(Ivanhoe Newswire) — A recent study finds a gene linked to attention deficit hyperactivity disorder (ADHD) leads to daydreaming. Researchers believe these findings are the first to show ““ through brain scanning ““ the dissimilarities in the brain network relationships between individuals with this specific form of gene and others with a different form.
“Our goal is to narrow down the function of candidate genes associated with ADHD, and in this study, we find this gene is tied to competition between brain networks. This could lead to increased inattention, but it likely has nothing to do with hyperactivity,” which the study’s lead author, Evan Gordon, a doctoral candidate in the interdisciplinary program in neuroscience at Georgetown University Medical Center, was quoted as saying. “This is just one gene, and it does not cause ADHD but likely contributes to it. The disorder is believed to be due to a myriad of genetic factors.”
DAT1 is the gene in question. Its protein produces the dopamine transporter that aids in regulating dopamine transmission between brain cells. Furthermore, the DAT1 gene comes in two alleles (forms): DAT1 10 and DAT1 9. Individuals who inherit two 10 alleles (10/10) are at greater risk for developing ADHD than those who inherit one of each allele (10/9). Gordon adds that people rarely inherit two 9 alleles, and that the 10 allele is more frequent than the 9 allele.
The biological significance in regards to inheriting a DAT1 10 allele is that the brain produces excess quantities of dopamine transporters, which results in less dopamine signaling between neurons. If too many dopamine transporters scoop up the dopamine released by those neurons, then fewer of them are able to actually reach other neurons and pass on a signal. If there are fewer transporters, more dopamine stays in the synapse between neurons, resulting in a triggered reaction.
The dopamine is important for “gating” the transfer of information between brain regions ““ allowing or preventing new information to come in. “The belief is that dopamine helps teach certain brain regions how and when to gate, and that 10/10 carriers are not gating as quickly or effectively as is possible,” Gordon said. That is exactly what the researchers discovered when they used functional MRI (fMRI) on 38 individuals who participated in the study. Half of the groups were 10/10 carriers and half were 10/9 carriers; none of them were diagnosed with ADHD.
Researchers ultimately investigated the activity in two areas of the brain, the default mode network (DMN) ““ associated with mind wondering or daydreaming ““ and task-positive networks (TPNs) ““ which are triggered and stay active during problem solving as well as other cognitive work. In the study, participants were asked to remember letters they saw on a screen inside the fMRI machine, and to recall them, thus activating TPNs.
Scanning determined that in 10/10 carriers, the mind wandering areas tended to communicate with regions engaged in memory tasks much stronger than it did in 10/9 carriers.
“Dopamine in the 10/10 carriers was not doing a good enough job in preventing the mind wandering regions from interfering with memory performance regions, resulting in less efficient cognition,” Gordon adds.
They also found no differences between genotype when the participants were at rest after their memory tasks. “That tells us that the DAT1 genotype affects gating only when release of dopamine is high, such as during a memory task, and that less dopamine signaling leads to increased inattention,” he concluded.
SOURCE: Annual Meeting of the Society for Neuroscience, November 2010
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