The National Institute of Mental Health strategic plan for advancing psychiatric neuroscience calls for an acceleration of discovery and the delineation of developmental trajectories for risk and resilience across the lifespan. To attain these objectives, sufficiently powered datasets with broad and deep phenotypic characterization, state-of-the-art neuroimaging, and genetic samples must be generated and made openly available to the scientific community. The enhanced Nathan Kline Institute-Rockland Sample (NKI-RS) is a response to this need. NKI-RS is an ongoing, institutionally centered endeavor aimed at creating a large-scale (N > 1000), deeply phenotyped, community-ascertained, lifespan sample (ages 6–85 years old) with advanced neuroimaging and genetics. These data will be publically shared, openly, and prospectively (i.e., on a weekly basis). Herein, we describe the conceptual basis of the NKI-RS, including study design, sampling considerations, and steps to synchronize phenotypic and neuroimaging assessment. Additionally, we describe our process for sharing the data with the scientific community while protecting participant confidentiality, maintaining an adequate database, and certifying data integrity. The pilot phase of the NKI-RS, including challenges in recruiting, characterizing, imaging, and sharing data, is discussed while also explaining how this experience informed the final design of the enhanced NKI-RS. It is our hope that familiarity with the conceptual underpinnings of the enhanced NKI-RS will facilitate harmonization with future data collection efforts aimed at advancing psychiatric neuroscience and nosology.

Despite the common co-occurrence of symptoms of attention deficit hyperactivity disorder (ADHD) in individuals with autism spectrum disorders (ASD), the underlying mechanisms are under-explored. A potential candidate for investigation is response time intra-subject variability (RT-ISV), a hypothesized marker of attentional lapses. Direct comparisons of RT-ISV in ASD versus ADHD are limited and contradictory. We aimed to examine whether distinct fluctuations in RT-ISV characterize children with ASD and with ADHD relative to typically developing children (TDC). We applied both a priori-based and data-driven strategies to RT performance of 46 children with ASD, 46 with ADHD, and 36 TDC (aged 7–11.9 years). Specifically, we contrasted groups relative to the amplitude of four preselected frequency bands as well as to 400 frequency bins from 0.006 to 0.345 Hz. In secondary analyses, we divided the ASD group into children with and without substantial ADHD symptoms (ASD+ and ASD−, respectively). Regardless of the strategy employed, RT-ISV fluctuations at frequencies between 0.20 and 0.345 Hz distinguished children with ADHD, but not children with ASD, from TDC. Children with ASD+ and those with ADHD shared elevated amplitudes of RT-ISV fluctuations in frequencies between 0.18 and 0.345 Hz relative to TDC. In contrast, the ASD− subgroup did not differ from TDC in RT-ISV frequency fluctuations. RT-ISV fluctuations in frequencies 0.18–0.345 Hz (i.e., periods between 3 and 5 s) are associated with ADHD symptoms regardless of categorical diagnosis and may represent a biomarker. These results suggest that children with ADHD and those with ASD+ share common underlying pathophysiological mechanisms of RT-ISV.

Despite the success of available medical and psychosocial treatments, a sizable subgroup of individuals with commonly co-occurring disorders, generalized anxiety disorder (GAD) and major depressive disorder (MDD), fail to make sufficient treatment gains thereby prolonging their deficits in life functioning and satisfaction. Clinically, these patients often display temperamental features reflecting heightened sensitivity to underlying motivational systems related to threat/safety and reward/loss (e.g., somatic anxiety) as well as inordinate negative self-referential processing (e.g., worry, rumination). This profile may reflect disruption in two important neural networks associated with emotional/motivational salience (e.g., salience network) and self-referentiality (e.g., default network, DN). Emotion Regulation Therapy (ERT) was developed to target this hypothesized profile and its neurobehavioral markers. In the present study, 22 GAD patients (with and without MDD) completed resting state MRI scans before receiving 16 sessions of ERT. To test study these hypotheses, we examined the associations between baseline patterns of intrinsic functional connectivity (iFC) of the insula and of hubs within the DN (anterior and dorsal medial prefrontal cortex [MPFC] and posterior cingulate cortex [PCC]) and treatment-related changes in worry, somatic anxiety symptoms and decentering. Results suggest that greater treatment linked reductions in worry were associated with iFC clusters in both the insular and parietal cortices. Greater treatment linked gains in decentering, a metacognitive process that involves the capacity to observe items that arise in the mind with healthy psychological distance that is targeted by ERT, was associated with iFC clusters in the anterior and posterior DN. The current study adds to the growing body of research implicating disruptions in the default and salience networks as promising targets of treatment for GAD with and without co-occurring MDD.

Results underscore the importance of parental anger and sense of competency in predicting parental behavior, specifically parental accommodation.

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