Form of vitamin B3 shows improvements in treating Alzheimer’s – on mouse model
February 7, 2018Alzheimer’s disease can be with prevended neurological damage and improved cognitive and physical function with the supplement nicotinamide riboside (NR) – a form of vitamin B3 – in a new mouse model, a study says.
Researchers at the National Institute on Aging (NIA) part of the National Institutes of Health, suggest a potential new target for treating Alzheimer’s disease. The findings published in the Feb. 5, 2018, issue of Proceedings of the National Academy of Sciences.
According to the study, NR acts on the brain by normalizing levels of nicotinamide adenine dinucleotide (NAD+), a metabolite vital to cellular energy, stem cell self-renewal, resistance to neuronal stress and DNA repair. In Alzheimer’s disease, the brain’s usual DNA repair activity is impaired, leading to mitochondrial dysfunction, lower neuron production, and increased neuronal dysfunction and inflammation.
Richard J. Hodes, director of the NIA. “We are encouraging the testing of a variety of new approaches, and this study’s positive results suggest one avenue to pursue further.”
Based on their studies in human postmortem brain, they developed a new strain of mice mimicking major features of human Alzheimer’s such as tau pathology, failing synapses, neuronal death and cognitive impairment. The researchers tested the effects of an NR supplement by adding it to the drinking water of the mice. Over a three-month period, the mice who received NR showed reduced tau in their brains, but no change in amyloid-beta, study revealed.
Possible tests of NR for treating dementia?
“We are encouraged by these findings that see an effect in this Alzheimer’s disease model,” said Dr. Bohr. He also said that the team will be further testing of how NR or similar compounds might be pursued for their possible therapeutic benefit for people with dementia.
Next steps for the research team include further studies on the underlying mechanisms and preparations towards intervention in humans.
Source: www.nih.gov
