About nine per cent of people have at least one copy of a gene for 5HT2a that call for the amino acid tyramine at one point in the receptor protein. The rest call for histamine. People with the tyramine variant make receptors that are less readily stimulated by serotonin.
De Quervain's team compared 70 people with the tyramine form to 279 with the histamine form. The tyramine group was 21 per cent worse at remembering a list of five words or simple shapes five minutes after seeing them.
There is going to be a veritable torrent of additional such discoveries in the next 10 or so years. Lots of genetic variations that contribute to intelligence will be identified. The identification of these variations will be useful for breeding decisions and offspring genetic engineering. The use of the term "breeding decisions" may seem cold but depending on how quickly offspring genetic engineering becomes available a great many people may make decisions about mating for reproduction based on the genetic profiles of potential mates. If many genetic variations that contribute to cognitive differences are identified in many years before offspring genetic engineering becomes possible then people will opt to choose their mates based on what genetic contributions their prospective mates can make to the cognitive ability of their offspring.
Some of the variations that raise and lower intelligence will turn out to do so by changing levels of expression of genes. Attempts will be made to develop drugs that will bind at targets in the regulatory chains that control the expression of those genes in order to make those genes express in less mentally capable people in ways that mirror their expression levels in smarter people. Also, attempts will be made to develop drugs that bind to receptors and change their shapes to be more like the shapes found in smarter people. The bottom line is that many of the genetic variations that contribute to cognitive ability will provide targets for pharmaceutical development. Every such discovery is another potential target for drug development.
It was already known that some anti-depressants that work on the 5HTa gene's receptor product and that those drugs have the side effect of interfering with short term memory. Another recent published report found that there is also a genetic variation in 5HT2a that appears to impact whether anti-depressant Paroxetine (a.k.a. Paxil) causes intolerable side effects in patients.
One variation of the 5HT2a gene, based on a single nucleotide change in the DNA sequence, is thought to affect the amount of the receptor on nerve cells. When the researchers compared the version of this gene that a patient had to his or her experience taking the drug, the differences due to gene variation were striking. People with the one version of the gene were much more likely to discontinue therapy due to intolerable side effects when compared to the two other versions (46 percent vs. 16 percent).
Unfortunately the press release for the second report doesn't state whether the same nucleotide is involved as in the first case.
|Share |||Randall Parker, 2003 October 19 10:28 PM Brain Genetics|