Noise-Induced Hearing Loss in the 21st Century: A Research and Translational Update

[Juan]

Noise-induced hearing loss in the 21st century: A research and translational update

The article describes in detail the reaction of the hearing system triggered by excessive noise, which causes noise-induced hearing loss (NIHL).

It talks about an opportunity window of typically 7 - 10 days after noise exposure:

"This prolonged oxidative stress is proposed to induce the delayed and continued cochlear injury. This time might, therefore, provide a "window of opportunity" for post-noise otoprotective interventions to ameliorate or repair injury to the cochlea and reduce the impact of hearing loss."​

I read other articles that talked about a period of 2 months during which the hearing system changes after being exposed to excessive noise (cochlear changes, changes to the spiral ganglion neuron (SNGs), nerve fiber etc). In this article there are also references about damage that extends for months after noise exposure:

"An established mechanism of NIHL damage is the excess release of the excitatory neurotransmitter glutamate at the IHC afferent synapse. Glutamate excitotoxicity resulting from excessive glutamate release following noise overstimulation leads to an influx of cations such as Ca2+ across the post-synaptic membrane. The osmotic imbalance results in swelling of the postsynaptic afferent dendrites. Secondary to this cellular degeneration is calcium-dependent caspase-mediated apoptosis by intrinsic (mitochondria-mediated) pathway. This may lead to degeneration of type 1 SGN weeks and months after a noise exposure. The inhibitory neurotransmitter γ-amino butyric acid (GABA) is also associated with the regulation of auditory function. Mice lacking the GABAB1 receptor subunit have elevated hearing thresholds but increased resistance to permanent acoustic injury."​

The article also talks about oxidative stress and free radicals:

"Free radicals (ROS and RNS) can cause damage by reacting with DNA, proteins, cytosolic molecules, cell surface receptors, and breaking down membrane lipids."​

Psychological stress as a reaction or consequence of noise exposure, and the use of corticoids:

"Noise causes psychological stress. The hypothalamic-pituitary-adrenal (HPA) axis can be activated by noise stress and directly modulate the sensitivity of the auditory system. Glucocorticoid receptors are expressed in human and rodent cochlea. Systemic glucocorticoids or steroid hormones are widely used to treat sudden hearing loss with variable success. For example, dexamethasone decrease the auditory thresholds in mice subjected to a moderate acoustic trauma, while the pre-treatment with glucocorticoid receptor antagonists exacerbates threshold shifts."​

Genetic predisposition to NIHL:

NIHL is a complex condition caused by the interaction of genetic and environmental factors. Therefore, individual vulnerability to NIHL is highly variable. Understanding the genetic makeup of people susceptible to NIHL will assist in early interventions and may lead to personalized therapies. Knockout mouse studies have implicated deficits in genes involved in antioxidative pathways or the structure of the cochlea to increase susceptibility to acoustic overstimulation. These include genes encoding proteins of the hair cell (Cdh23, Pmca2), oxidative stress (Sod1; Gpx1), stress-activated heat shock factor (Hsf1) and potassium recycling."​

Therapeutic strategies discussed include:

- Gene therapy for NIHL
- Otoprotective agents for the prevention and mitigation of NIHL (drugs and supplements)
- Otoprotective agents against glutamate excitotoxicity, apoptosis and intracellular calcium overload
- Otoprotective agents against noise-induced oxidative and metabolic stress
- Otoprotective agents against inflammation and reduced blood flow​

 

[Tezcatlipoca]

Pretty old article. I guess when it came out it was pretty novel, but now all of these things are common knowledge. Nothing new.

And the opportunity windows for acute noise exposure are not set in stone. Nobody really knows.

 

[twa]

Pretty old article. I guess when it came out it was pretty novel, but now all of these things are common knowledge.

Pretty interesting, nonetheless.

 

[Juan]

Pretty old article. I guess when it came out it was pretty novel, but now all of these things are common knowledge. Nothing new.

And the opportunity windows for acute noise exposure are not set in stone. Nobody really knows.

Yeah, I know it's old. I though it was pretty interesting as a summary.

Also it shows that in 8 years things have not advanced an inch in terms of results from hearing research. I have been hearing there would be a solution for NIHL for the past like 20 years... or more... and still nothing.

About the opportunity window, I think the interesting part is that most people agree on a timeframe up to 3 weeks in which something can be done (ideally less than 10 days, but anyway). However, there may be changes not only in hair cells but also in SGNs and nerve fibers months after a noise exposure... I think that's interesting and worth to explore.

 

[Diesel]

Also it shows that in 8 years things have not advanced an inch in terms of results from hearing research.

Not exactly... there is new research / findings in the hearing loss space that is shared on this site regularly. Some of it builds upon what you've shared above.

 

[Juan]

Not exactly... there is new research / findings in the hearing loss space that is shared on this site regularly. Some of it builds upon what you've shared above.

I mean in terms of the so much advertised "hearing pill" that would protect ears from excessive noise.