Nature Communications

An oral supplement protected rat retinas from degeneration

Rats with an inherited retinal disease received nicotinamide mononucleotide for up to four weeks, with less retinal thinning than controls given water without the supplement.

Paper by Lujia Feng, Yuwen Wen, Ting Zhang, +21 more authorsShaochong Zhang · Southern Medical University Shenzhen Hospital
Studied:
Experiments in RCS rats with retinitis pigmentosa, against rats given water without the supplement
What changed:
Supplemented rats had less retinal thinning and degeneration than rats given water without the supplement
The catch:
Treatment lasted only up to four weeks, too short to assess lasting retinal protection
In the record:
One of 729 papers on nicotinamide mononucleotide on record: 104 with results in people, 329 in animals.
Why it’s aging research:
It studies an intervention with evidence of extending healthy life.

Editor of record: Boris Djordjevic · AgingResearch.News

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RCS rats with retinitis pigmentosa, an inherited disease that causes retinal degeneration and blindness, had abnormal mitochondria—the cell structures that supply energy—in light-sensing cells and retinal support cells. In these animal experiments, researchers also found lower retinal levels of nicotinamide adenine dinucleotide, a molecule needed for energy metabolism.

They gave rats nicotinamide mononucleotide, a substance used to make that molecule, orally at 1,000 milligrams per kilogram of body weight daily. Supplementation began at 21 days old and lasted up to four weeks; controls received water without the supplement. After four weeks, supplemented rats had better mitochondrial function. Imaging and tissue analysis showed less retinal thinning and degeneration than in controls.

Why it matters

Retinal degeneration involves progressive loss of light-sensing cells and their supporting cells. The authors propose that sustaining energy metabolism may make these cells more resilient to disease-related stress.

Caveats

These were laboratory experiments, not a trial in people. The protection was found in a particular inherited rat model; the researchers reported that mitochondrial dysfunction was not universal across retinitis pigmentosa models.

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