Nicotinamide ribose ameliorates cognitive impairment of aged and Alzheimer’s disease model mice

Xie, Xiaogao; Gao, Yubin; Zeng, Min; Wang, Yi; Wei, Taofeng; Lu, Yun-Bi; Zhang, Wei‐Ping

doi:10.1007/s11011-018-0346-8

Cited by 64 publications

(49 citation statements)

References 46 publications

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“…However, the de novo biosynthesis pathway only occurred in limited cell types (Yoshino, Baur & Imai, 2018). NAD level reduction and unbalance between its synthesis and consumption is proved to be related to aging-associated diseases such as Parkinson’s disease (PD) (Jeśko et al., 2017) and Alzheimer’s disease (AD) (Xie et al., 2019). Hence, NAD supplementation might be a promising strategy to restore the cellular function.…”

Section: Introductionmentioning

confidence: 99%

“…Modulation of the cellular NAD level can attenuate hepatic steatosis and inflammation in mice fed with methionine-choline-deficient diet (Katsyuba et al., 2018). Evidences also display that replenish NR has beneficial effects on NAFLD, insulin sensitivity and AD in mice (Gariani et al., 2016; Cantó et al., 2012; Xie et al., 2019). In short, NAD has pronounced effects on hepatic homeostasis.…”

Section: Introductionmentioning

confidence: 99%

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Nicotinamide riboside exerts protective effect against aging-induced NAFLD-like hepatic dysfunction in mice

Han

Bao

Lou

et al. 2019

PeerJ

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Background & Aims Aging is one of the risk factors of non-alcoholic fatty liver disease (NAFLD). Yet, the mechanism underlying the aging-associated NAFLD-like syndrome is not fully understood. Nicotinamide adenine dinucleotide (NAD), a ubiquitous coenzyme, has protective effects against aging. Here, we investigated the actions of NAD precursors nicotinamide riboside (NR) on the development of aging-induced NAFLD. Methods NR supplemented food (2.5 g/kg food) was applied to aged mice for three months while normal chow to the other groups. Body weight, food intake, liver weight and fat pat mass were measured. The serum concentrations of lipid content, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and NAD were determined by biochemical assays. Pathological assessment and immunohistochemistry analysis of hepatic tissues were used to evaluate the effect of NR on NAFLD development and inflammatory infiltration. Results NR repletion significantly reduced fat pat mass in aged mice, while not altered the body weight, food intake, and liver weight. NR repletion significantly rescued the NAD reduction in aged mice. The total cholesterol and triglyceride levels could be lowered by NR repletion in aged mice. The AST level was also significantly reduced by NR repletion in aged group, while the ALT level lowered but without significance. Notably, moderate NAFLD phenotypes, including steatosis and hepatic fibrosis could be markedly corrected by NR repletion. In addition, Kupffer cells accumulated and inflammatory infiltration could also be remarkably reversed by NR repletion in aged mice. Conclusion Aging was associated with NAFLD-like phenotypes in mice, which could be reversed by oral NR repletion. Therefore, oral NR uptake might be a promising strategy to halt the progression of NAFLD.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nicotinamide riboside exerts protective effect against aging-induced NAFLD-like hepatic dysfunction in mice

Han

Bao

Lou

et al. 2019

PeerJ

Self Cite

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“…For example, NR treatment prevented dopaminergic neuronal loss in Parkinson’s disease model flies [ 29 ]. Moreover, NR treatment ameliorated selective cognitive impairment in aged mice and decreased the number of amyloid beta plaques in cortex of Alzheimer’s disease model mice [ 30 ]. Furthermore, NR treatment decreased glial activation and delayed motor neuron loss in the spinal code of amyotrophic lateral sclerosis model mice [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Axonal Protection by Nicotinamide Riboside via SIRT1-Autophagy Pathway in TNF-Induced Optic Nerve Degeneration

et al. 2020

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Nicotinamide adenine dinucleotide (NAD+) synthesis pathway has been involved in many biological functions. Nicotinamide riboside (NR) is widely used as an NAD+ precursor and known to increase NAD+ level in several tissues. The present study aimed to examine the effect of NR on tumor necrosis factor (TNF)-induced optic nerve degeneration and to investigate whether it alters SIRT1 expression and autophagic status in optic nerve. We also examined the localization of nicotinamide riboside kinase 1 (NRK1), which is a downstream enzyme for NR biosynthesis pathway in retina and optic nerve. Intravitreal injection of TNF or TNF plus NR was performed on rats. The p62 and LC3-II protein levels were examined to evaluate autophagic flux in optic nerve. Immunohistochemical analysis was performed to localize NRK1 expression. Morphometric analysis showed substantial axonal protection by NR against TNF-induced axon loss. TNF-induced increment of p62 protein level was significantly inhibited by NR administration. NR administration alone significantly increased the LC3-II levels and reduced p62 levels compared with the basal levels, and upregulated SIRT1 levels in optic nerve. Immunohistochemical analysis showed that NRK1 exists in retinal ganglion cells (RGCs) and nerve fibers in retina and optic nerve. NR administration apparently upregulated NRK1 levels in the TNF-treated eyes as well as the control eyes. Pre-injection of an SIRT1 inhibitor resulted in a significant increase of p62 levels in the NR plus TNF treatment group, implicating that SIRT1 regulates autophagy status. In conclusion, NRK1 exists in RGCs and optic nerve axons. NR exerted protection against axon loss induced by TNF with possible involvement of upregulated NRK1 and SIRT1-autophagy pathway.

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“…Whilst some patients with Alzheimer’s Disease given nicotinamide adenine dinucleotide (NADH; 10mg daily) did show improvement in mini mental state examination and global deterioration scores [11], others did not [12]. Nicotinamide derivatives such as nicotinamide mononucleotide, nicotinamide riboside [13] and nicotinamide loaded lipid nanoparticles [14] have, at extremely high doses, shown some cognitive benefits in Alzheimer’s disease animal models and in aged mice but their effects on cognition in humans, and at tolerable doses, are unknown [15].…”

Section: Discussionmentioning

confidence: 99%

Neurocognitive Function and Quality of Life Outcomes in the ONTRAC Study for Skin Cancer Chemoprevention by Nicotinamide

et al. 2019

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Nicotinamide (vitamin B3) has photoprotective effects and reduces skin cancer incidence in high risk patients. Nicotinamide also improves cognition in animal models. As part of the ONTRAC (Oral Nicotinamide To Reduce Actinic Cancer) phase III placebo-controlled, randomized trial to assess nicotinamide’s efficacy in skin cancer prevention, we included clinical neurocognitive function and patient-reported quality of life assessments at baseline and after 12 months of intervention in individuals with previous skin cancer in order to assess any effect of oral nicotinamide (500 mg po twice daily) on cognitive function and quality of life. In our sample of 310 participants who completed neurocognitive function testing at baseline and at 12 months, we were not able to detect any significant effect of oral nicotinamide on cognitive function nor on quality of life. Further studies of nicotinamide’s effects on cognition in humans might include individuals with pre-existing mild cognitive impairment, and it may be that higher doses of nicotinamide are required to significantly influence cognitive function compared to doses required to reduce skin cancer.

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Nicotinamide ribose ameliorates cognitive impairment of aged and Alzheimer’s disease model mice

Cited by 64 publications

References 46 publications

Nicotinamide riboside exerts protective effect against aging-induced NAFLD-like hepatic dysfunction in mice

Nicotinamide riboside exerts protective effect against aging-induced NAFLD-like hepatic dysfunction in mice

Axonal Protection by Nicotinamide Riboside via SIRT1-Autophagy Pathway in TNF-Induced Optic Nerve Degeneration

Neurocognitive Function and Quality of Life Outcomes in the ONTRAC Study for Skin Cancer Chemoprevention by Nicotinamide

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