistent evidence regarding the association among childhood adversity, inflammation, and internalizing symptoms, perhaps because previous studies have yet to adequately integrate important factors such as the timing of the adversity, genetic variation, and other relevant processes such as neuroendocrine regulation. The aims of the present study were threefold: (a) to determine whether the effect of the timing of child maltreatment on C-reactive protein (CRP), an inflammatory marker, varies by CRP gene variation; (b) to explore whether links between salivary CRP and childhood internalizing symptoms depend on the presence and timing of maltreatment experiences; and (c) to investigate the role of CRP in the relations between child neuroendocrine regulation and internalizing symptoms and examine whether these associations are moderated by the presence and timing of child maltreatment. Participants included a sample of 267 maltreated and 222 nonmaltreated children ( M age = 9.72, SD = 0.99; 52.4% male; 66% African American) who attended a summer day camp research program designed for school-aged low-income children. Department of Human Services records were examined to determine the onset and recency of maltreatment for children in the maltreated group. The results indicated that among children with recent onset maltreatment, those with at least one A allele from CRP single nucleotide polymorphism rs1417938 evidenced significantly higher CRP levels compared to recently maltreated children carrying the TT genotype. Moreover, higher levels of CRP were associated with higher levels of internalizing symptoms only for recently maltreated children. Finally, we did not find support for salivary CRP as a mechanism in the relation between neuroendocrine regulation and childhood internalizing symptoms. Our findings highlight the importance of the timing of child maltreatment and have important implications for characterizing variability in inflammation and internalizing symptoms among youth.
    Development and Psychopathology 05/2015; 27(02):553-566. DOI:10.1017/S0954579415000152
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    ABSTRACT: Epigenetic modifications to the genome are a key mechanism involved in the biological encoding of experience. Animal studies and a growing body of literature in humans have shown that early adversity is linked to methylation of the gene for the glucocorticoid receptor (GR), which is a key regulator of the hypothalamic-pituitary-adrenal axis as well as a broad range of physiological systems including metabolic and immune function. One hundred eighty-four families participated, including n = 74 with child welfare documentation of moderate-severe maltreatment in the past 6 months. Children ranged in age from 3 to 5 years, and were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors, and a composite variable assessed the number exposures to these adversities. Methylation of regions 1D, 1F, and 1H of the GR gene was measured via sodium bisulfite pyrosequencing. The composite measure of adversity was positively correlated with methylation at exons 1D and 1F in the promoter of the GR gene. Individual stress measures were significantly associated with a several CpG sites in these regions. GR gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children.
    Development and Psychopathology 05/2015; 27(2):577-585. DOI:10.1017/S0954579415000176
  • [Show abstract] [Hide abstract]
    ABSTRACT: Exposure to early life adversity is linked to impaired affective, cognitive, and behavioral functioning and increases risk for various psychiatric and medical conditions. Stress-induced increases in pro-inflammatory cytokines may be a biological mechanism of these effects. Few studies have examined cytokine levels in children experiencing early life adversity, and very little research has investigated cytokines or other markers of inflammation in saliva. In the present study, we examined salivary interleukin (IL)-1β and C-reactive protein (CRP) levels in relation to stress exposure in 40 children aged 3 to 5 years who were enrolled in a larger study of early life adversity. Childhood maltreatment status was assessed via review of child welfare records. Contextual stress exposure, traumatic life event history, and symptoms of psychopathology were assessed via caregiver interviews at a home visit. In a subsequent visit, salivary IL-1β and CRP were obtained before and after participation in four emotion-eliciting tasks. The number of past-month contextual stressors, lifetime contextual stressors, and traumatic life events each demonstrated a significant main effect on IL-1β. Baseline IL-1β was positively associated with each of the significant main-effect adversities. Postchallenge IL-1β displayed positive associations with each adversity variable, but these were not significant. CRP was not significantly associated with any of the adversity variables. Given the evidence suggesting the involvement of IL-1β in the neuropathology of psychiatric conditions, these results may have important implications for developmental outcomes.
    Development and Psychopathology 05/2015; 27(Special Issue 02):567-576. DOI:10.1017/S0954579415000164
  • Development and Psychopathology 05/2015; 27(02):319-320. DOI:10.1017/S0954579415000012