4 years. That would be awesome.
4 years. That would be awesome.
4 years. That would be awesome.
Elon did say if we don't increase our bandwidth interface speed (input and output, mostly output), it's over for humans when AGI gets here. So this is really good news to hear... thanks for showing me that.https://apnews.com/Business Wire/856d3482387741d5937af2fcec9d2314
Musk and Jepsen aren't the only ones with BCIs, DARPA is making injectible ones now too.
No brother, we are shooting for the stars, like the Mars mission.I'll gladly keep the hearing loss if they can just reduce my tinnitus!
@Silvio Sabo @Jab4Elon did say if we don't increase our bandwidth interface speed (input and output, mostly output), it's over for humans when AGI gets here. So this is really good news to hear... thanks for showing me that.
As I said don't confuse machine learning with AI. And also, as we can learn from tinnitus research, they always over sell the idea in articles.
Actually technology already exists for that, it's called CRISPR and it's been being improved since created.Even if you can identify the tinnitus problem in the DNA that does not mean an instant cure... don't think you can just change your DNA.
CRISPR exists but in the very early stages and that's even if they find "the tinnitus problem in the DNA"Actually technology already exists for that, it's called CRISPR and it's been being improved since created.
Or it could be more of the neuroinflammation in response to the hearing damage, like the recent research from the University of Arizona has been showing. Personally I'm looking forward to that in the long term, inflammation is a cause for many issues in the body and it sure would help explain the variability of tinnitus.
I am aware of that, but it is a double edged sword. Mind you cancer is a result of over inflammation. I believe neuroinflammation is causing hyperactivity. As for the part of the brain most responsible, research points to hyperactivity of fusiform cells in the Dorsal Cochlear Nucleus.Inflammation increases the perception of tinntus because tinnitus is directly linked to the limbic system, so it stands to reason that resolving inflammation would decrease, if not eliminate the perception of tinntus, this is however not the direct cause for tinnitus and inflammation is a necessary mechanism for a lot of functions in the body, including such things as the immune system, it is therefore not something sustainable long term on a systemic level (and one of the many reasons you can't use cortico steroids for your entire life), that said an anti inflammatory drug may work if it was specifically targeting the areas of the brain responsible for handling the repetitive noise (which I would assume, would be the nucleus accumbens). Rather than having a systemic effect. I would assume this is where some of the clinical research is heading.
Well not available for all, but FX-322 might have made it a reality in this world, and if proven to be effective in its next trial, it might be on the market within 3 years if they get the FDA fast track like they plan to.Looks like the prediction failed. :-/
3 years is pretty optimistic, more realistically, considering clinical trial follow-ups, you are looking at 10 to 15 years before commercial availability.Well not available for all, but FX-322 might have made it a reality in this world, and if proven to be effective in its next trial, it might be on the market within 3 years if they get the FDA fast track like they plan to.
Wouldn't this then oppose Dr. Josef Rauschecker's theories? Or go against Neuromod's new treatment if it's "nothing to do with plasticity"?It's nothing to do with your DNA and everything to do with the type of damage you sustained. It turns out stereocillia damage on its own only induces hearing loss, however (peripheral) neuropathy induces both tinnitus and hearing loss. At least that's what the latest research shows, this is why some people (for instance during the aging process) have hearing loss but no tinnitus.
It's nothing to do with the "gateway in your brain" or plasticity and instead everything to do with the type of damage your inner ear sustained.
At least as far as hearing loss induced tinnitus is concerned.
Plasticity allows for habituation, and possibly a lower (or higher) perception of the tinnitus, as it involves the nucleus accumbens and the auditory cortex, but it has nothing to do with the actual cause of tinnitus, in fact what is defined as plasticity is nothing more than a deregulation of multiple receptors (most likely dopamine related receptors) within the nucleus accumbens which processes repetitive sounds (which eventually leads to habituation), which is a natural process that occurs in most (but not all, for unknown reason) brains and takes at the very least 6 months of residual chronic exposure to a specific noise. This deregulation only starts to happen after the noise is perceived through the prefrontal cortex gateway (as opposed to the amygdala), which means the noise goes from a threatening state to an annoying, albeit non threatening state, as noises perceived through the amygdala are not processed by the nucleus accumbens, this can be (and often is) one of the reasons for which the habituation process can be blocked/not start, as a lot of people can be stuck in a negative feedback look through which the noise perception can remain in the amygdala for years.Wouldn't this then oppose Dr. Josef Rauschecker's theories? Or go against Neuromod's new treatment if it's "nothing to do with plasticity"?
Also, definitely agree on the Frequency Therapeutics product being a good decade away, people are getting far too carried away with 3 years.
There is such a thing as hidden hearing loss, this is why a lot of people have noise induced tinnitus and show normal, if not perfect hearing on their audiograms. It turns out the auditory cortex is pretty good at compensating and masking hearing loss/deficiencies (and not so much at masking tinnitus).Personally I don't need it because I have normal hearing. These are just my obviously non-expert estimates on it (none of us are experts here). Now if it works for tinnitus, it will be a different story.
They started the phase 1 trial July 2018 and finished April this year. That's 10 months. They also plan on starting the phase 2 trial later this year. Assuming they keep moving at this pace, the product works as they claim it does, and are granted the FDA fast track since, 3 years is a realistic estimate.
Now you two are saying it will be 10 years or more. Hmm.. Quite a difference. Can either of you fill me in on why? Since we all know "clinical trial follow ups", aren't always necessary to begin commercialization of a treatment.
I've heard of it. That still doesn't address the difference in FX-322's availability estimates.There is such a thing as hidden hearing loss, this is why a lot of people have noise induced tinnitus and show normal, if not perfect hearing on their audiograms. It turns out the auditory cortex is pretty good at compensating and masking hearing loss/deficiencies (and not so much at masking tinnitus).
3 years is pretty optimistic, more realistically, considering clinical trial follow-ups, you are looking at 10 to 15 years before commercial availability.