Emerging findings suggest that compromised cellular bioenergetics
and DNA repair contribute to the pathogenesis of Alzheimer’s disease
(AD), but their role in disease-defining pathology is unclear.
The findings of this study conducted on mice, suggest that NR is beneficial to neuroinflammation and oxidative stress.
Specifically, NR shows greater effects on learning and memory, LTP (long term potentiation of the brain), neuroinflammation, gait function, DNA damage, and sirtuin activity in a DNA repair-defective mouse model. This justifies additional research on the use of NR or other NAD+ precursors for treating AD in humans.
NR has shown beneficial effects in other DNA repair-deficient disease models, including ataxia-telangiectasia, xeroderma pigmentosum group A, and Cockayne syndrome.
NAD+ precursors such as NMN and NAM also improve memory and learning and mitochondrial function and increase lifespan in animal models of AD, Parkinson’s disease, and hearing loss.
This suggests that NAD+ up-regulation can reverse the impaired brain-energy metabolism and possibly oxidative stress that are implicated in cognitive decline.
To read the full study: ncbi.nlm.nih.gov/pubmed/29432159