Justice-involved youth experience significantly higher rates of adverse childhood experiences (ACEs) compared to the general population, which lead to negative outcomes such as greater criminal involvement and mental health disorders. Such effects emphasize the need to examine the role of protective factors on the development of these negative outcomes. This study uses data from 519 youth referred to a probation department in Southeast Texas to examine the effects of ACEs and the direct and mitigating effects of protective factors on a youth’s criminal involvement and mental health symptoms. Results from hierarchical linear regression models emphasize the negative effects of ACEs on these outcomes, as well as the potential ceiling effect of protective factors based on ACE severity.

Background/Objectives: Adverse childhood experiences (ACEs) are potent drivers of psychopathology and neurological disorders, especially within minoritized populations. Nonetheless, we lack a coherent understanding of the neuronal mechanisms through which ACEs impact gene expression and, thereby, the development of psychopathology. Methods: This observational pilot study used a novel marker of neuronal functioning (brain-derived micro ribonucleic acids, or miRNAs) collected via saliva to explore the connection between ACEs and neuronal gene expression in 45 adolescents with a collectively high ACE exposure (26 males and 19 females of diverse races/ethnicities, with six cumulative ACEs on average). We aimed to determine the feasibility of using salivary microRNA for probing neuronal gene expression with the goal of identifying cellular processes and genetic pathways perturbed by childhood adversity. Results: A total of 274 miRNAs exhibited reliable salivary expression (raw counts > 10 in > 10% of samples). Fourteen (5.1%) were associated with cumulative ACE exposure (p < 0.05; r’s ≥ 0.31). ACE exposure correlated negatively with miR-92b-3p, 145a-5p, 31-5p, and 3065-5p, and positively with miR-15b-5p, 30b-5p, 30c-5p, 30e-3p, 199a-3p, 223-3p, 338-3p, 338-5p, 542-3p, and 582-5p. Most relations remained significant after controlling for multiple comparisons and potential retrospective bias in ACE reporting for miRNAs with particularly strong relations (p < 0.03). We examined KEGG pathways targeted by miRNAs associated with total ACE scores. Results indicated putative miRNA targets over-represented 47 KEGG pathways (adjusted p < 0.05) involved in neuronal signaling, brain development, and neuroinflammation. Conclusions: Although preliminary and with a small sample, the findings represent a novel contribution to the understanding of how childhood adversity impacts neuronal gene expression via miRNA signaling.

This study examines the convergent validity of the substantive scales of the Minnesota Multiphasic Personality Inventory-2-Restructured Form (MMPI-2-RF) in the Veteran Affairs (VA) population. The sample includes test protocols drawn from all administrations of the MMPI-2-RF or MMPI-2 entered into the electronic medical record system between January 1, 2008 and May 31, 2015 at any VA across the United States. After excluding invalid protocols, substantive scale scores were correlated with external measures of depression, anxiety, and posttraumatic stress disorder if they were administered within |14| days of the MMPI-2/-RF. Results supported the convergent validity of the MMPI-2-RF emotional dysfunction domain scores. Discriminant validity for the remaining MMPI-2-RF substantive scale scores was also adequate. Limitations and implications of these findings are discussed.

Background/Objectives: Justice-involved (JI) youth frequently endorse a history of traumatic brain injury (TBI). TBI, even mild TBI, can have substantial implications for long-term neurocognitive and psychosocial functioning. However, reliable, noninvasive biological indicators of chronic brain changes remain elusive. Micro-ribonucleic acids (miRNAs) are small non-coding segments of RNA that regulate a host of cellular processes. miRNAs are perturbed immediately following TBI but may continue to show changes in the chronic phase of TBI recovery. Methods: We investigated miRNA expression in a group of JI youth (n = 42, ages 12–17 [M = 14.42, SD = 1.21; 57.1% male]) with (n = 22) and without reported histories of TBI. Results: After controlling multiple comparisons, independent samples t-tests revealed five miRNAs (miR-425-3p, miR-30b-5p, miR-582-5p, miR-200c-3p, and miR-150-5p) were significantly different between youth with and without a history of TBI. Among these, four (miR-425-3p, miR-30b-5p, miR-582-5p, and miR-200c-3p) showed higher expression in youth with TBI history, whereas miR-150-5 showed lower expression in youth with TBI history. Three miRNAs (miR-584-5p, miR-10b-5p, and miR-30b-5p) were significantly different between youth with and without a history of loss of consciousness (LOC). MiR-584-5p was lower in youth with LOC history, whereas miR-30b-5p and miR-10b-5p were higher in youth with a history of LOC. Many of these miRNAs have been implicated in prior studies as being involved with inflammatory processes, including neuroinflammation. Conclusions: These results, although preliminary, provide a starting point for understanding the cellular processes related to long-term TBI outcomes within adolescents. For example, they suggest that molecular pathways involved in stress and inflammation (as well as in certain types of behavioral disorders such as substance abuse) may be implicated in long-term brain changes following TBI during development. If replicated, it may suggest future targets for pharmacological intervention.