In research published in the journal Cell Metabolism, nicotinamide riboside (NR) successfully prevented short- and long-term hearing loss in mice when administered before and after noise exposure.
The researchers at Weill Cornell Medical College and the Gladstone Institutes pointed out that their findings may lead to better treatments in the future, as current antidotes for inner-ear disorders— including hearing loss— are limited.
During the animal trial, researchers used NR to protect the nerves that innervate the cochlea. The cochlea transmits sound information through these nerves to the spiral ganglion, which sends those messages to the brain. Exposure to loud noises damages the synapses connecting the nerves and the hair cells in the cochlea, causing noise-induced hearing loss. NR proved successful at protecting these synaptic connections from damage.
Nicotinamide Riboside (NR) is a precursor to the chemical compound nicotinamide adenine dinucleotide (NAD+), which Dr. Brown and co-senior author Samie Jaffrey, pharmacology professor at Weill Cornell, previously observed could protect cochlea nerve cells from injury.
It was also noticed in the study that Nicotinamide Riboside (NR) and NAD+ work together to increase the activity of the protein sirtuin 3 (SIRT3), which plays a crucial role in the function of mitochondria, the powerhouses of the cell.
Study authors tested the power of SIRT3 by eliminating the gene in mice, which eliminated any of the protective properties of NR. A new strain of mice engineered to express high levels of SIRT3 also was resistant to noise-induced hearing loss— even without the administration of NR.
SIRT3 decreases naturally as the body ages. The study suggests that targeting SIRT3 using NR could be a viable target for treating all sorts of aging-related disorders including metabolic syndromes like obesity, pulmonary hypertension, and even diabetes researchers said.
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