ADHD Gene #7: SNAP 25 Gene, T1065G allele, Human location: Chromosome #20 (20p11.2) This will be our final installment in a series of 7 ADHD genes. Much of the information here is summarized in a publication by Faraone and Khan in a 2006 article in the Journal of Clinical Psychiatry. There will be further discussions on the topic of genes related to ADHD, so please stay tuned for future posts.
Nevertheless, the final ADHD gene, referred to in this post as SNAP 25, is of importance for discussion. SNAP 25 is short for the term "Synaptosomal-Associated Protein 25 Gene", which is located in the "p11.2" region on human chromosome #20. For more details on genes and gene locations and how they are relevant to our discussion on ADHD, please click here.
Of particular interest is the fact this SNAP25 gene is found to have a 100% match (meaning the DNA sequences are identical) in both chickens and mice. Because of this close match-up among the different species, genetic studies of this "ADHD gene" in mice (of which there are many) may provide information which is much more relevant to humans than other "ADHD genes" that have been covered. In other words, although the relative number of human studies involving this gene and ADHD is limited, a number of studies of the "mouse form" of this gene should be taken seriously.
In mice, a deletion (removal of part of a gene) for this gene results in spontaneous hyperactive behavior. Furthermore, motor abilities are noticeably compromised and physical changes to a part of the brain called the hippocampus (a part of the brain responsible for learning, memory development, emotional responses and various personality traits) were also seen. Therefore, some of the deficient "side effects" that are often seen in ADHD, such as poor memory, inappropriate emotional responses to certain situations and social maladjustments, may be affected, in part, by having the "ADHD form" of this gene. While the information surrounding this in humans should be viewed as only speculative at the present time, the direct behavioral correlations with the gene in mice are tough to ignore.
Unlike other ADHD genes, such as one in a previous post, where most of the "ADHD" behavior is tied to one single block of DNA, the correlation between the SNAP 25 gene and ADHD is more likely affected by multiple blocks of DNA on the gene. Nevertheless, the most statistically dominant form of the gene (also called allele, for more information on this, please click here) is thought to be what is called the T1065G allele. This "T1065G" notation means that the presence of a Thymine DNA base (Thymine is referred to as "T") instead of a Guanine ("G") at the DNA base 1065 (this a number is reference to where on the gene this replacement is located) results in a statistically-increased likelihood of developing ADHD.
If you are unfamiliar with the concept of DNA bases, please click here for a more detailed explanation.
While not of the statistical significance as the T1065G form, there is another nearby section of the gene that also may affect ADHD. In fact these two regions may "work together" to increase the likelihood of developing ADHD. This second form, which is backed by less statistical evidence than T1065G, is called the T1069Callele. This refers to a substitution of a Thymine (T) for a Cytosine (C) located on the 1069th base position in the gene. Keep in mind that these two regions are very close, separated by only 4 individual DNA bases. For more on what DNA bases are, please click here.
Among the key findings that we should draw from this research (as well as from other related studies) is this: Individuals who have the "T" form at position 1065 in the gene instead of the "G" form are more likely to develop ADHD. Additionally, but to a lesser statistical degree, individuals who have the "T" form instead of the "C" at position 1069 are more likely to have ADHD as well. When combined (i.e. "T's" at both spots), the statistical likelihood of having ADHD goes up even further. Therefore, the SNAP 25 gene, located on the 20th chromosome in humans, is a good candidate gene to study and investigate for insight into an individuals genetic susceptibility to ADHD.
Again, if this explanation is difficult to visualize, please click here for another post with a relevant explanation.
Of course, SNAP25 is just one of many potential ADHD genes. However, if one is to have several of the "right forms" or alleles of multiple ADHD genes, the statistical likelihood of developing ADHD will continue to climb. Look for another post in the near future where I will summarize the results of the 7 "ADHD genes" that have been discussed in this section.