Search results

Adolescents are more susceptible to dysregulation in positive social contexts, compared to children. We investigated whether maternal presence would buffer these effects in adolescence. Fifty‐four adolescents and children (age range = 8–17 years, Mage = 13.38 years) completed a social go‐nogo task during an fMRI scan alone and in the presence of their mother. We found age‐related patterns, such that older relative to younger youth displayed more disinhibition toward socially appetitive than socially aversive stimuli, which was buffered by maternal presence. Furthermore, with age, maternal buffering in socially appetitive contexts elicited heightened activation in the ventromedial prefrontal cortex and amygdala–medial prefrontal cortex connectivity. Findings underscore the importance of caregivers in promoting the neural regulation of their offspring during adolescence.

School commitment typically declines across adolescence, but the family‐level factors that explain this decline have not been fully characterized. This study investigated sibling support as a family resource in predicting school commitment across 7th–10th grade using a sample of 444 adolescents (Mages = 12.61, 13.59, 14.59, 15.58 years). Results showed that sibling support linearly increased and school commitment decreased and stabilized, independently, over time. Sibling support positively predicted school commitment in seventh grade and across time, suggesting that having supportive siblings may help to offset adolescents' declines in school commitment. Furthermore, having a brother enhanced this association versus having a sister. These findings provide insight into ways to help youth maintain school commitment across the middle‐ to high school transition.

Neuroimaging work has examined neural processes underlying risk taking in adolescence, yet predominantly in low‐risk youth. To determine whether we can extrapolate from current neurobiological models, this functional magnetic resonance imaging study investigated risk taking and peer effects in youth with conduct problems (CP; N = 19) and typically developing youth (TD; N = 25). Results revealed higher real‐life risk taking, lower risky decisions, and no peer effects on a risk‐taking task in CP youth. CP youth showed greater ventral striatum (VS) activity during safe than risky decisions, whereas TD youth showed greater VS activation during risky decisions. Differential VS activity explained higher real‐life risk taking in CP youth. Findings provide preliminary evidence that risk‐taking behavior in youth with CD problems is characterized by differential neural patterns.

The present study examined adolescents' neural responses to social exclusion as a mediator of past exposure to a hostile school environment (HSE) and later social deviance, and whether family connectedness buffered these associations. Participants (166 Mexican‐origin adolescents, 54.4% female) reported on their HSE exposure and family connectedness across Grades 9–11. Six months later, neural responses to social exclusion were measured. Finally, social deviance was self‐reported in Grades 9 and 12. The HSE–social deviance link was mediated by greater reactivity to social deviance in subgenual anterior cingulate cortex, a region from the social pain network also implicated in social susceptibility. However, youths with stronger family bonds were protected from this neurobiologically mediated path. These findings suggest a complex interplay of risk and protective factors that impact adolescent behavior through the brain.

Abstract
High engagement in lifestyle health behaviors appears to be protective against cognitive decline in aging. We investigated the association between patterns of modifiable lifestyle health behaviors and common brain neuropathologies of dementia as a possible mechanism. We examined 555 decedents from the Rush Memory and Aging Project, free of dementia at their initial concurrent report of lifestyle health behaviors of interest (physical, social, and cognitive activities, and healthy diet), and who underwent a postmortem neuropathology evaluation. First, we used latent profile analysis to group participants based on baseline behavior patterns. Second, we assessed the associations of profile membership with each neurodegenerative (global Alzheimer's disease [AD] pathology, amyloid-beta load, density of neurofibrillary tangles, and presence of cortical Lewy bodies and TAR DNA-binding protein 43 cytoplasmic inclusions) and neurovascular pathologies (presence of chronic gross or microscopic infarcts, arteriolosclerosis, atherosclerosis, and cerebral amyloid angiopathy), using separate linear or logistic regression models, adjusted for age at death, sex (core model), vascular disease risk factors, and vascular conditions (fully adjusted model). Participants had either consistently lower (N = 224) or consistently higher (N = 331) engagement across 4 lifestyle health behaviors. We generally found no differences in neuropathologies between higher and lower engagement groups in core or fully adjusted models; for example, higher engagement in lifestyle health behaviors was not associated with global AD pathology after core or full adjustment (both p > .8). In conclusion, we found no evidence of associations between patterns of lifestyle health behaviors and neuropathology. Other mechanisms may underlie protective effects of health behaviors against dementia.