Researchers at University of California-Irvine are testing the effects of nicotine to see if it will reduce or reverse auditory decline.
The research is part of a new project funded by the NIA division of the U.S. National Institutes of Health.
The project was recently awarded $640,473 in grant money for 2021 to determine, in humans and mice, whether nicotine’s effects can restore auditory function.
It began a few months ago and will continue until at least the end of 2021. (If successful, it could continue to receive more funding every year, until the end of 2025.)
Worth pointing out: nicotine, in this context, is NOT related to tobacco, smoking, or vaping. This is some sort of pharmaceutical nicotine, apparently:
“Because nicotine enhances cortical and cognitive function, pharmaceutical companies are developing nicotine-like drugs … These drugs are non-addictive (unlike nicotine in tobacco), yet nicotine also is non-addictive when given topically or orally.”
And, according to the project description, a positive outcome “will facilitate the translation of nicotine-based therapeutic treatments for hearing loss to clinical populations.”
Here is a shortened version of the project Abstract and Public Health Relevance Statement (formatting and emphasis ours):
Ideally, a combination of drug treatment with hearing aids and behavioral training could restore auditory function, but the development of pharmacological treatments requires a better understanding of the mechanisms by which candidate drugs improve hearing.
The goals of this proposal are to develop biomarkers of altered auditory processing in aging mice and humans, and using these biomarkers, to test the hypothesis that nicotine can normalize these age-related central auditory deficits.
Because nicotine enhances cortical and cognitive function, pharmaceutical companies are developing nicotine-like drugs to target cognitive deficits in aging. These drugs are non-addictive (unlike nicotine in tobacco), yet nicotine also is non-addictive when given topically or orally. However, its clinical benefits have not been exploited except as an aid to stop smoking.
We hypothesize that: 1) acute nicotine compensates for the age-related decline in inhibition by exciting the remaining inhibitory neurons; 2) chronic nicotine exposure (CNE) upregulates nicotinic acetylcholine receptors (nAChRs); and, as a result, 3) acute nicotine and/or CNE will reduce or reverse the age-related auditory decline.
We will test these hypotheses in both mouse and human at the level of cells (mouse in vitro brain slice), neural systems (mouse in vivo physiology; human brain imaging and EEG) and behavior (human psychoacoustics).
- Aim 1 will determine in mouse whether age-related decline in auditory spectrotemporal processing is reversed by acute nicotine or CNE, and characterize the associated cellular mechanisms.
- Aim 2 will identify, in humans, age-related changes in receptive field properties in auditory cortex using novel fMRI techniques and determine if nicotine reverses these changes using psychoacoustics, fMRI and EEG.
This project features a multifaceted, parallel approach in mouse and human. Each Aim will:
- examine auditory processing at multiple adult ages;
- use similar acoustic stimuli in both species, accounting for species differences in hearing, to target common mechanisms;
- test the effects of nicotine.
A successful outcome will promote an integrated understanding across levels, from cellular mechanisms to perception, and facilitate translation of nicotine-based therapeutic treatments to clinical populations.
Public Health Relevance Statement
Nicotine enhances auditory and cognitive functions because it mimics the brain’s system for “paying attention” to important sounds amid distractions (for example, understanding speech in a noisy environment). In part, nicotine does this by activating inhibitory neurons in the auditory cortex. Since age-related hearing deficits result in part from the loss of inhibitory neurons, this project will determine, in humans and mice, whether nicotine’s effects can compensate for reduced inhibition in aging and thereby restore auditory function.
For some more background on the science and theory behind nicotine and hearing, here is a good paper from last year:
Nicotine Enhances Auditory Processing in Healthy and Normal-Hearing Young Adult Nonsmokers March 2020
Nicotine improves auditory performance in difficult listening situations. The present results support future investigation of nicotine effects in clinical populations with auditory processing deficits or reduced cholinergic activation.
The UC Irvine project described in this post is part of the story. There is also a separate project, also at UC Irvine, titled, “Nicotinic enhancement of auditory-cognitive processing.” (Also awarded a grant worth over $600,000.)
From the project narrative section of the description:
The drug nicotine enhances auditory-cognitive function because it “hijacks” the brain’s endogenous system for directing attention to important sounds (for example, understanding speech in a noisy environment). This project seeks to determine if one kind of nicotine receptor (a2 subtype) and one kind of neuron (VIP) in two key regions of the cerebral cortex (auditory cortex and prefrontal cortex) play essential roles in nicotine’s effects. The long-term goal is to understand brain mechanisms of auditory processing and guide development of novel drug treatments for auditory-cognitive disorders.
We will be following this research and these nicotine/hearing improvement projects and posting updates as important milestones are met.
This article is an unfinished draft and a work in progress. You are accessing it early because this not-yet-public link is sent to email subscribers.
Exported on 05/01/2021 from the HHS Tracking Accountability in Government Grants System (TAGGS), http://taggs.hhs.gov, Project Number 1R01AG067073-01A1