New Study in Mice Proposes the First Gene That Could Help Prevent Tinnitus

This discovery was just posted TODAY

New study in mice proposes the first gene that could help prevent tinnitus, that ringing in the ears inside one's head when no external sound is present. This discovery is a first step to identify the molecules that could be targeted in treatments to silence the phantom noises, and help thousands of people.

https://www.sciencedaily.com/releases/2016/09/160901102734.htm


Let's see if someone finds this interesting...

 

@Mario martz AWESOME FIND MARIO! Its good to know science is moving forward and discovering key pieces to prevent and cure. Kudos to Christopher R. Cederroth for knowing "tinnitus is a multi-disciplinary affair, and current knowledge is scattered". And to mention, "This work is part of an effort to gather all the expertise to solve problems of heterogeneity, in how tinnitus becomes a problem to some but not all people and why they respond differently to treatments."

 

First "prevent" (which suggest this will do nothing for us who already have T) and they they say "silence the phantom noises" (which suggest it will treat already existing T). What's it gonna be?

 

I think when you can detect and eliminate the problematic gene, it literally erases whatever issue it was causing like it was never there.

 

i agree, it makes lots of sense Mricha37

 

I just wish they would hurry up

 

i agree

 

This is what CRISPR is for:

Genetic Engineering Will Change Everything...

 

This ^

 

I assume they are talking about Potassium channel blocker and Sodium channel blockers. Pinky and the Brain got their T cured. I was a list of drug names. AM-101 was one of the first but there are a few that out right cure T in some rats and T proofed a few other. Its about some people's brains plasticity, and neuronal hyperactivity. I think they will have a few treatments in the next few years for some peoples T.

for example: Ifenprodil, 7-Chlorokynurenate, Taurine, Retigabine, AUT3, and Sildenafil

 

I think we are looking at years out. They have to do pretrials, phase 1, 2, 3 out testing. Then if all is good, government approval if we are lucky. This entire process is years after research and design.

 

More than a decade really.

 

this was very informative!! and pleasant to watch

 

We are all so screwed beyond belief.

@Alue how do you manage the pain someone else caused this? I'm in the same place, and it kills me someone inflected this one me.

 

Any time I think about it I get angry. And I work with the person that caused this...

The person that caused it was apologetic, but how I was treated by the company after the injury is even worse.

I don't know, I don't manage it too well to be honest, and I haven't gotten over it even though everyone else has moved on.

If you live in the USA don't ever get a subjective injury on the job. If you get a broken leg or something obvious WC is fine, if it's a subjective permanent injury you are completely screwed. It's considered a no fault system, pain and suffering is irrelevant, and if it's subjective you must be making it up.

 

Maybe you should get some information about a qEEG, they might be able to "measure" over-activity in the brain compared with other tinnitus sufferers.

 

I know exactly how you feel. I am not dealing with that part very well.

 

I was going to respond, but I don't want to derail this thread.

 

While this is all interesting, it's a long way from mice models to reality. Sorry.

 

Most Likely!
but still its awesome to find out, that there are more and more scientist working and researching, people that we werent even aware that were working on it,
like this guy in the article that has been researching since 2009

 

This is the same article but with a video.
http://www.eurekalert.org/pub_releases/2016-09/f-wsp090116.php

 

I'm assuming people are aware that these are links to press releases, and press releases should be treated like any other advertising.

Has anyone actually read the paper? I've posted the title and abstract below as well as a link to the paper which I believe is freely available. It's worth noting up front that this isn't a paper about testing drugs or some type of genetic modification to treat tinnitus. Moreover, they induced tinnitus via salicylate administration (i.e. aspirin) so it isn't clear how the conclusions would apply more generally though they do discuss noise induced tinnitus.

At a minimum it seems like the results should improve the measurement of tinnitus in mice - assuming the acoustic startle response measurements are doing what the people using them think they are doing. There is some debate for the effectiveness of ASR in measuring tinnitus (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4411996/).

The possibility that varying levels of GLAST are related to vulnerability to tinnitus or other hearing issues is quite interesting. It would be very useful to be able to screen for such vulnerability, and I hope someone follows up on their suggestion for genetic analysis of people with and without tinnitus (or potentially other hearing issues). It wouldn't prove a causal relationship, but it may provide another piece of the puzzle. Hopefully some of the places that do genetic testing for hearing issues will include EAAT1 in their tests. MORL at U of Iowa does not presently (http://www.medicine.uiowa.edu/morl/otoscopegenes/) test EAAT1.

Finally, the relationship of GLAST to anxiety and schizophrenia is noteworthy. They raise the possibility that low levels of GLAST result in increased baseline anxiety and that this may exacerbate tinnitus intensity if not cause the tinnitus.

Regarding a few of the comments...

If the authors are correct, reducing or eliminating the expression of this gene will increase vulnerability to tinnitus. What would be required would be to increase its expression.

There is no mention in the text of channel blockers though a couple of papers are referenced. This isn't a paper about testing drugs.

Title:

GLAST Deficiency in Mice Exacerbates Gap Detection Deficits in a Model of Salicylate-Induced Tinnitus

Abstract:

Gap detection or gap pre-pulse inhibition of the acoustic startle (GPIAS) has been successfully used in rat and guinea pig models of tinnitus, yet this system has been proven to have low efficacy in CBA mice, with low basal GPIAS and subtle tinnitus-like effects. Here, we tested five mouse strains (CBA, BalbC, CD-1, C57BL/6 and 129sv) for pre-pulse inhibition (PPI) and gap detection with varying interstimulus intervals (ISI) and found that mice from a CBA genetic background had the poorest capacities of suppressing the startle response in the presence of a pre-pulse or a gap. CD-1 mice displayed variable responses throughout all ISI. Interestingly, C57BL/6, 129sv and BalbC showed efficient suppression with either pre-pulses or gaps with shorter ISI. The glutamate aspartate transporter (GLAST) is expressed in support cells from the cochlea and buffers the excess of glutamate. We hypothesized that loss of GLAST function could sensitize the ear to tinnitus-inducing agents, such as salicylate. Using shorter ISI to obtain a greater dynamic range to assess tinnitus-like effects, we found that disruption of gap detection by salicylate was exacerbated across various intensities of a 32-kHz narrow band noise gap carrier in GLAST knockout (KO) mice when compared to their wild-type (WT) littermates. Auditory brainstem responses (ABR) and distortion-product otoacoustic emission (DPOAE) were performed to evaluate the effects on hearing functions. Salicylate caused greater auditory threshold shifts (near 15 dB) in GLAST KO mice than in WT mice across all tested frequencies, despite similarly reduced DPOAE. Despite these changes, inhibition using broad-band gap carriers and 32 kHz pre-pulses were not affected. Our study suggests that GLAST deficiency could become a useful experimental model to decipher the mechanisms underlying drug-induced tinnitus. Future studies addressing the neurological correlates of tinnitus in this model could provide additional insights into the mechanisms of tinnitus.

Paper: http://journal.frontiersin.org/arti...campaign=ECO_FNBEH_20160901_cederrothtinnitus

 

A century in fact

 

My T is

It's very cool that they identified GLAST, it would be great if they could measure a decrease in T from modulating GLAST. That would be so huge. My T very literally sounds like a bird chirping, can't pretend this one doesn't exist, I would be the perfect volunteer because there are no good days or days where I'm at a 2 instead of an 8. I can't pretend the birdy isn't there.. I could accurately say if any treatment works..

 

A century? Lol. Really, the human is something we really haven't perfected yet. Everything else is on auto pilot in terms of development, such as cars, phones, computers all private companies but it took a little while for people to see how much $$ you can make. The minute one of these trials is even remotely successful you will have companies throwing funds at it.

 

i had a look and the GLAST is SLC1A3. So i checked the ones i have in my genetic info from 23andme. i'm not sure if it covers all of them.

https://ghr.nlm.nih.gov/gene/SLC1A3#resources

 

And flying cars are just a few months away! Hope I'm alive in 100 years

 

Can we just cryogenically freeze ourselves until a cure is found.

 

A cure is always at least 6 years away. This is a basic law of medicine.

 

Lol, within the next few years we should have a good idea on a time line. There are a lot of clinical trials that have never been done before. When I got my condition eight years ago there were almost zero clinical trials on the horizon.