The Etiological Structure of Cognitive-Neurophysiological Impairments in ADHD in Adolescence and Young Adulthood.
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ABSTRACT:
SUBMITTER: Michelini G
PROVIDER: S-EPMC7750664 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature
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The Etiological Structure of Cognitive-Neurophysiological Impairments in ADHD in Adolescence and Young Adulthood.
Michelini Giorgia G Cheung Celeste H M CHM Kitsune Viryanaga V Brandeis Daniel D Banaschewski Tobias T McLoughlin Gráinne G Asherson Philip P Rijsdijk Frühling F Kuntsi Jonna J
Journal of attention disorders 20180503 1
<b>Objective:</b> Previous studies in children with ADHD identified two partially separable familial factors underlying cognitive dysfunction, but evidence in adolescents and adults is lacking. Here, we investigate the etiological structure of cognitive-neurophysiological impairments in ADHD in adolescents and young adults. <b>Method:</b> Factor analyses and multivariate familial models were run in 356 participants from ADHD and control sibling pairs aged 11 to 27 years on data on IQ, digit span ...[more]
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Project description:Previous studies in children with ADHD identified two partially separable familial factors underlying cognitive dysfunction, but evidence in adolescents and adults is lacking. Here, we investigate the etiological structure of cognitive-neurophysiological impairments in ADHD in adolescents and young adults.Factor analyses and multivariate familial models were run in 356 participants from ADHD and control sibling pairs aged 11 to 27 years on data on IQ, digit span forward (DSF) and backward (DSB), and cognitive-performance and event-related potential (ERP) measures from three cognitive tasks.Three familial factors (cF1-3), showing substantial familial overlap with ADHD, captured the familial covariation of ADHD with nine cognitive-ERP measures. cF1 loaded on IQ, mean reaction time (MRT), and reaction-time variability (RTV); cF2 on DSF and DSB; and cF3 on number of errors and ERPs of inhibition and error processing.These results identify three partially separable etiological pathways leading to cognitive-neurophysiological impairments in adolescent and adult ADHD.
| S-EPMC7116505 | biostudies-literature
Project description:BackgroundUsing a nationally representative longitudinal cohort, we examine how cognitive aptitude in early adolescence is associated with heterogeneous pathways of marijuana use from age sixteen through young adulthood. We also examine whether this relationship can be explained by the role of cognitive aptitude in the social organization of peer group deviance.MethodsUsing the National Longitudinal Survey of Youth 1997, we identified 5 latent trajectories of frequency of marijuana use between ages 16 and 26: abstainers, dabblers, early heavy quitters, consistent users, and persistent heavy users. Multinomial regression assessed the relationship of cognitive aptitude in early adolescence with these latent trajectories, including the role of peer group substance use in this relationship.ResultsA one decile increase in cognitive aptitude in early adolescence is associated with greater relative risk of the dabbler trajectory (RR = 1.048; p < .001) and consistent user trajectory (RR = 1.126; p < .001), but lower relative risk of the early heavy quitter trajectory (RR = 0.917; p < .05) in comparison with the abstainer trajectory. There was no effect for the persistent heavy user trajectory. The inclusion of peer group substance use-either via illegal drugs or smoking-had no effect on these relationships.ConclusionsAdolescents who rate higher in cognitive aptitude during early adolescence may be more likely to enter into consistent but not extreme trajectories of marijuana use as they age into young adulthood. Cognition may not influence patterns of marijuana use over time via the organization of peer groups.
| S-EPMC6814275 | biostudies-literature
Project description:Objective: We investigated whether "late-onset" ADHD that emerges in adolescence/adulthood is similar in risk factor profile to: (1) child-onset ADHD, but emerges later because of scaffolding/compensation from childhood resources; and (2) depression, because it typically onsets in adolescence/adulthood and shows symptom and genetic overlaps with ADHD. Methods: We examined associations between late-onset ADHD and ADHD risk factors, cognitive tasks, childhood resources and depression risk factors in a population-based cohort followed-up to age 25 years (N=4224-9764). Results: Parent-rated late-onset ADHD was like child-onset persistent ADHD in associations with ADHD polygenic risk scores and cognitive task performance, although self-rated late-onset ADHD was not. Late-onset ADHD was associated with higher levels of childhood resources than child-onset ADHD and did not show strong evidence of association with depression risk factors. Conclusions: Late-onset ADHD shares characteristics with child-onset ADHD when parent-rated, but differences for self-reports require investigation. Childhood resources may delay the onset of ADHD.
| S-EPMC7612898 | biostudies-literature
Project description:BackgroundDepression and anxiety persist within and across diagnostic boundaries. The manner in which common v. disorder-specific genetic and environmental influences operate across development to maintain internalizing disorders and their co-morbidity is unclear. This paper investigates the stability and change of etiological influences on depression, panic, generalized, separation and social anxiety symptoms, and their co-occurrence, across adolescence and young adulthood.MethodA total of 2619 twins/siblings prospectively reported symptoms of depression and anxiety at mean ages 15, 17 and 20 years.ResultsEach symptom scale showed a similar pattern of moderate continuity across development, largely underpinned by genetic stability. New genetic influences contributing to change in the developmental course of the symptoms emerged at each time point. All symptom scales correlated moderately with one another over time. Genetic influences, both stable and time-specific, overlapped considerably between the scales. Non-shared environmental influences were largely time- and symptom-specific, but some contributed moderately to the stability of depression and anxiety symptom scales. These stable, longitudinal environmental influences were highly correlated between the symptoms.ConclusionsThe results highlight both stable and dynamic etiology of depression and anxiety symptom scales. They provide preliminary evidence that stable as well as newly emerging genes contribute to the co-morbidity between depression and anxiety across adolescence and young adulthood. Conversely, environmental influences are largely time-specific and contribute to change in symptoms over time. The results inform molecular genetics research and transdiagnostic treatment and prevention approaches.
| S-EPMC4673666 | biostudies-literature
Project description:ImportanceDepressive symptoms have increased among US adolescents since 2010. It remains unclear as to what extent this increase will persist into young adulthood, potentially turning the youth mental health crisis into a young adult mental health crisis.ObjectiveTo test the association between birth cohort and adolescent depressive symptoms at ages 18, 19 to 20, and 21 to 22 years and changes in these symptoms by cohort.Design, setting, and participantsThis panel cohort study analyzed data from the Monitoring the Future longitudinal survey from 1990 to 2019, including birth cohorts from 1972 to 2001. Survey respondents were recruited from US high schools in 12th grade and were approximately aged 18 years (at baseline) through age 21 to 22 years (during mail and web follow-up). Data analysis was conducted from April to October 2023.ExposureDepressive symptoms score (>12 vs ≤12, with >12 representing top-decile scores) on a scale examining affective items (eg, "Life often seems meaningless").Main outcomes and measuresHigh (vs lower) depressive symptoms at ages 19 to 20 years and 21 to 22 years.ResultsThe 36 552 respondents included 18 597 females (50.5%), and most reported having a parent who graduated from college (44.8%). Among females, 19.1% (95% CI, 16.7%-21.4%) of the most recent birth cohort (born: 1997-2001) had high depressive symptoms at age 18 years, higher than any previous birth cohort. While prevalence declined by age 21 to 22 years, it remained higher than previous cohorts at that age. Among males, 13.4% (95% CI, 11.2%-15.6%) of the most recent birth cohort had high depressive symptoms at age 18 years, and prevalence increased through young adulthood. Males with high baseline depressive symptoms had 10.24 (95% CI, 7.01-14.97) times the odds of symptoms at age 19 to 20 years and 6.20 (95% CI, 3.93-9.78) times the odds of symptoms at age 21 to 22 years. Females with high baseline depressive symptoms had 9.16 (95% CI, 6.57-12.76) times the odds of symptoms at age 19 to 20 years and 7.28 (95% CI, 4.92-10.78) times the odds of symptoms at age 21 to 22 years. The magnitude of the associations did not vary over time. Population attributable fractions indicated that the total proportion of young adult symptoms associated with depressive symptoms at age 18 years among females has increased; in the most recent birth cohort, 55.25% (95% CI, 38.11%-65.13%) of depressive symptoms at age 21 to 22 years were associated with symptoms at age 18 years.Conclusions and relevanceThis panel cohort study found that increases in depressive symptoms in adolescence persisted into young adulthood, suggesting the need for primary prevention and mental health resources during the adolescent years.
| S-EPMC11325205 | biostudies-literature
Project description:BackgroundPreterm birth is associated with an increased risk for cognitive-neurophysiological impairments and attention-deficit/hyperactivity disorder (ADHD). Whether the associations are due to the preterm birth insult per se, or due to other risk factors that characterise families with preterm-born children, is largely unknown.MethodsWe employed a within-sibling comparison design, using cognitive-performance and event-related potential (ERP) measures from 104 preterm-born adolescents and 104 of their term-born siblings. Analyses focused on ADHD symptoms and cognitive and ERP measures from a cued continuous performance test, an arrow flanker task and a reaction time task.ResultsWithin-sibling analyses showed that preterm birth was significantly associated with increased ADHD symptoms (β = 0.32, p = 0.01, 95% CI 0.05 to 0.58) and specific cognitive-ERP impairments, such as IQ (β = -0.20, p = 0.02, 95% CI -0.40 to -0.01), preparation-vigilance measures and measures of error processing (ranging from β = 0.71, -0.35). There was a negligible within-sibling association between preterm birth with executive control measures of inhibition (NoGo-P3, β = -0.07, p = 0.45, 95% CI -0.33 to 0.15) or verbal working memory (digit span backward, β = -0.05, p = 0.63, 95% CI -0.30 to 0.18).ConclusionsOur results suggest that the relationship between preterm birth with ADHD symptoms and specific cognitive-neurophysiological impairments (IQ, preparation-vigilance and error processing) is independent of family-level risk and consistent with a causal inference. In contrast, our results suggest that previously observed associations between preterm birth with executive control processes of inhibition and working memory are instead linked to background characteristics of families with a preterm-born child rather than preterm birth insult per se. These findings suggest that interventions need to target both preterm-birth specific and family-level risk factors.
| S-EPMC7322548 | biostudies-literature
Project description:ImportanceCognitive deficits are core features of mental disorders and are important in predicting long-term prognosis. However, it is still unknown whether individual patterns of cognitive deficits predate specific mental disorders.ObjectiveTo investigate the specificity of the associations of attention, working memory, and inhibition in childhood with borderline personality disorder (BPD), psychosis, depression, and hypomania in adolescence and young adulthood.Design, setting, and participantsThis cohort study obtained data from the Avon Longitudinal Study of Parents and Children in the United Kingdom. All pregnant women resident in Avon, United Kingdom, with an expected date of delivery from April 1, 1991, and December 31, 1992, were eligible. Data analysis was conducted from April 1 to September 30, 2020. The sample initially comprised 13 988 participants who were alive at 1 year of age. For this study, data were available for 6333 individuals reporting on any psychopathological measure at ages 11 to 12 years, 4903 individuals at ages 17 to 18 years, and 2963 individuals at 22 to 23 years.ExposuresSustained attention, selective attention, and attentional control were assessed with the Test of Everyday Attention for Children at age 8 years, and working memory and inhibition were assessed at age 10 years with the Counting Span Task and the stop-signal paradigm, respectively.Main outcomes and measuresSymptoms of BPD were assessed at ages 11 to 12 years, psychotic experiences and depression were examined at ages 17 to 18 years, and hypomania was examined at ages 22 to 23 years.ResultsAmong 5315 individuals included in the statistical analysis, 2551 (48.0%) were male and 2764 (52.0) were female. Higher sustained attention at 8 years was associated with decreased risk of BPD symptoms at ages 11 to 12 years (adjusted odds ratio [aOR], 0.964; 95% CI, 0.933-0.996; P = .03), better performance on inhibition at age 10 years with decreased risk of psychotic experiences at ages 17 to 18 years (aOR, 0.938; 95% CI, 0.890-0.989; P = .02), higher sustained attention at age 8 years with decreased risk of depressive symptoms at ages 17 to 18 years (aOR, 0.969; 95% CI 0.938-0.9997; P = .048), and better performance in working memory at age 10 years with decreased risk of hypomania symptoms at ages 22 to 23 years (aOR, 0.694; 95% CI, 0.529-0.911; P = .008). After controlling for potential psychopathological overlay, all the associations remained, except for working memory and hypomania. Higher sustained attention at age 8 years was associated with decreased risk of BPD symptoms at ages 11 to 12 years (β = -0.05; P < .001) and of depression at ages 17 to 18 years (β = -0.03; P = .04), and better performance in inhibition at age 10 years was associated with decreased risk of psychotic experiences at ages 17 to 18 years (β = -0.03; P = .04).Conclusions and relevanceThese findings suggest that specific cognitive deficits in childhood are distinctively associated with different psychopathological symptoms in young people. Furthermore, these results suggest the potential of early cognitive interventions in childhood as a way of modifying or attenuating risk for subsequent psychopathological symptoms.
| S-EPMC8027911 | biostudies-literature
Project description:This study evaluated how patterns of mothers' depressive symptoms across their child's childhood relate to children's psychosocial adjustment at adolescence and young adulthood and to cognitive functioning at adolescence. Depressive symptoms were measured in 1,273 mothers when their children were 1, 5, 10, and 14.6 years of age. Children (53.5% male; n = 1,024) completed the Youth Self-Report at adolescence (M = 14.6y), and the Adult Self-Report in young adulthood (M = 20.5y; n = 817) to assess internalizing and externalizing symptoms. Adolescents also completed standardized cognitive tests to assess verbal and mathematical skills. Growth mixture modeling analyses identified four patterns of maternal depressive symptom trajectories: infrequent (55%), increasing at adolescence (20%), decreasing at adolescence (14%), and chronic severe (11%). Results indicated that exposure to maternal depression of any duration, severity or time period during childhood portended higher levels of externalizing and attention problems at both adolescence and adulthood and higher levels of internalizing problems at adulthood. Adolescents whose mothers had chronic severe depressive symptoms had lower language, vocabulary, reading comprehension and mathematical test scores than youth whose mothers had stable infrequent depressive symptoms. Findings illustrate the significance and long-term ramifications of mothers' depressed mood for their children's mental and psychosocial health into adulthood. Findings also demonstrate that the lower cognitive abilities among children of severely depressed mothers persist beyond childhood and pertain to a broad range of cognitive abilities.
| S-EPMC7992359 | biostudies-literature
Project description:ObjectiveThis study tested two opposing hypotheses on the continuity of psychopathology throughout adolescence and young adulthood; differentiation versus dynamic mutualism. Differentiation predicts that co-occurrence decreases, while dynamic mutualism predicts that co-occurrence increases due to causal interactions amongst mental health problems.MethodUsing data from the Dutch TRacking Adolescents' Individual Lives Survey (n = 2228, 51% female), we studied the development of self-reported internalizing, externalizing, and attention problems at ages 11 to 26 across six waves. Random-intercept cross-lagged panel modeling was employed to distinguish within-person development from stable between-person processes.ResultsLarge stable between-person associations indicated that adolescents with internalizing problems tended to have both externalizing and attention problems as well. On a within-person level, mental health problems showed partial stability and strong cross-sectional co-occurrence. Within-wave associations of internalizing with externalizing or attention problems decreased between age 11 and 16 years, after which they increased again. Little heterotypic continuity was found: age 11 externalizing predicted age 13 attention, which in turn predicted age 16 externalizing problems, and internalizing predicted externalizing problems across ages 22 to 26. Findings were similar for males and females.ConclusionsOur findings suggest co-occurrence decreases during early and middle adolescence, supporting differentiation. While co-occurrence increased again into young adulthood, this could not be labeled as dynamic mutualism because little evidence for heterotypic continuity was found in this phase of life. The strong stable links between internalizing, externalizing, and attention problems stress the importance of targeting these mental health problems and their shared risk factors together.
| S-EPMC11318507 | biostudies-literature
Project description:ObjectiveAmong untreated adults, functional impairments associated with ADHD are widespread and cumulative, and can include social, educational, and professional impairments, increased risk of accidents and mortality, and reduced quality of life. Here, we review the most prominent functional impairments in adults with ADHD and summarize evidence describing the potential role of medication in improving outcomes.MethodArticles related to the search terms "ADHD," "adult," and functional impairments were identified through Google Scholar and PubMed and selected for inclusion based on four criteria: strength of evidence, relevance to current challenges in adult ADHD, impact on the field, and recency of the results.ResultsWe identified 179 papers to support the conclusions on the relationship between ADHD and functional impairments, and the impact of pharmacological therapy on functional impairments.ConclusionThis narrative review provides evidence that pharmacological treatment can be effective in minimizing not only the symptoms of ADHD, but its functional consequences as well.
| S-EPMC10173356 | biostudies-literature