Behind the headlines: Could a genetic defect lead to ADHD?

A genetic error can triple a child's risk of developing ADHD, according to news reports.

A study by South Korean researchers suggested that ADHD is linked to a fault in a single gene in humans.

What did the researchers find?
Researchers from the Korea Advanced Institute of Science and Technology in Daejeon, South Korea, studied the DNA of 388 Korean children with ADHD and 196 controls.

Researchers discovered that an error in a single DNA letter near the GIT1 gene was associated with reduced expression of the GIT1 protein.

Children with at least one copy of the faulty version of the gene had a 2.66-fold increased risk of the disorder.

Researchers then examined the effect of GIT1 in the brains of mice to test whether a lack of normal protein leads to ADHD-like symptoms.

Half of all mice bred to lack any functioning GIT1 protein died soon after birth.

Survivors had reduced weight, a two-fold increase in hyperactivity, and impaired learning and memory.

Are new treatments likely?
News sources said the finding 'paves the way for new drugs', but the study authors make no such suggestion in their paper.

The researchers pointed out that their findings in mice are only a model of what may occur in humans.

For instance, mice only showed ADHD-like symptoms if they had two abnormal copies of the GIT1 gene, but humans only required one abnormal copy of the gene, and one 'normal' copy.

Researchers said this may be due to differences in how mice and humans maintain excitation and inhibition of electrical signals in the brain.

The results suggest that if this balance is upset, such as in mice lacking the GIT1 gene, this may contribute to ADHD-like symptoms. However, the researchers concluded that this idea needs to be explored further to prove its effect in humans.

Informing patients
  • Children with a single-letter DNA fault are more likely to develop ADHD.
  • Tests in mice showed errors in the affected gene lead to ADHD-like symptoms.
  • The gene's role in the disorder in humans remains unclear.

Stephen Robinson recommends

Nature Medicine online 2011

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