Alzheimer’s disease is a common form of dementia that affects memory and cognitive function. Recently, NAD+ (Nicotinamide Adenine Dinucleotide) – an important coenzyme in energy maintenance and cell function – has attracted attention in Alzheimer’s research. A decline in NAD+ levels is thought to be linked to neurodegeneration, opening up the potential for new therapies.
1. NAD+ and the Hallmarks of Alzheimer’s Disease
NAD fluctuations + affects several signs of aging, such as mitochondrial dysfunction, neurogenesis, immune response, DNA repair, damaged phagocytes, chromatin and epigenetics, cell division, Redox reactions and neuronal networks. AD is the most common type of dementia, but still
There is no effective treatment that affects the progression of AD.
Pathological signs of AD are characterized by the accumulation of amyloid-β (Aβ) plaques, as well as tau neurofibrillary tangles (NFTs) and mitochondrial dysfunction in the brain. Emerging evidence suggests an important role for NAD depletion + and impairment of NAD-dependent metabolic pathways + associated with pathophysiological markers of AD and NAD repletion + may improve cognitive deficits in cross-species models of AD.

NAD+ depletion is associated with pathophysiological markers of AD: As we age, or under several genetic and non-genetic factors, increased NAD+ consumption (CD38, PARP1 and SARM1) promotes promotes NAD+ depletion, leading to impaired DNA repair, mitochondrial homeostasis, and neuronal function, as well as inflammation, all of which can worsen disease progression.
Evidence suggests that NAD+ depletion and impairment of NAD+-dependent metabolic pathways are associated with important pathophysiological markers of AD (Aβ plaque, hyperphosphorylation, and dysfunction). mitochondria); and enhancing NAD+ by exercise, diet, or pharmacological enhancers may improve cognitive deficits in AD models by inhibiting these pathologies.
2. NAD+ precursors as a potential therapeutic intervention for Alzheimer’s disease models
Pretreatment of neurons with NAD+ precursor protects against axonal degeneration after axonectomy or even noise-induced hearing loss in mice, demonstrating a neuroprotective effect. Furthermore, induction of NAD+ levels after calorie restriction reduces A accumulationβ. It is worth noting that transgenic AD mice improved memory loss with NR treatment. We should note that NAD+ precursors, such as NAM, NMN and NR, may be a way to prevent cUgh Alzheimer’s disease.
3. Systematic review of preclinical trials of NAD+ for Alzheimer’s disease models
The researchers systematically searched PubMed, Google Scholar, and the Cochrane Library from inception to May 30, 2020. Ultimately, they identified 14 eligible preclinical trials. precursors NAD+ improves memory for AD models.
In short, NAD + is an important metabolite related to the pathophysiology of AD. This comprehensive review of emerging findings has revealed the important role of NAD precursors + and related metabolites in AD models and shows NAD + may influence the pathological signs of AD. Advances in understanding the molecular mechanisms of NAD-based neuronal resilience + will lead to new approaches to treating AD.
Data from included studies were included indicates that the addition of NAD precursors + seems to be an anti-strategy Alzheimer’s dementia effective and safe with adequate bioavailability to prevent neurological and behavioral symptoms. The stage is now set to test whether these exciting pre-clinical trials are precursors for tsuccessfully in large-scale randomized clinical trials and whether the results can be translated clinically to improve the phenotype of AD patients.
Author contributions: W-WW and LF implemented the idea and searched for related documents. H-JH contributed significantly to the concept and design, images and tables. XW, SZ, and XX drafted and edited the manuscript. C-LX and RH participated in drafting the manuscript and supervised the process. All authors contributed to the article and approved the submitted version.
References: Pnas.org, Pubmed.ncbi.nlm.nih.gov
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