Cilcare's CIL001 Targets Cochlear Synaptopathy — An American/French Collaboration

Thanks for sharing. I'll keep an eye out for sign-ups for the clinics in France and Germany.

Are there any other members here who would potentially be interested in signing up?
If there's one in the UK, what have I got to lose? Another 10 to 20 years as a hermit with an aching, hissing ear while I wait for it to come to market?
 
How would targeting cochlear synaptopathy "fix" tinnitus?
Well, presumably the brain will have to adapt to its restored hearing and might decide at that point that the tinnitus sound is no longer necessary — or perhaps integrate the new audio into that pathway.

But it's anyone's guess, really, isn't it? For all we know, it could make everything worse since it's never been done in humans before.
 
I have been in contact with the researcher; however, I'm a little reluctant. Intratympanic injections are no longer seen as the best route to the cochlea. All trials using this method have failed, with companies often blaming the lack of permeability.

Many institutions are now moving away from this approach and have discovered new proprietary routes.
 
I have been in contact with the researcher; however, I'm a little reluctant. Intratympanic injections are no longer seen as the best route to the cochlea. All trials using this method have failed, with companies often blaming the lack of permeability.

Many institutions are now moving away from this approach and have discovered new proprietary routes.
I'm relatively new to all this, so forgive me if I'm totally off base, but even if it fails to pass through the round window and restore synaptopathy, since neurotrophin-3 has CNS potential, might this still potentially help with some types of noxacusis caused by middle ear damage?
 
I have been in contact with the researcher; however, I'm a little reluctant. Intratympanic injections are no longer seen as the best route to the cochlea. All trials using this method have failed, with companies often blaming the lack of permeability.

Many institutions are now moving away from this approach and have discovered new proprietary routes.
Is it known whether they're also exploring other forms of administration?
 
I have been in contact with the researcher; however, I'm a little reluctant. Intratympanic injections are no longer seen as the best route to the cochlea. All trials using this method have failed, with companies often blaming the lack of permeability.

Many institutions are now moving away from this approach and have discovered new proprietary routes.
That really is something the guys and gals in white coats need to figure out. I recall one research group mentioning that their drug had difficulty accessing the lower frequencies of the cochlea. Kind of fundamental, don't you think? It's like saying, "We have the wonder drug, but we can't deliver it."
 
I have been in contact with the researcher; however, I'm a little reluctant. Intratympanic injections are no longer seen as the best route to the cochlea. All trials using this method have failed, with companies often blaming the lack of permeability.

Many institutions are now moving away from this approach and have discovered new proprietary routes.
I hope they share these new routes of delivery.
 
How would targeting cochlear synaptopathy "fix" tinnitus?
Tinnitus is caused by cochlear synaptopathy.

For example, if you go to a club without earplugs, the loud music can damage cochlear synapses, destroying many of them. As a result, your hair cells still pick up sound, but there are far fewer synapses to receive and process the sound information. It is like a damaged microphone that cannot pick up sound properly.

To compensate for the loss of sound clarity and reduced signal input, your central nervous system increases central gain in an attempt to restore normal hearing levels. However, in the process of turning up central gain, tinnitus develops—just like how turning up the gain too high on a sound system to compensate for a poor-quality microphone would create buzzing and ringing. This also leads to a loss of sound clarity and fidelity.

If Cilcare's drug worked, it would restore sound input, allowing central gain to return to normal levels. As a result, hearing would improve with better clarity and fidelity, and the ringing would go away. That is why targeting cochlear synaptopathy could potentially fix tinnitus.
Well, presumably the brain will have to adapt to its restored hearing and might decide at that point that the tinnitus sound is no longer necessary — or perhaps integrate the new audio into that pathway.

But it's anyone's guess, really, isn't it? For all we know, it could make everything worse since it's never been done in humans before.
No, it could not make everything worse. If the synapses were regenerated, it could only lead to improvement—better sound fidelity and clarity, increased sound input, and less or no tinnitus and hyperacusis.
 

The brain scientist linked above conducted a comparative study on the brains of London taxi drivers and other groups, such as bus drivers. The study revealed that taxi drivers, who had to memorize not only street names and locations but also how they were interconnected, had much larger hippocampi than bus drivers, who only needed to memorize a single route, or the average person.

Perhaps a comparative study on the brains of patients with tinnitus, hyperacusis, hearing loss or deafness, and misophonia—or some combination of these—could reveal new insights.

It would also be valuable to examine the brains of healthy children, adolescents, and young adults for comparison.
Tinnitus is caused by cochlear synaptopathy.

For example, if you go to a club without earplugs, the loud music can damage cochlear synapses, destroying many of them. As a result, your hair cells still pick up sound, but there are far fewer synapses to receive and process the sound information. It is like a damaged microphone that cannot pick up sound properly.

To compensate for the loss of sound clarity and reduced signal input, your central nervous system increases central gain in an attempt to restore normal hearing levels. However, in the process of turning up central gain, tinnitus develops—just like how turning up the gain too high on a sound system to compensate for a poor-quality microphone would create buzzing and ringing. This also leads to a loss of sound clarity and fidelity.

If Cilcare's drug worked, it would restore sound input, allowing central gain to return to normal levels. As a result, hearing would improve with better clarity and fidelity, and the ringing would go away. That is why targeting cochlear synaptopathy could potentially fix tinnitus.

No, it could not make everything worse. If the synapses were regenerated, it could only lead to improvement—better sound fidelity and clarity, increased sound input, and less or no tinnitus and hyperacusis.
Ha! It is all about the flow.

Just like plumbing! 😉

To restore the water supply, first, you make sure the connection to the water main is working. Then, check if there is water in the tank. You have to make sure the faucet is not blocked, and so on.

Once everything is in order, you are good to go!

Or, for that matter, it is just like fixing the electrics.
 
Tinnitus is caused by cochlear synaptopathy.

For example, if you go to a club without earplugs, the loud music can damage cochlear synapses, destroying many of them. As a result, your hair cells still pick up sound, but there are far fewer synapses to receive and process the sound information. It is like a damaged microphone that cannot pick up sound properly.

To compensate for the loss of sound clarity and reduced signal input, your central nervous system increases central gain in an attempt to restore normal hearing levels. However, in the process of turning up central gain, tinnitus develops—just like how turning up the gain too high on a sound system to compensate for a poor-quality microphone would create buzzing and ringing. This also leads to a loss of sound clarity and fidelity.

If Cilcare's drug worked, it would restore sound input, allowing central gain to return to normal levels. As a result, hearing would improve with better clarity and fidelity, and the ringing would go away. That is why targeting cochlear synaptopathy could potentially fix tinnitus.

No, it could not make everything worse. If the synapses were regenerated, it could only lead to improvement—better sound fidelity and clarity, increased sound input, and less or no tinnitus and hyperacusis.
Tinnitus and hyperacusis do not always originate from the ears. The thalamus is also involved, for your information.
 
No, it could not make everything worse. If the synapses were regenerated, it could only lead to improvement—better sound fidelity and clarity, increased sound input, and less or no tinnitus and hyperacusis.
I was just being a little facetious, sorry! 🙂

Although, if their drug does not work as intended in trials, I suppose that could make things worse.
 

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