MicroRNA Markers of Previous Traumatic Brain Injury in Juvenile Offenders: Implications for Neuronal Dysfunction and Repair

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.