Objectives:Pediatric bipolar disorders(PBD) presents with high comorbidity, and poor psychosocial functioning. The first episode of the disorder is always almost depression and difficult to clinically differentiate the symptoms of depression of BD from those of the unipolar depression(UD). Identifying biomarkers during depression may help facilitate early diagnosis and appropriate treatment interventions. Early onset biomarkers could be change prior to the conversion to BD and can be detected in the genetically at-risk population. Active model of psychoeducation of brain changes in PBD and impact of medications will be presented to help clinicians who can then educate families to grasp how cognitive and emotional domain dysfunction is addressed. The symposium addresses (1) Brain and peripheral epigenetic markers of at-risk and youth with BD, and pharmacotherapy impact on brain plasticity, (2) identifying bipolar depression in terms of neural markers and clinical indicators(3) a model for translation of science to service in educating families on brain changes in PBD and an evidence based model for neuropharmacotherapy, and (4) CBT model to reverse mood dysregulation.

Methods: We will review (1) our work on early neuromarkers of neuroplasticity and environmental, and genetic influences and treatment of the disorder,(2)findings from functional neuroimaging studies(FNS) in youth with BD versus UD,(3)findings from neurocognitive and FNS that are relevant to educate families towards assessment and intervention, (4)neuroscience informed CBT will be presented.

Results: There is a pattern of increase in biomarkers on long-term treatment with medications.BD offspring group showed significantly more family dysfunction with the association between the BDNF genotype and anxiety symptoms. Neural activity during processing of emotion processing and working memory can help differentiate BD depression from UD in adolescents. Cognitive circuitry impairment across multiple domains impact PBD and experimental pharmacotherapy probes revealed distinct mechanistic changes in emotion regulation.CBT was feasible and acceptable.
Conclusion: Neuroscience can serve as a bridge to educate on the complexity of the illness and help formulate pharmacotherapy in psychosocial, academic, and combination interventions. Early neural markers can help early recognition and differentiation.The CBT models are useful for emotional regulation.