Stuttering Devices

'More genes found.

You must listen to the Stutter Talk interview with Dennis Drayna on his team's discovery of a genetic mechanism for stuttering in 10% of people who stutter. Not once but twice or three times! I did, and here is my summary (and comments in brackets)

8.9% of stutterers have mutations in one of the three related genes, but this number can change. (I agree: there is a large statistical error in drawing a sub sample from the population of stutterers. Not sure about the magnitude, but from 5% to 15% is definitely possible.)

Roughly 10% appear to stutter because of mutations in one of three genes.The first gene was first discovered in large Pakistani stuttering families on chromosome 12, and then looked for and found in other stuttering Pakistanis, and US and UK samples of stutterers.
The gene is one of two genes responsible for constructing an enzyme used for a specific cellular metabolism.They looked at mutations in the second gene, and found that it also correlates to stuttering. Then they looked at a third gene that is responsible for a second enzyme that is responsible for the second step of the metabolic pathway.
And again it correlated to stuttering.Special kinds of cells seem to be especially sensitive to a breakdown of this metabolic pathway, but most others are not.Because mutation carriers do not have any other noticeable symptoms apart from stuttering.

We don't know what happens to the remaining 90%. They found more genes correlated to stuttering! (As I said before, if you talk to Dennis, it's like talking to the Dennis one or more years younger! I am convinced he has much more information, and again it will take years until everyone else knows about it.

A scandal of the current publishing system in medical sciences!)One could scan for the mutations, but Dennis' team is about science and not a client service provider.A company could well come up with such a service.There is some predictive factor.

There has little correlation with severity. Already in the 70s, Prof Kidd found that family history is not related to severity.  (I am not surprised. Severity is very likely due to learned behaviours and physiological reactions to jams in the brain.)
Enzyme treatment is feasible, but gene treatment is very delicate. (That's pretty obvious. You just add enzymes to the body, but you would have to add or replace a gene in all cells?) No Pagoclone relationship. (He did not mention that a Chinese team has found a genetic dopamine relationship. What ever happened to research?)

Recovery is unclear. (I think his understanding on and thinking about recovery is superficial as I once told him! He also seems to think that it is the same mechanism than in persistent stuttering and the brain compensates. I am not so sure. Has someone ever recover from these mutations?)Brain plasticity is not strong enough for those with the gene mutation. (As I said many times.)A couple of female mutation carriers did not develop stuttering. (Interesting! Did they study them in more details?)

Future avenues:Metabolic pathway study: what is the biochemical description?Where are those cells sensitive to the lack of enzyme? They have hints that these cells play a role in emotion. (Maybe the cells keep speech unjammed at strong emotional states?)Make mice with such mutations and try to establish as an experimental model. (I am highly skeptical.
byTom Weidig