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Vitamin B-3 has previously been proposed as an alternative for treating Alzheimer's disease.
In an older study, large doses of nicotinamide — also referred to as B-3 — reversed Alzheimer's-related memory loss in mice.
A new study, however, focused on the effect of nicotinamide riboside (NR), which is a form of vitamin B-3, on Alzheimer's-related brain damage in mice.
More specifically, the researchers — who were jointly led by Dr. Vilhelm A. Bohr, the chief of the National Institute on Aging's (NIA) Laboratory of Molecular Gerontology, and Dr. Yujun Hou, a postdoctoral investigator in the laboratory — focused on how NR affects the brain's ability to repair its DNA, a function that is compromised in Alzheimer's disease.
As the scientists explain, a deficiency in the brain's ability to repair its DNA leads to dysfunction in the cells' mitochondria — the energy-creating organelles inside the cells — which, in turn, leads to neuronal dysfunction and lower neuron production.
But NR is "critical for mitochondrial health and biogenesis, stem cell self-renewal, and neuronal stress resistance." Thus, Dr. Bohr and his colleagues wanted to explore the effects of NR supplementation in a mouse model of the neurological disease.
The team added NR to the drinking water of mice that had been genetically engineered to develop the hallmarks of the neurodegenerative disorder. These included toxic buildups of the proteins tau and amyloid beta, dysfunctional synapses, and neuronal death — all of which resulted in cognitive deficits.
The mice drank the water for 3 months, and their brains and cognitive health were compared with those of control mice. The findings were published in the journal Proceedings of the National Academy of Sciences.
NR promotes neuronal and cognitive health
Compared with the controls, the NR-treated mice had less of the protein tau in the brain, less DNA damage, and more neuroplasticity — that is, the brain's ability to "rewire" itself when it learns new things, stores new memories, or becomes damaged.
Additionally — probably as a result of NR's ability to aid the self-renewal of stem cells, or cells that have the ability to transform into any other type of cell that the body needs — the mice in the intervention group produced more neurons from neuronal stem cells.
Also, fewer neurons died or were damaged in these mice. Intriguingly, however, their levels of the beta-amyloid protein stayed the same as those of the control mice.
Finally, the researchers say that in the hippocampi — a brain area involved in memory that often shrinks or is damaged in Alzheimer's — of the mice that received the treatment, NR appeared to get rid of the existing DNA damage or stop it from spreading.
All the brain changes were backed up by results from cognition and behavioral tests. All of the NR-treated mice performed better at maze tasks and object recognition tests, and they demonstrated stronger muscles and better gait.
Commenting on the results of the study, Dr. Richard J. Hodes — director of the NIA — says, "The pursuit of interventions to prevent or delay Alzheimer's and related dementias is an important national priority."
"We are encouraging the testing of a variety of new approaches, and this study's positive results suggest one avenue to pursue further," he adds.
"We are encouraged by these findings that see an effect in this Alzheimer's disease model. [...] We are looking forward to further testing of how NR or similar compounds might be pursued for their possible therapeutic benefit for people with dementia."
Dr. Vilhelm A. Bohr
In future, the researchers plan to further investigate the mechanisms by which NR may be used to prevent Alzheimer's-related cognitive deficits, and to set the stage for human clinical trials.
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