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A new study used genetic variations to determine whether certain brain activity patterns influence the risk for developing ADHD, or vice versa. Results showed that genetic variants leading to lower levels of a specific type of brain activity when a person is at rest (resting alpha-band EEG activity) increase the risk for ADHD. No evidence was found that genetic liability to ADHD influences these brain activity patterns. The paper was published in the Journal of Attention Disorders.
Attention-deficit/hyperactivity disorder (ADHD) is a mental health condition that affects attention, behavior, and emotional regulation. People with ADHD may struggle to concentrate, stay organized, or complete tasks that require sustained mental effort. Its key symptoms fall into two categories: inattention and hyperactivity-impulsivity. Hyperactivity can manifest as constant movement, fidgeting, or an inability to sit still, while impulsivity can lead to acting or speaking without thinking.
Although ADHD is usually diagnosed in childhood, many adults continue to experience its symptoms throughout life. It can influence academic performance, work productivity, and relationships if left untreated. Genetic factors play a strong role, though environmental influences like stress or early childhood experiences also contribute.
The study authors, led by Kwangmi Ahn, note that previous studies established an association between brain activity patterns at rest, as measured by electroencephalography (EEG), and ADHD. They aimed to determine the causal direction of this relationship: do these brain patterns contribute to ADHD risk, or does having ADHD cause the changes in brain activity?
They conducted a Mendelian randomization analysis. The authors analyzed summary statistics from two large-scale data sources. The first, from the ENIGMA-EEG consortium, included resting-state EEG recordings from 7,983 individuals in twin and family studies.
They combined this with genetic data for ADHD from 225,534 individuals, sourced from the Psychiatric Genomics Consortium (PGC).
The analysis revealed that genetic variants leading to lower resting alpha-band activity were causally linked to an increased risk of ADHD. Conversely, they found no evidence for reverse causation; a genetic predisposition for ADHD did not appear to cause changes in alpha-band activity.
“Our findings provide genetic evidence that reduced resting-state alpha power is not merely correlated with ADHD but may causally predispose individuals to developing the disorder,” the study authors concluded. “This supports previous observational studies linking lower alpha activity to ADHD and establishes a causal pathway from altered EEG activity to ADHD risk, with important implications for understanding ADHD pathophysiology and potential biomarker development.”
The study contributes to the scientific understanding of the neural underpinnings of ADHD. However, the authors note that while Mendelian randomization provides strong evidence for causality, it is an inferential method and not definitive proof. Another limitation is that the EEG data was sourced from a single electrode location on the scalp. The authors suggest that findings could differ when examining other brain regions.
The paper, “ADHD and Differences in Brain Function as Measured by EEG: Cause or Effect?” was authored by Kwangmi Ahn, Jenny Jean, Luke J. Norman, and Philip Shaw.
