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Supplement improved movement in mice modeling Parkinson’s disease

Male and female mice received nicotinamide riboside in drinking water for 21 weeks, improving movement without preventing the loss of dopamine-producing brain cells.

Paper by Sukanya Saha, Chengbo Meng, Jie Dong, +5 more authorsGuohong Cui · National Institute of Environmental Health Sciences
Studied:
Preprint: experiments in double-hit Parkinson's model mice, 21 weeks, against untreated double-hit mice (Randomized, blinded)
What changed:
NR-treated Parkinson's model mice stayed on a rotating rod longer than untreated model mice
The catch:
Treatment began with disease induction; movement benefits from starting after symptoms appeared were not measured
In the record:
One of 608 papers on nicotinamide riboside on record: 114 with results in people, 248 in animals.

Editor of record: Boris Djordjevic · AgingResearch.News

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Male and female mice aged 3–10 months were studied in experiments using a Parkinson’s disease model that combined excess production of the protein alpha-synuclein with benomyl exposure. Nicotinamide riboside was given at 12 millimolar in drinking water for 21 weeks, starting when researchers began creating the model.

Supplemented model mice moved more and showed partial improvement in coordination compared with untreated model mice. Supplementation did not prevent the loss of brain cells that produce dopamine, a signaling chemical. Separate experiments used injections of 1,000 milligrams per kilogram of body weight twice daily for five days. These increased ongoing and stimulated dopamine release in control and model mice. Repeated injections also increased a measure of cellular energy supply in several types of nerve cells.

Why it matters

Aging can worsen problems in mitochondria, the cell structures that supply energy. The authors propose boosting cellular energy as a promising add-on strategy for easing Parkinson’s-related functional impairments.

Caveats

Supplementation began as the disease model was being created, rather than after disease was established. The findings came from mice, and the preprint has not been peer-reviewed.

From the paper

Events by group

In PD mice, histological analyses revealed > 50% loss of DA neurons in the SNc and ~ 30% loss in the ventral tegmental area (VTA), as well as > 50% reductions in DA terminals within the dorsolateral striatum (DLS), compared to the littermate control mice.

Results, NR does not prevent the loss of DA neurons or their striatal innervation.

Quoted word for word from the full text on PubMed Central.

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