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Related Experiment Video

Updated: Jul 18, 2026

A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene

A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene

Published on: April 1, 2019

No association between TPH2 gene polymorphisms and ADHD in a UK sample.

Karen Sheehan¹, Ziarih Hawi, Michael Gill

¹Neuropsychiatric Genetics, Trinity Centre for Health Sciences, St. James' Hospital, Dublin 8, Ireland. sheehak@tcd.ie

Neuroscience Letters

|November 25, 2006

Summary

This study investigated the link between Tryptophan Hydroxylase 2 (TPH2) gene variants and Attention Deficit Hyperactivity Disorder (ADHD). The findings did not replicate previous associations, suggesting larger studies are needed to confirm any genetic connection.

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Event Related Potentials (ERPs) and other EEG Based Methods for Extracting Biomarkers of Brain Dysfunction: Examples from Pediatric Attention Deficit/Hyperactivity Disorder (ADHD)

Event Related Potentials (ERPs) and other EEG Based Methods for Extracting Biomarkers of Brain Dysfunction: Examples from Pediatric Attention Deficit/Hyperactivity Disorder (ADHD)

Published on: March 12, 2020

Area of Science:

Neurogenetics
Psychiatric Genetics
Molecular Psychiatry

Background:

Tryptophan Hydroxylase 2 (TPH2) is the key enzyme for serotonin synthesis in the brain.
Previous research suggested a link between TPH2 gene markers and Attention Deficit Hyperactivity Disorder (ADHD).
Serotonin plays a crucial role in various brain functions and mood regulation.

Purpose of the Study:

To examine the association between specific TPH2 single nucleotide polymorphisms (SNPs) and ADHD.
To attempt replication of previously reported associations between TPH2 markers and ADHD in an Irish cohort.
To investigate potential sex-specific effects in the transmission of TPH2 alleles to ADHD probands.

Main Methods:

Analysis of four single nucleotide polymorphisms (SNPs) in the TPH2 gene.
Utilized transmission disequilibrium analysis (TDA) to assess marker-ADHD association.
Examined parental transmission patterns, including sex-specific over-transmission analysis.

Main Results:

No significant association was found between the examined TPH2 SNPs and ADHD in the study sample.
The previously reported paternal over-transmission of associated alleles to ADHD probands was not replicated.
The results indicate a lack of genetic association for the studied TPH2 markers with ADHD in this cohort.

Conclusions:

The current study failed to establish a genetic link between the investigated TPH2 variants and ADHD.
Replication of prior findings was unsuccessful, highlighting the need for further investigation.
Larger sample sizes are recommended to definitively clarify the role of TPH2 alleles in ADHD etiology.