After questioning the practical significance of evidence that parenting influences brain development - while highlighting the scientific importance of such work for understanding how family experience shapes human development - this paper reviews evidence suggesting that brain structure and function are 'chiselled' by parenting. Although the generalisability of most findings is limited due to a disproportionate, but understandable focus on clinical samples (e.g., maltreated children with post-traumatic stress disorder (PTSD)) and causal inferences are difficult to draw because of the observational nature of most of the evidence, it is noteworthy that some work with community samples and very new experimental work (e.g., parent training) suggests that tentative conclusions regarding effects of parenting on the developing brain may well be substantiated in future research. Such efforts should focus on parenting in the normal range, experimental manipulations of parenting, differential susceptibility to parenting effects and pathway models linking parenting to brain development and, thereby, to behavioural development. Research on parenting and children's brain development may be regarded as at 'the end of the beginning'.

Annual research review: Parenting and children’s brain development: The end of the beginning.

Many of the major neuropsychiatric illnesses, including schizophrenia, have a typical age of onset in late adolescence. Late adolescence may reflect a critical period in brain development making it particularly vulnerable for the onset of psychopathology. Neuroimaging studies that focus on this age range may provide unique insights into the onset and course of psychosis. In this review, we examine the evidence from 2 unique longitudinal cohorts that span the ages from early childhood through young adulthood; a study of childhood-onset schizophrenia where patients and siblings are followed from ages 6 through to their early twenties, and an ultra-high risk study where subjects (mean age of 19 years) are studied before and after the onset of psychosis. From the available evidence, we make an argument that subtle, regionally specific, and genetically influenced alterations during developmental age windows influence the course of psychosis and the resultant brain phenotype. The importance of examining trajectories of development and the need for future combined approaches, using multimodal imaging together with molecular studies is discussed.

/pdf/age-of-onset-of-schizophrenia-perspectives-from-structural-5be6og8pqy.pdf

Age of Onset of Schizophrenia: Perspectives From Structural Neuroimaging Studies

Adolescence is a time of transition from childhood to adulthood during which significant changes occur across multiple domains, including emotional experience. This article reviews the relevant lit...

https://journals.sagepub.com/doi/pdf/10.1177/1754073918768878

Understanding Emotion in Adolescents: A Review of Emotional Frequency, Intensity, Instability, and Clarity:

Neural aspects of reward function have been conceptualized as critical to the etiology, development, pathophysiology, and treatment of depression (e.g., Forbes & Dahl, 2005; Hasler, Drevets, Manji, & Charney, 2004). This direction of research helps to shift the field away from a narrow focus on increased negative affect in depression and toward consideration of diminished positive affect, and it contributes to the search for mechanisms underlying mood and subjective experience.

A developmental psychopathology perspective could be especially valuable to understanding the role of reward function in depression and to reconciling seemingly conflicting findings on this topic, such as mixed results on low striatal response to reward. Because depression typically begins during adolescence (Kessler, Avenevoli, & Merikangas, 2001), and adolescent depression confers a high risk of recurrence in adulthood (Lewinsohn, Rohde, Klein, & Seeley, 1999), adolescent depression provides a valuable scientific opportunity. Examining reward function during adolescent depression can elucidate the larger course of the disorder and place its etiology within the context of typical, dramatic changes in reward function that occur during this developmental period (Somerville, Jones, & Casey, 2010).

This review examines the evidence for what in particular about reward function is disrupted in adolescent depression, when in the development of depression reward function is disrupted, and how disruption in neural reward circuits occurs. We propose testable hypotheses to guide future work on this compelling topic, and we briefly consider how a deeper understanding of these issues may inform intervention strategies. To obtain material for this conceptual review, we searched for peer-reviewed empirical papers in English published between 1990 and 2010 using PubMed, PsycInfo, and ScienceDirect indices, with terms such as depress*, reward, decision-making, dopamine, fMRI, striatum, and adolescen* (with the * wild card allowing retrieval of terms with the same stem, such as depressed and depression). Papers identified by the search were included if (1) they focused on topics relevant to the focus of the review (e.g., depression and striatal or medial prefrontal cortex (mPFC) response to reward; depression and decision-making behavior; adolescence and reward function; dopamine and depression), (2) used fMRI with a reward processing paradigm; (3) reported results of statistical tests; and (4) compared currently depressed and healthy control groups (e.g., not remitted depressed). Extending the stance of our previous reviews (Forbes, 2011; Forbes & Dahl, 2005; Forbes, et al., 2009), the specific goals of this review are to integrate recent neuroimaging findings; provide an overview of key related topics, such as reward-related decision-making; and develop an explicit foundation for future research.

Research Review: altered reward function in adolescent depression: what, when and how?

Social connectedness, mental health and the adolescent brain

One of the most striking aspects of the epidemiology of depressive disorders across the lifespan is the rapid rise in the incidence of depression that is observed in early adolescence (Lewinsohn et al., 1993, 1998). A recent metaanalysis of epidemiological studies estimated the prevalence of unipolar depressive disorders to be approximately 5.6% in adolescents as compared with 2.8% in children below age 13 (Costello et al., 2006). Lifetime estimate rates for adolescents, ranging from 15–20%, are comparable with those of adults (Birmaher et al., 1996). Further, longitudinal data indicate that an episode of depression is a substantial risk factor for subsequent episodes, both within adolescence and into adulthood (Birmaher et al., 1996; Harrington & Vostanis, 1995). This increased vulnerability likely reflects the adverse impact of depressive episodes on neurobiological and cognitive development (Harrison, 2002; Vythilingam et al., 2002) as well as on emotional, social, and occupational functioning (Bardone et al., 1996; Rohde et al., 1994). These data indicate the important public health significance of adolescent depressive syndromes. Moreover, they direct our attention to the likelihood that some causative mechanism, or mechanisms, underlie this population-wide increase in vulnerability, and in so doing highlight the need to understand the relationships between early adolescent development and the psychopathological processes that give rise to depressive conditions. Explicating these relationships will yield important insights not only for understanding depressive disorders during adolescence (a critically important life stage if we are to provide effective prevention and early intervention), but likely also for understanding vulnerability throughout the life span. In other words, the developmentally driven changes that occur during early adolescence and result in an increased cohort-wide vulnerability to depression may provide clues as to

Adolescent Emotional Development and the Emergence of Depressive Disorders: The importance of affective development for the emergence of depressive disorders during adolescence

The way that parents express their emotions during interactions with their adolescent children is important for adolescent adjustment, and predicts adolescent emotional problems such as depression. In the current study, we assessed whether adolescent depressive symptoms were associated with neural activity during exposure to their mother's affective behavior. Thirty adolescents (18 females, mean age 17.35, s.d. 0.43) participated in an fMRI task that used digitized video segments of their own mother's, as well as an unfamiliar mother's affective behavior as stimuli. Exposure to one's own (compared to an unfamiliar) mother's positive (compared to neutral) behavior was associated with activation in the anterior and posterior cingulate, precuneus and ventrolateral prefrontal cortex. In contrast, exposure to positive behavior across own and an unfamiliar mother (controlling for neutral behavior) was associated with superior temporal sulcus, occipital pole, amygdala and striatum activity. Adolescent depressive symptoms were associated with reduced rostral anterior cingulate activity during exposure to one's own (compared to an unfamiliar) mother's positive behavior, and reduced striatal activity during exposure to positive behavior in general. This study represents an important step in furthering our understanding of the neural basis of affective processing in adolescents. Further, the results support a disruption of reward function in depression.

Adolescents’ depressive symptoms moderate neural responses to their mothers’ positive behavior

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Adolescent Emotional Development and the Emergence of Depressive Disorders: Towards a developmental psychopathology of adolescent-onset depression: implications for research and intervention

Emotional interactions between parents and their children are known to have a significant effect on the development and recurrence of clinical depression in children. While speech models used by existing conversation modeling algorithms can provide information about frequency of speech-silence states, the modeling process itself does not provide qualitative insights into the nature of the emotional process that underlies the speakers’ behavior. To address this issue, a recently proposed higher order emotional influence model (HOEIM) was applied to determine the extent to which “emotional influences” (interpreted as the values of the model coefficients) differed between families with depressed and non-depressed adolescents. The analysis was based on four speaker states: positive emotion, negative emotion, neutral emotion, and silence. The HOEIM estimated the conditional probabilities of these states in parent-child conversations in 29 families with clinically depressed adolescents (14-18 years old) and in 31 families with non-depressed adolescents. The trajectories of the model coefficients displayed across model orders increasing from 1 to 5 (corresponding to the memory time of past emotional states ranging from 1 to 5 seconds) indicated that parent-child interactions were significantly different between these two types of family environments, and the nature of these interactions clearly depended on the topic of conversation.

Quantitative and qualitative insights into emotional interaction patterns in families with clinically depressed and non-depressed adolescents

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