2025 NEI Fall Congress Young Investigator Poster Awards
Friday, November 7, 2025
The 2025 NEI Fall Congress Scientific Poster Session was held on Friday, November 7th and featured 146 posters covering the full spectrum of mental health research and clinical data. Among them, three particularly stood out for the quality of their data and contributions to the field. Presented below are the winners of the 2025 NEI Fall Congress Young Investigator Poster Competition.
Impact of Parental ADHD Status on Screen Time Allowance in Children: Insights from NHIS Data
Chase Moscovic BS1, Andrew Lemmen BS1, Rebecca Klisz-Hulbert, MD1
1Wayne State School of Medicine, Detroit, MI. 540 E Canfield, Detroit, MI, USA
Introduction: Children's screen use has become a major public health concern, with excessive exposure linked to adverse developmental, cognitive, and behavioral outcomes. While much of the literature focuses on childhood ADHD, limited research has examined how parental ADHD may influence screen time regulation. ADHD-related deficits in executive function, impulse control, and consistency in parenting may undermine screen time management. This study investigates whether parents with ADHD allow more screen time for their children compared to non-ADHD parents, using nationally representative survey data.
Methods: We analyzed data from the 2019–2023 National Health Interview Survey (NHIS), focusing on 11,571 parents who reported both their ADHD status and their child’s screen time allowance. Parental ADHD status was determined by self-report. The primary outcome was daily screen time permitted for children, categorized as either <2 hours or =2 hours. Descriptive statistics, chi-squared analyses, and Z-scores assessed the significance of differences between ADHD and non-ADHD groups. Stratified analyses explored variation by sex, race, education level, income-to-poverty ratio, and possible ADHD treatment. No adjustments for confounders were performed due to the exploratory nature of the study.
Results: Among 1,185 parents with ADHD, 76% allowed =2 hours of daily screen time for their children, compared to 62.6% of 10,386 non-ADHD parents (Z = 9.10; X2 = 87.64; p < 0.001). Effect sizes (e.g., Gamma = 0.31, Tau-b = 0.08) indicated a moderate but significant positive association between parental ADHD and increased screen time allowance. This relationship remained significant across most demographic subgroups. Notably, parents with ADHD who had taken medication for emotional, concentration, or behavioral problems showed a slight reversal in the trend, suggesting a potential moderating effect of treatment.
Conclusions: Parental ADHD is significantly associated with more permissive screen time practices, possibly due to impairments in executive functioning and self-regulation. These findings underscore the need to integrate parental mental health considerations into pediatric screen time interventions. Supporting ADHD parents with executive function coaching, ADHD-specific CBT, and digital behavior management tools may enhance family-level media regulation. Public health guidelines should reflect the neurodiverse needs of families, and future research should explore treatment-mediated intergenerational benefits.
Funding: No Funding.
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Inflammatory Biomarkers and Treatment-Resistant Depression: A Targeted Review of Recent Clinical Evidence
Enque Endeshaw, MD1; Ishani Mehta, MD2; Amun Mustafa, MBBS3; Ashwin Mathai, MD1
1Saint Elizabeths Hospital - Department of Behavioral Health, Washington, DC, USA; 2 Maharaja Agrasen Medical College, Agroha; 3Fatima Memorial Hospital - College of Medicine and Dentistry, Lahore, Pakistan
Introduction: Treatment-resistant depression (TRD) presents a major clinical challenge, affecting up to one-third of individuals with major depressive disorder (MDD). A growing body of evidence implicates chronic low-grade inflammation and neuroimmune dysregulation in the pathophysiology of TRD, offering potential biomarkers for prognosis and personalized treatment. This review synthesizes recent clinical evidence on the role of inflammatory and immune biomarkers in TRD, highlighting their prognostic and therapeutic implications.
Methods: A targeted narrative review of clinical studies published in the last five years was conducted using PubMed and Google Scholar. The review included 16 randomized controlled trials, observational studies, and meta-analyses focusing on clinical utility. Inclusion criteria were limited to human studies examining the relationship between peripheral biomarkers (e.g., CRP, cytokines, BDNF), treatment response, and inflammation-targeted interventions in TRD.
Results: Findings suggest that elevated levels of pro-inflammatory cytokines (e.g., IL-6, TNF- α, IL-1 β), ESR, and CRP are associated with poorer antidepressant response to SSRIs and ketamine and may serve as predictive markers of TRD, though results remain mixed. In some studies, null findings were attributed to small sample sizes and study design limitations. A sex-specific pattern emerged for IL-8: increased levels following ketamine infusion were associated with improved response in females but worsened outcomes in males. One study demonstrated that whole-blood mRNA profiling of genes including P2RX7, CXCL12, and ones related to IL-1B, IL-6, TNF-alpha, and the glucocorticoid receptor more effectively distinguished TRD patients from responders than conventional inflammatory markers. Adjunctive use of anti-inflammatory agents—such as minocycline, celecoxib, and biologics like adalimumab—showed benefit in selected patients, though findings were inconsistent. In another trial, metyrapone, an anti-glucocorticoid agent, worsened depressive symptoms and increased IL-6, possibly due to compensatory HPA axis activation. Additional studies suggest roles for BDNF and kynurenine pathway metabolites (e.g., higher tryptophan/lower kynurenine) as treatment biomarkers in ECT. EEG vigilance has also emerged as a potential predictor of TRD treatment outcomes.
Conclusions: Peripheral inflammatory biomarkers hold promise for identifying treatment resistance in depression and guiding adjunctive immunomodulatory strategies. Integrating biomarker-based stratification into clinical decision-making may advance precision psychiatry for TRD. Larger-scale studies are needed to validate predictive value and develop standardized protocols for biomarker-informed care.
Funding: No Funding.
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The Role of Brexpiprazole in Treating Irritability in Borderline Personality Disorder: A Hypothesized Mechanism of Action
Gryan Garcia, PhD, PsyD, FNP-BC, PMHNP-BC1; Christy Cotner, DNP, FNP-C, PMHNP-BC1
1Western University of Health Sciences, Pomona, California
Introduction: Borderline Personality Disorder (BPD) is a severe and enduring psychiatric condition characterized by affective instability, impulsivity, chronic interpersonal dysfunction, and high levels of irritability and anger. These symptoms often result in functional impairment, recurrent psychiatric crises, and increased healthcare utilization. Despite the clinical burden, there are no FDA-approved pharmacologic treatments for BPD, and off-label medication use is common. Brexpiprazole, an atypical antipsychotic with partial agonism at dopamine D2 and serotonin 5-HT1A receptors and antagonism at serotonin 5-HT2A and alpha-1 adrenergic receptors, is currently approved for major depressive disorder (MDD) and schizophrenia. Given its pharmacologic profile, brexpiprazole may exert modulatory effects on neural circuits implicated in affective dysregulation. This abstract proposes a hypothesized mechanism of action (MoA) by which brexpiprazole may attenuate irritability in individuals with BPD and presents a brief case series to illustrate real-world clinical observations.
Methods: This hypothesized MoA analysis is based on a targeted review of brexpiprazole’s receptor pharmacodynamics and the neurobiological mechanisms underlying BPD-related affective dysregulation. Emphasis was placed on corticolimbic circuitry, particularly the amygdala and prefrontal cortex. To support clinical plausibility, a retrospective review was conducted on three adult patients (n=3) with DSM-5–confirmed BPD treated in a community-based outpatient psychiatric clinic. All presented with prominent irritability, impulsive aggression, and difficulty with affect modulation. Each patient was initiated on low-dose brexpiprazole (0.5 mg to 1 mg daily) and monitored for symptom changes over a 6-week period.
Results: All three patients reported clinically meaningful improvements in irritability, with decreased verbal outbursts, improved frustration tolerance, and enhanced capacity for emotional regulation. Symptom improvement was observed within 2 to 4 weeks of treatment initiation. No extrapyramidal symptoms, sedation, or metabolic adverse effects were reported. One patient demonstrated marked improvement in interpersonal boundaries, suggesting broader affect stabilization.
Conclusions: Brexpiprazole may represent a novel off-label pharmacologic option for managing irritability and affective dysregulation in BPD. Its multimodal receptor activity is hypothesized to normalize dysregulated corticolimbic pathways. In this limited case series (n=3), low-dose brexpiprazole was well tolerated and associated with early subjective and functional improvements. These findings support further investigation into its role as an adjunctive treatment in BPD, particularly in patients with prominent irritability and poor response to first-line psychotherapies.
Funding: No Funding.
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