It has been suggested that interconnected brain areas evolve in tandem because evolutionary pressures act on complete functional systems rather than on individual brain areas. The cerebellar cortex has reciprocal connections with both the prefrontal cortex and motor cortex, forming independent loops with each. Specifically, in capuchin monkeys cerebellar cortical lobules Crus I and Crus II connect with prefrontal cortex, whereas the primary motor cortex connects with cerebellar lobules V, VI, VIIb, and VIIIa. Comparisons of extant primate species suggest that the prefrontal cortex has expanded more than cortical motor areas in human evolution. Given the enlargement of the prefrontal cortex relative to motor cortex in humans, our hypothesis would predict corresponding volumetric increases in the parts of the cerebellum connected to the prefrontal cortex, relative to cerebellar lobules connected to the motor cortex. We tested the hypothesis by comparing the volumes of cerebellar lobules in structural MRI scans in capuchins, chimpanzees and humans. The fractions of cerebellar volume occupied by Crus I and Crus II were significantly larger in humans compared to chimpanzees and capuchins. Our results therefore support the hypothesis that in the cortico-cerebellar system, functionally related structures evolve in concert with each other. The evolutionary expansion of these prefrontal-projecting cerebellar territories might contribute to the evolution of the higher cognitive functions of humans.
Background and purpose: Sleep disturbances in autism spectrum disorder (ASD) are common and may impair daytime functioning as well as add to parental burden. In this well characterized sample of young children with ASD and disruptive behaviors, we examine the association of age and IQ in sleep disturbances using the Child Sleep Habits Questionnaire modified for ASD (CSHQ-ASD). We also test whether children with poor sleep have greater daytime behavioral problems than those with better sleep. Finally, we examine whether parental stress is higher in children with greater disruptive behaviors and sleep disturbances. Participants and methods: One hundred and seventy-seven children with complete data out of 180 (mean age 4.7) with ASD participated in a randomized clinical trial. Parents completed the CSHQ-ASD and several other measures at study enrollment. The sample was divided into “poor sleepers” (upper quartile on the total score of the CSHQ-ASD) and “good sleepers” (lower quartile) for comparisons. Analyses were conducted to evaluate group differences on age, IQ, daytime disruptive behavior, social disability and parental stress. Results: The two groups of young children with ASD, good sleepers versus poor sleepers, were not different on age or cognitive level. Children in the poor sleeping group had significantly higher daytime behavioral problems including irritability, hyperactivity, social withdrawal and stereotypical behaviors. Parents in this group reported significantly higher levels of stress. Conclusions: The finding of no age difference between good and poor sleepers in young children with ASD and disruptive behaviors suggests that sleep problems are unlikely to resolve as might be expected in typically developing children. Likewise, the good and poor sleepers did not significantly differ in IQ. These findings add strong support for the need to screen for sleep disturbances in all children with ASD, regardless of age and cognitive level. Poor sleepers exhibited significantly greater daytime behavioral problems and parents of children in this group reported significantly higher levels of stress. Above and beyond the co-occurring disruptive behavior, poor sleep quality appears to pose substantial additive burden on child and parents.
It has been long recognized that parents exert profound influences on child development. Dating back to at least the seventeenth-century Enlightenment, the ability for parents to shape child behavior in an enduring way has been noted. Twentieth-century scholars developed theories to explain how parenting histories influence psychological development, and since that time, the number of scientific publications on parenting influences in both human and nonhuman animal fields has grown at an exponential rate, reaching numbers in the thousands by 2015. This special issue describes a symposium delivered by Megan Gunnar, Regina Sullivan, Mar Sanchez, and Nim Tottenham in the Fall of 2014 at the Society for Social Neuroscience. The goal of the symposium was to describe the emerging knowledge on neurobiological mechanisms that mediate parent–offspring interactions across three different species: rodent, monkey, and human. The talks were aimed at designing testable models of parenting effects on the development of emotional and stress regulation. Specifically, the symposium aimed at characterizing the special modulatory (buffering) effects of parental cues on fear- and stress-relevant neurobiology and behaviors of the offspring and to discuss examples of impaired buffering when the parent–infant relationship is disrupted.
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Lisa Rosenthal;
Valerie A. Earnshaw;
Joan M. Moore;
Darrah N. Ferguson;
Tene Lewis;
Allecia E. Reid;
Jessica B. Lewis;
Emily C. Stasko;
Jonathan N. Tobin;
Jeannette R. Ickovics
Objective: Racial/ethnic and socioeconomic disparities in infant development in the United States have lifelong consequences. Discrimination predicts poorer health and academic outcomes. This study explored for the first time intergenerational consequences of women's experiences of discrimination reported during pregnancy for their infants' social-emotional development in the first year of life. Methods: Data come from a longitudinal study with predominantly Black and Latina, socioeconomically disadvantaged, urban young women (N = 704, M age = 18.53) across pregnancy through 1 year postpartum. Women were recruited from community hospitals and health centers in a Northeastern US city. Linear regression analyses examined whether women's experiences of everyday discrimination reported during pregnancy predicted social-emotional development outcomes among their infants at 6 months and 1 year of age, controlling for potentially confounding medical and sociodemographic factors. Path analyses tested if pregnancy distress, anxiety, or depressive symptoms mediated significant associations. Results: Everyday discrimination reported during pregnancy prospectively predicted greater inhibition/separation problems and greater negative emotionality, but did not predict attention skills or positive emotionality, at 6 months and 1 year. Depressive symptoms mediated the association of discrimination with negative emotionality at 6 months, and pregnancy distress, anxiety, and depressive symptoms mediated the association of discrimination with negative emotionality at 1 year. Conclusion: Findings support that there are intergenerational consequences of discrimination, extending past findings to infant social-emotional development outcomes in the first year of life. It may be important to address discrimination before and during pregnancy and enhance support to mothers and infants exposed to discrimination to promote health equity across the life span.
The preponderance of causal influence on total population attributable risk for autism is polygenic in nature, but it is not known how such liability engenders the development of the syndrome. In 348 epidemiologically ascertained toddler twins, we explored associations between autistic traits and three robust, highly heritable predictors of familial autism recurrence: variation in attention, motor coordination, and parental autistic trait burden. We observed that these predictors—despite collectively accounting for over one third of variance in clinical recurrence—are genetically independent in early childhood, and jointly account for a comparable share of inherited influence on early reciprocal social behavior in the general population. Thus, combinations of what are otherwise discrete, inherited behavioral liabilities—some not specific to autism—appear to jointly mediate common genetic risk for autism. Linking genetic variants and neural signatures to these independent traits prior to the onset of the development of autism will enhance understanding of mechanisms of causation in familial autistic syndromes. Moreover, ongoing biomarker discovery efforts will benefit from controlling for the effects of these common liabilities, which aggregate in individuals with autism but are also continuously distributed in “controls”. Finally, early inherited liabilities that participate in the early ontogeny of autistic syndromes represent parsimonious intervention targets for polygenic forms of the condition, and represent candidate trans-diagnostic endophenotypes of potential relevance to a diversity of neuropsychiatric syndromes.
Semantic memory, defined as our store of knowledge about the world, provides representational support for all of our higher order cognitive functions. As such, it is crucial that the contents of semantic memory remain accessible over time. Although memory for knowledge learned through direct observation has been investigated previously, we know very little about the retention of knowledge derived through integration of information acquired across separate learning episodes. The current research investigated cross-episode integration in 4-year-old children. Participants were presented with novel facts via distinct story episodes and tested for knowledge extension through cross-episode integration as well as for retention of the information over a 1-week delay. In Experiment 1, children retained the self-derived knowledge over the delay, although performance was primarily evidenced in a forced-choice format. In Experiment 2, we sought to facilitate the accessibility and robustness of self-derived knowledge by providing a verbal reminder after the delay. The accessibility of self-derived knowledge increased irrespective of whether participants successfully demonstrated knowledge of the integration facts during the first visit. The results suggest that knowledge extended through integration remains accessible after delays even in a population where this learning process is less robust. The findings also demonstrate the facilitative effect of reminders on the accessibility and further extension of knowledge over extended time periods.
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Emily Hotez;
Christina Shane-Simpson;
Rita Obeid;
Danielle DeNigris;
Michael Siller;
Corinna Costikas;
Jonathan Pickens;
Anthony Massa;
Michael Giannola;
Joanne D'Onofrio;
Kristen Gillespie-Lynch
Students with Autism Spectrum Disorder (ASD) face unique challenges transitioning from high school to college and receive insufficient support to help them navigate this transition. Through a participatory collaboration with incoming and current autistic college students, we developed, implemented, and evaluated two intensive week-long summer programs to help autistic students transition into and succeed in college. This process included: (1) developing an initial summer transition program curriculum guided by recommendations from autistic college students in our ongoing mentorship program, (2) conducting an initial feasibility assessment of the curriculum [Summer Transition Program 1 (STP1)], (3) revising our initial curriculum, guided by feedback from autistic students, to develop a curriculum manual, and (4) pilot-testing the manualized curriculum through a quasi-experimental pre-test/post-test assessment of a second summer program [Summer Transition Program 2 (STP2)]. In STP2, two autistic college students assumed a leadership role and acted as "mentors" and ten incoming and current autistic college students participated in the program as "mentees." Results from the STP2 pilot-test suggested benefits of participatory transition programming for fostering self-advocacy and social skills among mentees. Autistic and non-autistic mentors (but not mentees) described practicing advanced forms of self-advocacy, specifically leadership, through their mentorship roles. Autistic and non-autistic mentors also described shared (e.g., empathy) and unique (an intuitive understanding of autism vs. an intuitive understanding of social interaction) skills that they contributed to the program. This research provides preliminary support for the feasibility and utility of a participatory approach in which autistic college students are integral to the development and implementation of programming to help less experienced autistic students develop the self-advocacy skills they will need to succeed in college.
This study investigated the influences of neighborhood factors (residential stability and neighborhood disadvantage) and variants of the serotonin transporter linked polymorphic region (5-HTTLPR) genotype on the development of substance use among African American children aged 10-24 years. To accomplish this, a harmonized data set of five longitudinal studies was created via pooling overlapping age cohorts to establish a database with 2,689 children and 12,474 data points to span ages 10-24 years. A description of steps used in the development of the harmonized data set is provided, including how issues such as the measurement equivalence of constructs were addressed. A sequence of multilevel models was specified to evaluate Gene × Environment effects on growth of substance use across time. Findings indicated that residential instability was associated with higher levels and a steeper gradient of growth in substance use across time. The inclusion of the 5-HTTLPR genotype provided greater precision to the relationships in that higher residential instability, in conjunction with the risk variant of 5-HTTLPR (i.e., the short allele), was associated with the highest level and steepest gradient of growth in substance use across ages 10-24 years. The findings demonstrated how the creation of a harmonized data set increased statistical power to test Gene × Environment interactions for an under studied sample.
Puberty is accompanied by numerous psychological and interpersonal challenges, including a dramatic rise in the prevalence of depression among girls. Pubertal timing has been identified as a potent predictor of depressive symptoms among females, but less is known about other features of puberty. The present study sought to address this gap in the literature by examining the effect of pubertal synchrony, the degree to which morphological indicators of puberty develop concurrently, on depressive symptoms in adolescence and emerging adulthood in a longitudinal sample. Among 355 female participants, asynchronous development at age 13 was associated with increased depressive symptoms at age 20, but not age 15. Additional analyses indicated that pubertal timing moderated the association between synchrony and depressive symptoms at age 20, such that girls who exhibited asynchronous development had the highest levels of depressive symptoms when they matured later than peers. Results provide initial empirical support for the role of pubertal synchrony in the development of depression among females and are discussed with regard to the biopsychosocial processes that may connect features of puberty with the long-term development of psychopathology.
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Gamola Z. Fortenberry;
John D. Meeker;
Brisa N. Sanchez;
Dana Boyd Barr;
Parinya Panuwet;
David Bellinger;
Lourdes Schnaas;
Maritsa Solano-Gonzalez;
Adrienne S. Ettinger;
Mauricio Hernandez-Avila;
Howard Hu;
Martha Maria Tellez-Rojo
Attention Deficit Hyperactivity Disorder (ADHD) is the most commonly diagnosed and studied cognitive and behavioral disorder in school-age children. The etiology of ADHD and ADHD-related behavior is unclear, but genetic and environmental factors, such as pesticides, have been hypothesized. The objective of this study was to investigate the relationship between in utero exposure to chlorpyrifos, chlorpyrifos-methyl, and/or 3,5,6-trichloro-2-pyridinol (TCPY) and ADHD in school-age Mexican children using TCPY as a biomarker of exposure. The temporal reliability of repeated maternal urinary TCPY concentrations across trimesters was also explored (N= 21). To explore associations with ADHD-related outcomes in children, third trimester urinary TCPY concentrations in were measured in 187 mother-child pairs from a prospective birth cohort. Child neurodevelopment in children 6-11 years of age was assessed using Conners' Parental Rating Scales-Revised (CRS-R), Conners' Continuous Performance Test (CPT), and Behavior Assessment System for Children-2 (BASC-2). Multivariable linear regression models were used to test relationships for all children combined and also stratified by sex. Intraclass correlation coefficients (ICC) calculations were based on a random effects model. The ICC was 0.41 for uncorrected TCPY, and ranged from 0.29 to 0.32 for specific gravity-corrected TCPY. We did not observe any statistically significant associations between tertiles of maternal TCPY concentrations and ADHD-related outcomes in children. However, compared to the lowest tertile we found suggestive evidence for increased ADHD index in the highest TCPY tertile in boys (β= 5.55 points; 95% CI (-0.19, 11.3); p= 0.06) and increased attention problems for the middle tertile in girls (β= 5.81 points; 95% CI (-0.75, 12.4); p= 0.08). Considering the continued widespread agricultural and possible residential use of chlorpyrifos and chlorpyrifos-methyl in Mexico and the educational implications of cognitive and behavior deficits, these relationships deserve further study.