Familial Risk For Depression Research Articles

Maternal Response to Positive Affect Moderates the Impact of Familial Risk for Depression on Ventral Striatal Response to Winning Reward in 6- to 8-Year-Old Children

BackgroundA growing body of research has demonstrated that adolescent offspring of depressed parents show diminished responding in the ventral striatum to reward. More recent work has suggested that altered reward responding may emerge earlier than adolescence in offspring at familial risk for depression, although factors associated with neural alterations in childhood remain poorly understood. MethodsWe tested whether 6- to 8-year-old children, 49% at heightened risk for depression via maternal history, showed altered neural responding to winning reward. We evaluated whether maternal socialization of positive emotion moderated the association between familial risk and child neural response to reward. Participants were 49 children 6 to 8 years of age (24 with a maternal history of recurrent or chronic depression, 25 with no maternal history of any psychiatric disorder). Children underwent functional magnetic resonance imaging while completing the Doors Guessing Task, a widely used reward guessing task. Mothers reported their use of encouraging and dampening responses to child positive affect. ResultsFindings demonstrated that children at high familial risk for depression showed lower ventral striatum responding to winning reward relative to low-risk children, but only when mothers used less encouragement or greater dampening responses to their child’s positive emotion expressions. ConclusionsNeural reward alterations in the ventral striatum may emerge earlier than previously thought, as early as 6 to 8 years of age, specifically in the context of maternal discouragement of child positive emotions. Clinical interventions that focus on coaching mothers on how to encourage child positive emotions may be beneficial for supporting child reward-related brain development.

Metabolic syndrome among young adults at high and low familial risk for depression.

Our study examined whether the early-onset depression phenotype among young adults (probands) is associated with the metabolic syndrome (MetS) and its components, and if MetS characterizes unaffected but high-risk siblings of probands. We studied three groups of young adults (Mage = 25 years, s.d. = 3.84 years): probands with histories of childhood onset depression - i.e. early-onset phenotype - (n = 293), their unaffected siblings (high-risk siblings, n = 273), and healthy controls (n = 171). Participants completed a full psychiatric interview, physical and laboratory assessments, and self-rating scales. MetS was defined using the criteria of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (). Early-onset depression phenotype and being a high-risk sibling were associated with higher MetS composite scores relative to that of controls, but did not differ from one another. With regard to MetS components: Probands and siblings had similarly larger waist circumference and lower HDL than did controls, while siblings and controls had lower triglyceride levels than did probands but did not differ from one another. Groups did not differ on glucose levels and SBP. Our study extends the literature on the association between MetS and depression and underscores the importance of depression phenotypes: failure to account for the clinical heterogeneity of depression may partly underlie the inconsistent findings regarding its relation to MetS. The results also suggest that, in depression-prone populations, MetS may predate and possibly function as a risk factor for eventual depression.

Age related sex differences in maladaptive regulatory responses to sadness: A study of youths at high and low familial risk for depression

Offspring of parents with depression histories are at increased risk of developing depression and also report maladaptive ways of self-regulating sadness. Maladaptive regulation of sadness tends to be more prevalent among females than males and has been proposed as one explanation of sex differences in depression rates that emerge around mid-adolescence. However, there is scant information about the age at which the sex differences in maladaptive regulatory responses become evident and whether such age-related sex differences vary depending on depression risk. The present study examined two samples aged 8-18 years: 86 offspring of emotionally healthy parents and 98 offspring of parents with depression histories. Subjects were clinically assessed and provided self-reports of maladaptive responses to sadness. In the combined samples, sex differences in maladaptive responses were significant at age 12.5 years and older ages (i.e., chronologically earlier than the documented emergence of sex differences in depression). While in the high-risk group, sex differences in maladaptive regulatory responses were significant at 12.11 years of age and older, in the low-risk group there was no age at which sex differences were significant. Our findings support the possible mechanistic role of maladaptive emotion regulation in the emergence of sex disparities in depression rates and have implications for prevention.

Motor Abnormalities, Depression Risk, and Clinical Course in Adolescence

BackgroundMotor abnormalities, such as psychomotor agitation and retardation, are widely recognized as core features of depression. However, it is not currently known whether motor abnormalities connote risk for depression. MethodsUsing data from the Adolescent Brain Cognitive Development (ABCD) Study, a nationally representative sample of youth (N = 10,835, 9–11 years old), the present paper examines whether motor abnormalities are associated with 1) depression symptoms in early adolescence, 2) familial risk for depression (familial risk loading), and 3) future depression symptoms. Motor abnormality measures included traditional (DSM) motor signs such as psychomotor agitation and retardation as well as other motor domains such as developmental motor delays and dyscoordination. ResultsTraditional motor abnormalities were less prevalent (agitation = 3.2%, retardation = 0.3%) than nontraditional domains (delays = 13.79%, coordination = 35.5%) among adolescents. Motor dysfunction was associated with depression symptoms (Cohen’s d = 0.02 to 0.12). Familial risk for depression was related to motor abnormalities (Cohen’s d = 0.08 to 0.27), with the exception of motor retardation. Family vulnerability varied in sensitivity to depression risk (e.g., retardation: 0.53%; dyscoordination: 32.05%). Baseline endorsement of motor abnormalities predicted future depression symptoms at 1-year follow-up. ConclusionsThese findings suggest that motor signs reflect a novel, promising future direction for examining vulnerability to depression risk in early adolescence.

Links between depressive symptoms and the observer perspective for autobiographical memories and imagined events: a high familial risk study

ABSTRACT Depression is associated with increased observer visual perspective for positive autobiographical memories. However, it is unclear if this relationship (1) is present in individuals at high familial risk of depression; (2) is a general bias extending to future imagined events; and (3) is independent of general cognition and other cognitive biases. We examined the association of observer perspective, valence (positive, negative, neutral) and temporality (memories, future imagined events) with depressive symptoms in 29 young adults at high familial risk for depression. Increased observer perspective for memories was associated with dimensional depressive symptoms controlling for IQ and autobiographical specificity. There was weak evidence that increased observer perspective for future events was associated with a diagnostic measure of depressive symptoms, but limited evidence that perspective by valence interactions were associated with depressive symptoms. Results indicate depressive symptoms are associated with an observer perspective bias in autobiographical thinking regardless of temporality or valence.

Contributions From Resting State Functional Connectivity and Familial Risk to Early Adolescent-Onset MDD: Results From the Adolescent Brain Cognitive Development Study

Abstract Background Family history of Major Depressive Disorder (MDD) is a robust predictor of MDD onset, especially in early adolescence. We examined the relationships between familial risk for depression and alterations to resting state functional connectivity (rsFC) within the default mode network (wDMN) and between the DMN and the left/right hippocampus (DMN-LHIPP/DMN-RHIPP) to the risk for early adolescent MDD onset. Methods We examined 9403 youth aged nine to eleven from the Adolescent Brain Cognitive Development study. Depressive symptoms were measured with the parent-reported Child Behavior Checklist. Both youth and their parents completed the Kiddie Schedule for Affective Disorders and Schizophrenia, which provided MDD diagnoses. A family history screen was administered to determine familial risk for depression. Youth underwent a resting state functional magnetic resonance imaging scan, providing us with rsFC data. Results Negative wDMN rsFC was associated with child-reported current depression, both child- and parent-reported past depression, and parent-reported current depressive symptoms. No difference was found in wDMN, DMN-LHIPP or DMN-RHIPP rsFC in children with or without familial risk for depression. Familial risk for depression interacted with wDMN rsFC in association with child-reported past MDD diagnosis and parent-reported current depressive symptoms. Limitations Information such as length of depressive episodes and age of onset of depression was not collected. Conclusions Altered wDMN rsFC in youth at familial risk for depression may be associated with increased risk for MDD onset in adolescence, but longitudinal studies are needed to test this hypothesis.

Depression and Familial Risk for Depression Associated With Motor Abnormalities in the ABCD Study

Motor abnormalities are a strong indicator of emerging neural network abnormalities and may provide critical early indications of psychopathology risk. In fact, motor abnormalities, such as motor slowing and agitation, are widely recognized as features of several neurodevelopmental disorders. However, our understanding of motor pathology in the course of depression remains poorly developed.

Emotion Regulation as a Mediator in the Relationship Between Cognitive Biases and Depressive Symptoms in Depressed, At-risk and Healthy Children and Adolescents

Contemporary cognitive models of depression propose that cognitive biases for negative information at the level of attention (attention biases; AB) and interpretation (interpretation biases; IB) increase depression risk by promoting maladaptive emotion regulation (ER). So far, empirical support testing interactions between these variables is restricted to non-clinical and clinical adult samples. The aim of the current study was to extend these findings to a sample of children and adolescents. This cross-sectional study included 109 children aged 9–14 years who completed behavioural measures of AB (passive-viewing task) and IB (scrambled sentences task) as well as self-report measures of ER and depressive symptoms. In order to maximize the variance in these outcomes we included participants with a clinical diagnosis of depression as well as non-depressed youth with an elevated familial risk of depression and non-depressed youth with a low familial risk of depression. Path model analysis indicated that all variables (AB, IB, adaptive and maladaptive ER) had a direct effect on depressive symptoms. IB and AB also had significant indirect effects on depressive symptoms via maladaptive and adaptive ER. These findings provide initial support for the role of ER as a mediator between cognitive biases and depressive symptoms and provide the foundations for future experimental and longitudinal studies. In contrast to studies in adult samples, both adaptive as well as maladaptive ER mediated the effect of cognitive biases on depressive symptoms. This suggests potentially developmental differences in the role of ER across the lifespan.

DLPFC volume is a neural correlate of resilience in healthy high-risk individuals with both childhood maltreatment and familial risk for depression.

Two prominent risk factors for major depressive disorder (MDD) are childhood maltreatment (CM) and familial risk for MDD. Despite having these risk factors, there are individuals who maintain mental health, i.e. are resilient, whereas others develop MDD. It is unclear which brain morphological alterations are associated with this kind of resilience. Interaction analyses of risk and diagnosis status are needed that can account for complex adaptation processes, to identify neural correlates of resilience. We analyzed brain structural data (3T magnetic resonance imaging) by means of voxel-based morphometry (CAT12 toolbox), using a 2 × 2 design, comparing four groups (N = 804) that differed in diagnosis (healthy v. MDD) and risk profiles (low-risk, i.e. absence of CM and familial risk v. high-risk, i.e. presence of both CM and familial risk). Using regions of interest (ROIs) from the literature, we conducted an interaction analysis of risk and diagnosis status. Volume in the left middle frontal gyrus (MFG), part of the dorsolateral prefrontal cortex (DLPFC), was significantly higher in healthy high-risk individuals. There were no significant results for the bilateral superior frontal gyri, frontal poles, pars orbitalis of the inferior frontal gyri, and the right MFG. The healthy high-risk group had significantly higher volumes in the left DLPFC compared to all other groups. The DLPFC is implicated in cognitive and emotional processes, and higher volume in this area might aid high-risk individuals in adaptive coping in order to maintain mental health. This increased volume might therefore constitute a neural correlate of resilience to MDD in high risk.

Further Evidence that Subsyndromal Manifestations of Depression in Childhood Predict the Subsequent Development of Major Depression: A Replication Study in a 10 Year Longitudinally Assessed Sample

BackgroundWe have previously shown that subsyndromal scores on the Child Behavior Checklist (CBCL)-Anxiety/Depression (Anx/Dep) scale at baseline predicted the subsequent development of Major Depressive Disorder (MDD) in youth with ADHD. The present study aimed to replicate these findings in a separate, long-term, longitudinal sample of children at high- and low- risk for depression. Methods219 children of parents with and without depression and/or anxiety, ages 2-25, were stratified into 3 groups: 1) children with familial risk for depression (by presence of parental MDD) plus subsyndromal scores on the CBCL-Anx/Dep scale, 2) children with familial risk for depression without subsyndromal scores, and 3) children with neither familial risk for depression nor subsyndromal scores. Subjects were reassessed at both 5 and 10 year follow-ups. ResultsChildren with both subsyndromal scores on the CBCL-Anx/Dep plus a familial risk for depression were at greater risk for developing MDD at the 10 year follow-up when compared with all other groups. Those with familial risk but no subsyndromal scores had an intermediate risk that was greater than the controls, who had the lowest risk. LimitationsThe recruitment of the study included families with parental panic disorder, so the sample likely included more families with anxiety disorders than the general population. ConclusionsOur results showed that subsyndromal scores of the CBCL-Anx/Dep scale increased the risk for the subsequent development of MDD, particularly in children at high risk for depression. These results confirm the CBCL-Anx/Dep scale's utility in identifying children at high risk for developing MDD.

Contributions from resting state functional connectivity and familial risk to early adolescent-onset MDD: Results from the Adolescent Brain Cognitive Development study

BackgroundFamily history of Major Depressive Disorder (MDD) is a robust predictor of MDD onset, especially in early adolescence. We examined the relationships between familial risk for depression and alterations to resting state functional connectivity (rsFC) within the default mode network (wDMN) and between the DMN and the left/right hippocampus (DMN-LHIPP/DMN-RHIPP) to the risk for early adolescent MDD onset. MethodsWe examined 9403 youth aged nine to eleven from the Adolescent Brain Cognitive Development study. Depressive symptoms were measured with the parent-reported Child Behavior Checklist. Both youth and their parents completed the Kiddie Schedule for Affective Disorders and Schizophrenia, which provided MDD diagnoses. A family history screen was administered to determine familial risk for depression. Youth underwent a resting state functional magnetic resonance imaging scan, providing us with rsFC data. ResultsNegative wDMN rsFC was associated with child-reported current depression, both child- and parent-reported past depression, and parent-reported current depressive symptoms. No difference was found in wDMN, DMN-LHIPP or DMN-RHIPP rsFC in children with or without familial risk for depression. Familial risk for depression interacted with wDMN rsFC in association with child-reported past MDD diagnosis and parent-reported current depressive symptoms. LimitationsInformation such as length of depressive episodes and age of onset of depression was not collected. ConclusionsAltered wDMN rsFC in youth at familial risk for depression may be associated with increased risk for MDD onset in adolescence, but longitudinal studies are needed to test this hypothesis.

48352 Mechanisms Underlying Lipidomic Changes in Major Depressive Disorder

ABSTRACT IMPACT: Lipidomics is emerging as a powerful strategy to identify biomarkers for Major Depressive Disorder, as well as therapeutic targets in lipid metabolic pathways. OBJECTIVES/GOALS: Lipidomics is increasingly recognized in precision psychiatry for global lipid perturbations in patients suffering from Major Depressive Disorder (MDD). We will test the hypothesis that lipid metabolism dysregulation is associated with familial risk of depression. METHODS/STUDY POPULATION: Patients with MDD (G1), children (G2), and grandchildren (G3) have been part of a longitudinal study since 1982. If a parent G2 and grandparent G1 have MDD, G3 is considered a high risk of depression. Biospecimens (saliva and serum) were collected for full exome sequencing and RNA analysis. Samples will also be extracted for lipid content and lipids will be identified by mass spectrometry. A panel of nearly 600 lipid species can reliably be identified and quantified using liquid chromatography paired with tandem mass spectrometry (LC-MS/MS). Dysregulated lipids will be correlated with familial risk of depression in samples of G3. RESULTS/ANTICIPATED RESULTS: We hypothesize that dysregulation of lipids and lipid metabolism will be apparent in biospecimens from the high risk compared to the low risk of depression. Also, alterations in RNA transcriptomics of genes involved in lipid metabolic networks are associated with familial risk of depression. Several differential lipid species were previously identified to be associated with MDD. Reduced phosphatidylcholine(PC), phosphatidylethanolamine(PE), phosphatidylinositol(PI), and increased LysoPC, LysoPE, ceramide, triacylglycerol, and diacylglycerol levels have been correlated to MDD. However, these results need to be replicated in independent studies using lipidomics analysis. DISCUSSION/SIGNIFICANCE OF FINDINGS: It is highly likely that completely novel cellular targets will emerge from these studies by uncovering the convergence of lipidomics and genetic variance of lipid metabolic enzymes as biomarkers for predisposition to MDD as well as potential targets for therapeutic development for MDD.

An Eye-Tracking Study of Attention Biases in Children at High Familial Risk for Depression and Their Parents with Depression

Attention biases (AB) are a core component of cognitive models of depression yet it is unclear what role they play in the transgenerational transmission of depression. 44 children (9–14 years) with a high familial risk of depression (HR) were compared on multiple measures of AB with 36 children with a low familial risk of depression (LR). Their parents: 44 adults with a history of depression (HD) and 36 adults with no history of psychiatric disorder (ND) were also compared. There was no evidence of group differences in AB; neither between the HR and LR children, nor between HD and ND parents. There was no evidence of a correlation between parent and child AB. The internal consistency of the tasks varied greatly. The Dot-Probe Task showed unacceptable reliability whereas the behavioral index of the Visual-Search Task and an eye-tracking index of the Passive-Viewing Task showed better reliability. There was little correlation between the AB tasks and the tasks showed minimal convergence with symptoms of depression or anxiety. The null-findings of the current study contradict our expectations and much of the previous literature. They may be due to the poor psychometric properties associated with some of the AB indices, the unreliability of AB in general, or the relatively modest sample size. The poor reliability of the tasks in our sample suggest caution should be taken when interpreting the positive findings of previous studies which have used similar methods and populations.

Familial risk and heritability of depression by age at first diagnosis in Danish twins.

Familial and genetic factors seem to contribute to the development of depression but whether this varies with age at diagnosis remains unclear. We examined the influence of familial factors on the risk of depression by age at first diagnosis. We included 23498 monozygotic and 39540 same-sex dizygotic twins from the population-based Danish Twin Registry, followed from 1977 through 2011 in nationwide registers. We used time-to-event analyses accounting for censoring and competing risk of death to estimate cumulative incidence, casewise concordance, relative recurrence risk, and heritability of first depression by age using monozygotic and same-sex dizygotic twin pairs. During follow-up, a total of 1545 twins were diagnosed with depression. For twins at age 35 or younger at first depression, heritability was estimated to be 24.8% (95% confidence interval [CI], 4.6-43.1%), whereas at age 90 it was 14.7% (95% CI, 3.1-26.3%). The relative recurrence risk was higher at younger ages: At age 35, the risk was 27.7-fold (95% CI, 20.0-35.5) and 6.9-fold (95% CI, 3.9-9.8) higher than the population risk for monozygotic and same-sex dizygotic twins, respectively, while the corresponding numbers were 3.0 (95% CI, 2.3-3.6) and 1.8 (95% CI, 1.3-2.2) at age 90. Heritability seemed similar for male and female twins. Familial risk of depression, caused either by genes or shared environment, seemed to slightly decrease with age at diagnosis and an elevated concordance risk for monozygotic over same-sex dizygotic pairs suggested a genetic contribution to the development of depression.

Sympathetic arousal during the processing of dysphoric affect by youths at high and low familial risk for depression.

Youths at high risk for depression have been shown to have problems in repairing their own sad mood. Given that sympathetic arousal has been implicated both in the experience and regulation of affect, an atypical pattern of arousal may be one of the factors that contribute to mood repair problems. In the current study, we measured sympathetic arousal of never-depressed youths at high (n=56) and low (n=67) familial risk for depression during sad mood induction and instructed mood repair. Sympathetic arousal was indexed by skin conductance level (SCL) and cardiac pre-ejection period (PEP); mood repair outcome was indexed by self-rated affect. High-risk youths demonstrated increased SCL during sadness induction, which persisted during mood repair; low-risk youths evidenced increased SCL only during mood repair. Shortened PEP was evident only among high-risk youths and only during mood repair. Furthermore, shortened PEP during mood induction predicted less successful mood repair in the low-risk but not in the high-risk group. The findings suggest that: (a) depression-prone youths differ from control peers in patterns of sympathetic responses to emotional stimuli, which may impair their ability to relieve sadness, and (b) activation patterns differ across subsystems (SCL vs. PEP) of sympathetic activity, in conjunction with depression risk status.

Social media use predicts later sleep timing and greater sleep variability: An ecological momentary assessment study of youth at high and low familial risk for depression

IntroductionSocial media (SM) use has been increasingly recognized as a potential contributor to poor sleep. Few studies have examined SM use and sleep using ecological momentary assessment (EMA), compared different types of media use (SM, television, gaming), or examined whether youth at high and low familial risk for depression are differentially affected by SM use. MethodsThe current study included 76 youth (46% female; Mean age = 11.28 years) who were recruited based on parental history of recurrent depression (N = 35 high risk; N = 41 low risk) in the United States. Youth completed a 9-day EMA protocol, which included current activity at time of prompt and daily sleep onset and offset times. Regression and multilevel models were conducted to examine the effects of media use on sleep. ResultsResults indicated that youth who used more SM (mean and number of days) went to sleep later, but did not have shorter sleep duration. Youth with more SM use also had higher levels of variability of both sleep timing and sleep duration across the 9-day period. There were no effects of gaming or TV on sleep, and youth at high risk for depression did not have differences in SM use or its effects on sleep compared to low-risk youth. ConclusionsThese findings indicate a unique impact of SM use on sleep timing and variability for youth (regardless of risk status), which may suggest a unique and modifiable pathway through which SM use contributes to poor health.

Familial risk for depressive and anxiety disorders: associations with genetic, clinical, and psychosocial vulnerabilities.

In research and clinical practice, familial risk for depression and anxiety is often constructed as a simple Yes/No dichotomous family history (FH) indicator. However, this measure may not fully capture the liability to these conditions. This study investigated whether a continuous familial loading score (FLS), incorporating family- and disorder-specific characteristics (e.g. family size, prevalence of depression/anxiety), (i) is associated with a polygenic risk score (PRS) for major depression and with clinical/psychosocial vulnerabilities and (ii) still captures variation in clinical/psychosocial vulnerabilities after information on FH has been taken into account. Data came from 1425 participants with lifetime depression and/or anxiety from the Netherlands Study of Depression and Anxiety. The Family Tree Inventory was used to determine FLS/FH indicators for depression and/or anxiety. Persons with higher FLS had higher PRS for major depression, more severe depression and anxiety symptoms, higher disease burden, younger age of onset, and more neuroticism, rumination, and childhood trauma. Among these variables, FH was not associated with PRS, severity of symptoms, and neuroticism. After regression out the effect of FH from the FLS, the resulting residualized measure of FLS was still associated with severity of symptoms of depression and anxiety, rumination, and childhood trauma. Familial risk for depression and anxiety deserves clinical attention due to its associated genetic vulnerability and more unfavorable disease profile, and seems to be better captured by a continuous score that incorporates family- and disorder-specific characteristics than by a dichotomous FH measure.

The neural basis of hot and cold cognition in depressed patients, unaffected relatives, and low-risk healthy controls: An fMRI investigation

BackgroundModern cognitive neuropsychological models of depression posit that negatively biased emotional (“hot”) processing confers risk for depression, while preserved executive function (“cold”) cognition promotes resilience. MethodsWe compared neural responses during hot and cold cognitive tasks in 99 individuals: those at familial risk for depression (N = 30 unaffected first-degree relatives of depressed individuals) and those currently experiencing a major depressive episode (N = 39 unmedicated depressed patients) with low-risk healthy controls (N = 30). Primary analyses assessed neural activation on two functional magnetic resonance imaging tasks previously associated with depression: dorsolateral prefrontal cortex (DLPFC) responsivity during the n-back working memory task; and amygdala and subgenual anterior cingulate cortex (sgACC) responsivity during incidental emotional face processing. ResultsDepressed patients exhibited significantly attenuated working memory-related DLPFC activation, compared to low-risk controls and unaffected relatives; unaffected relatives did not differ from low-risk controls. We did not observe a complementary pattern during emotion processing. However, we found preliminary support that greater DLPFC activation was associated with lower amygdala response during emotion processing. LimitationsThese findings require confirmation in a longitudinal study to observe each individual's risk of developing depression; without this, we cannot identify the true risk level of the first-degree relative or low-risk control group. ConclusionsThese findings have implications for understanding the neural mechanisms of risk and resilience in depression: they are consistent with the suggestion that preserved executive function might confer resilience to developing depression in first-degree relatives of depressed patients.

Here's looking at you, kid? Maternal depression and adolescent attention to self- or other-directed emotional faces

BackgroundMaternal depression history represents a significant risk factor for developing psychopathology in children, altered emotional responding may represent a central risk pathway. However, additional research is needed on factors that affect the strength or direction of response alterations in relation to depression-risk in youth. In particular, facial orientation and gaze direction may alter personal relevance, with emotions directed towards an individual heightening motivational salience, compared to emotions directed away. MethodsMother-daughter dyads (N = 56) were recruited based on presence or absence of maternal depression history and absence of youth depression. In line with theoretical perspectives suggesting diminished sensitivity to emotional context in relation to depression risk, we examined three Event-Related Potential (ERP) components in relation to forward versus averted emotional faces in a sample of girls with and without a maternal history of depression: the N200, N400, and Late Positive Potential (LPP). ResultsResults showed a significant maternal depression history by face-orientation effect. Low-risk girls exhibited more negative N200 and N400 amplitudes for straight (M = −3.72, SE = 0.83; M = −3.57, SE = 0.86) versus averted (M = −2.15, SE = 0.76; M = −1.68, SE = 0.81) faces, while girls of mothers with histories of depression showed undifferentiated N200 or N400 responses in relation to face orientation. For LPP amplitudes, low-risk girls exhibited significantly more positive LPP amplitudes than high-risk girls, but only for averted faces (M = 0.69, SE = 0.59 and M = −2.63, SE = 0.74, respectively). LimitationsCross-sectional design and limited sample. ConclusionsResults indicate that familial depression risk is associated with altered responsivity to face-orientation, these were interpreted as representing differential sensitivity to the personal-relevance of emotional stimuli.

The cross-sectional and longitudinal relationship between overgeneral autobiographical memory and adolescent depression in a UK population-based cohort

BackgroundOvergeneral autobiographical memory (OGM), the tendency to recall fewer specific memories and recall more repeated or extended events, is associated with subsequent adult depression. However, prospective associations are only found in adolescents with additional risk factors for depression (e.g. OGM for negative material is associated with subsequent depression in females and those at familial risk of depression) and not in community samples. It remains unclear whether OGM is associated with subsequent depression in population-based adolescent samples or just in high-risk adolescents. MethodsWe examined the relationship between OGM for negative cues (age 13) and adolescent depressive symptoms in a population-based cohort - the Avon Longitudinal Study of Parents and Children. Regression models investigated the association of OGM for negative cues with depressive symptoms at age 12.5 years (n = 3,145) and age 16.5 years (n = 2,345). Associations with alternative measures of OGM were also explored. Gender and maternal depression were examined as potential moderators of these relationships. ResultsOGM for negative cues was associated with both contemporaneous and prospective depressive symptoms. Only OGM for negative cues and total OGM were prospectively associated with depressive symptoms. There was no evidence of moderation by gender or maternal depression. LimitationsDepression was reported 6 months earlier than OGM. ConclusionsTo our knowledge, this is the first study to find a prospective link between OGM for negative material and depression in a population-based cohort. Results highlight memory biases can precede subsequent adolescent depression in the general population, not just high-risk samples.