# The Potential Future Role of Genetic Markers, Neurophysiological Insights, and AI Innovations in Personalized Attention-Deficit/Hyperactivity Disorder (ADHD) Management

**Authors:** Vimal Satodiya, Surendra Gupta

PMC · DOI: 10.7759/cureus.93949 · Cureus · 2025-10-06

## TL;DR

This paper explores how genetic markers, brain activity insights, and AI can improve personalized ADHD management and diagnosis.

## Contribution

The paper introduces a multi-modal approach combining genetics, neurophysiology, and AI for more precise ADHD diagnosis and treatment.

## Key findings

- Genetic markers like SLC6A3 and DRD4 influence ADHD risk and treatment responses.
- Neurophysiological biomarkers such as theta/beta ratio from EEG improve ADHD diagnosis.
- AI tools like EEG-based analysis and wearable devices offer scalable ADHD management solutions.

## Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder marked by inattention, hyperactivity, and impulsivity, with significant genetic and environmental influences. Its heritability rate is estimated with genetic markers such as SLC6A3, DRD4, ADRA2A, COMT, DRD5, and SLC6A2 influencing dopamine and norepinephrine regulation. These markers may impact ADHD risk, subtypes, and treatment responses, potentially enabling pharmacogenetic insights into stimulant efficacy and adverse effects. Neurophysiological biomarkers, particularly EEG-derived theta/beta ratio, may enhance diagnostic precision by identifying ADHD-specific cortical activity. Quantitative EEG (qEEG) and biofeedback further aid in treatment monitoring. Non-invasive biomarkers, including magnesium and zinc deficiencies, inflammatory cytokines like interleukin-6 (IL-6), and salivary markers, such as cortisol, alpha-amylase, and secretory immunoglobulins, expand ADHD diagnostic tools. Artificial intelligence (AI) may revolutionize ADHD management in the future with scalable tools like EEG-based motor analysis, eye-tracking systems, and wearable devices. AI-powered models, including socially assistive robots and hybrid algorithms, may enhance engagement and personalize therapy, particularly in underserved regions. Despite advancements, challenges remain in standardizing biomarkers, validating AI tools, and addressing ADHD heterogeneity. Future research should integrate genetic, neuroimaging, and AI-driven multi-modal approaches to improve diagnostics and optimize therapies. Holistic interventions, such as pharmacogenetics and magnesium supplementation, show promise for enhancing ADHD care. By uniting genetic, neurophysiological, and technological insights, these innovations pave the way for precise, accessible, and personalized ADHD management strategies.

## Linked entities

- **Genes:** SLC6A3 (solute carrier family 6 member 3) [NCBI Gene 6531], DRD4 (dopamine receptor D4) [NCBI Gene 1815], ADRA2A (adrenoceptor alpha 2A) [NCBI Gene 150], COMT (catechol-O-methyltransferase) [NCBI Gene 1312], DRD5 (dopamine receptor D5) [NCBI Gene 1816], SLC6A2 (solute carrier family 6 member 2) [NCBI Gene 6530]
- **Chemicals:** magnesium (PubChem CID 5462224), zinc (PubChem CID 23994), cortisol (PubChem CID 5754), alpha-amylase (PubChem CID 17396988)
- **Diseases:** Attention-deficit/hyperactivity disorder (MONDO:0007743), ADHD (MONDO:0007743)

## Full-text entities

- **Genes:** DRD5 (dopamine receptor D5) [NCBI Gene 1816] {aka DBDR, DRD1B, DRD1L2}, DRD4 (dopamine receptor D4) [NCBI Gene 1815] {aka D4DR}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, ADRA2A (adrenoceptor alpha 2A) [NCBI Gene 150] {aka ADRA2, ADRA2R, ADRAR, ALPHA2AAR, FPLD8}, COMT (catechol-O-methyltransferase) [NCBI Gene 1312] {aka HEL-S-98n}, SLC6A2 (solute carrier family 6 member 2) [NCBI Gene 6530] {aka NAT1, NET, NET1, SLC6A5}, SLC6A3 (solute carrier family 6 member 3) [NCBI Gene 6531] {aka DAT, DAT1, PKDYS, PKDYS1}
- **Diseases:** inflammatory cytokines (MESH:D000080424), hyperactivity (MESH:D006948), impulsivity (MESH:D007174), neurodevelopmental disorder (MESH:D002658), ADHD (MESH:D001289), magnesium and zinc deficiencies (MESH:D008275), inattention (MESH:D001308)
- **Chemicals:** dopamine (MESH:D004298), norepinephrine (MESH:D009638), magnesium (MESH:D008274), cortisol (MESH:D006854)

## Full text

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## References

115 references — full list in the complete paper: https://tomesphere.com/paper/PMC12588396/full.md

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Source: https://tomesphere.com/paper/PMC12588396