Tuesday, April 19, 2016

"Stuttering" mice make us fluent?

They managed to create a stuttering mouse, or let be more precise they created a mouse that has the same gene mutation than a subclass of people who stutter and that shows an abnormal "speech" pattern.

This is significant as we are moving out of the soft psychosocial research arena with weak research standards to a more rigorous research arena with full-time scientists who have been trained to this kind of stuff for many different disorders.

I predicted this development at the discovery of the gene mutation.

Read the article in Cell here.


Unknown said...

The paper was published in Current Biology, and has lots of caveats/flaws/inherent limitations - whatever you want to call them, but I would judge it as of high quality. A huge step towards the establishment of the very first (genuine) cause-effect association in stuttering.

Tom Weidig said...

if it was published in Current Biology, why has Cell a big article?

If you want to write a guest post on the caveats/flaws/inherent limitations, be my guest!

Tom Weber said...

Tom, if one person has this mutation and his stuttering is driven by this, what would be a therapy option? Is there - generally - a protein therapy available for people with genes causing anything undesired?

Anonymous said...

Tom, this is no doubt a HUGE step for the stuttering community, now having an animal model. Do you think this will lead to a "cure" or more effective treatment in our lifetime?....or do you feel like we are still decades and decades away from something of the like?

As always, thank you for your posts!

Unknown said...

I will drop some lines regarding the caveats/flaws/inherent limitations asap. They are rather technical, however. Meanwhile, folks, do not overexcite. There are many (more serious) diseases with simple (called mis-sense) mutations) like the one inserted in the murine model, whose treatment either do not exist or is not effective. For people who stutter due to specific mutations like that, the most promising strategy would be enzyme replacement, whose efficacy has been shown to be very limited in most rare diseases (Fabry's disease, mucopolysaccharidosis I, II e VI, Gaucher diseases, among others).

Tom Weidig said...

Still waiting for your lines, Tiago! :-)