Editor's Blog
Nicknamed "Sound Bullets," researchers at Caltech are developing a way of using an "acoustic lens" that can be used like a scalpel "to revolutionize applications from medical imaging and therapy to the nondestructive evaluation of materials and engineering systems." Link
Key Molecular Step to Fighting off Viruses Identified… sometimes you can’t improve upon a Science Daily headline. Quote: "’Activation of RIG-I is the first line of our immune defenses against viral infections,’ said Dr. Chen, an investigator for the Howard Hughes Medical Institute at UT Southwestern. ‘Understanding how it comes to life is a key step in developing new approaches to antiviral therapies. Having this test-tube system could help us identify substances that enhance the body’s antiviral immunity.’"
Scientific American revisits Ecstasy and Psilocybin as therapeutic tools. "Can The Peace Drug Clean Up the War Mess?" Ah? Ahhhhhhh…
This report in Salt Lake City Tribune on the discovery of a "gene linked to intelligence" seems like it may contradict our writer Athena Andreadis’ assertion:
"About half of our genes contribute directly to brain function; the rest do so indirectly, since brain function depends crucially on signal processing and body feedback. This makes the brain/mind a bona fide complex (though knowable) system. This attribute underlines the intrinsic infeasibility of instilling virtue, intelligence or good taste in clothes by changing single genes."
Quoting from the Tribune article:
"Korenberg’s team studied 10 genes, but the one that jumped out was STX1A, which helps control electrochemical processes at the synapses, the junction between nerve cells. It can account for 15.6 percent of variation in cognitive function."
Anyway, let the debate rage… or else leave in a Huff (the automobile preferred by online commentators with their knickers in a twist)…
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3 Comments
Actually, the report reinforces my point that we can easily find a cracked screw that causes a car to stall, but doesn’t make the car run by its lonesome. Korenberg’s group studied people who have Williams syndrome, which affects neuronal transmission and hence brain function. The gene they zeroed in on, STX1A (syntaxin 1A) belongs to a family — as most human genes do — that codes for docking proteins.
So what they did is identify one gene whose malfunction may cause Williams syndrome, just as the dual-activity kinase encoded by DYRK1A causes much of the Down syndrome cognitive problems but is not a single-entry point to high intelligence (however you define it).
The article is not yet available on PubMed, so I won’t be able to judge its substance until I see it. Much of the reporting in your link is standard PR blather to boost the university’s profile and donations (good for them!). Also, publication in PLoS One means the study is not as groundbreaking as the PR tries to imply.
There is no evidence in humans or in rodents that DYRK1A causes “much of the Down syndrome cognitive problems”. This assertion is a misreading of the literature which largely is based on a rodent model that overexpresses DYRK1A, one of over 250 genes on chromosome 21. Many of these genes likely contribute to DS cognitive abnormalities.
Similarly, Korenberg does not claim that STX1A is the only gene responsible for cognitive deficits in WS or normals, but rather that the variation of the gene in WS suggests that it is involved and may have a significant role in the variation of intelligence in WS. By extension, they contend that this is of interest to look at in the normal population. Moreover, they suggest that, based on this correlation and on the important role of STX1A at the synapse, parts of intelligence may be determined by this or other proteins that are located at or modify synaptic functions.
Exactly. No less, but also no more. Which is the point I made in the article I wrote for H+ magazine just before this report appeared.
Miranda Wrongs: Reading Too Much into the Genome
http://hplusmagazine.com/articles/bio/miranda-wrongs-reading-too-much-genome
Specifically regarding the many inputs to the DS phenotype — a third of my research focuses precisely on this issue. If DYRK1A were the only (or the major) determinant of the cognitive issues in DS, nobody would be bothering to investigate the phenomenon further.
So you’re really preaching to the choir here, even if it consists of a single a capella singer.