Table 1 Characteristics of the studies included in the systematic review
Author’s | Species/sex | Diseases | Treatment | Duration | Dose/Route | Cognitive Behavioral tests | Findings |
|---|---|---|---|---|---|---|---|
Tarantini et al. [21] | Male C57BL/6 Mice | Aging | NMN | 14 days | 500 mg /kg, i.p | Radial arms water maze, EPM, and NOR | Restoring endothelial NO mediation, mitochondrial oxidative stress ↓ and improved mitochondrial bioenergetics |
Rex et a. [22] | Male Wistar Rat | Aging | NADH | 10 days | 10, 50, and 100 mg/kg, i.p | MWM | Cognitive function↑ |
Koppen et a. [23] | Male Wistar Rat | Aging | NAM | Single | 1.2Â g/kg, s.c | MWM | Did not improve learning and memory |
Hosseini et al. [6] | Male Wistar Rat | Aging | NMN | 28 days, every other day | 100 mg/kg, i.p | Barnes maze and NOR tests | Memory impairment and apoptosis↓ |
Li et al. [17] | Male SAMP8 Mice | Aging | NMN | 15 weeks | 300 mg/kg | MWM | Decreased oxidative stress and mitochondrial dysfunction, learning and memory deficits, and inflammation |
Liu et al. [24] | 3xTgAD Mice | AD | NAM | 8 months | 40 µg/g, drinking water | MWM Open field | Increased levels of activated neuroplasticity-related kinases, and cognitive function↑ |
Yao et al. [25] | APPswe/PS1dE9 transgenic Mice | AD | NMN | Every other day for 28 days | 100 mg/kg s.c | MWM and Passive Avoidance | Inhibited JNK activation, Aβ and cognition deficits↓ |
Vakilinezhad et al. [26] | Male Sprague–Dawley Rat | AD | NAM | Every other day | i.p | MWM | Cognition impairment ↓ |
Green et al. [27] | 3xTg-AD Mice | AD | NAM | 4 months | 200 mg/kg. drinking water | MWM, NOR, and Passive Avoidance | Not affect Aβ pathology, Thr231, phosphorylated tau, and monoubiquitinated tau ↓ , improve spatial learning |
Rehman et al. [18] | Male C57BL/12N Mice | AD | NAM | 7 days | 250 mg/kg i.p | MWM and Y-Maze | Memory impairments ↓, oxidative stress ↓ , neuronal cell, and inflammation ↓ |
Xie et al. [28] | Male Mice | AD | NR | 3 months | 2.5 g/kg food | Open field, Y-Maze test, EPM, NOR, and Fear-conditioning | Improved the short-term spatial memory of aged mice, and the contextual fear memory of AD mice, accumulation of Aβ ↓ and the migration of astrocytes to Aβ ↓, activation of astrocytes ↓, and elevation of serum NAMPT of aged mice |
Gong et al. [29] | Tg2576 Mice | AD | NR | 3 months | 250 mg/kg, drinking water | NOR | NAD+ and PGC-1a ↑, improved synaptic plasticity, BACE1 levels and Aβ production |
Hou et al. [12] | Male and female adult Mice | AD | NR | 6 months | 12 mM in their drinking water | MWM, NOR, Y-Maze, and Fear-conditioning | Neuroinflammation, pTau,DNA damage, and synaptic dysfunction↓ and sirtuins activity↑ |
Wang et al. [30] | Male Wistar Rat | AD | NMN | 10 days | 500 mg/kg, i.p | MWM and Open field | Cognition function, neuron survival, and energy metabolism ↑ , ROS↓ |
Yang et al. [31] | Male Mice | VAD | NAM | 0, 2, 6 or 12Â h after the first and second injections of MPTP | 500Â mg/kg i.p | Step-down passive avoidance test and Step-through active avoidance test | Restored learning and memory |
Zhao et al. [15] | Male Sprague–Dawley Rat | VAD | NAD+ | 8 weeks | 250 μg/g i.p | MWM | Cognitive deficits and neuroinflammation ↓ |
Peterson et al. [32] | Male Sprague–Dawley Rat | TBI | NAM | 3 days | 75 mg/kg, i.p | MWM | Diminished tissue loss in the injured cortex and ipsilateral |
Hoane et al. [33] | Sprague–Dawley Rat | TBI | NAM | 15 min, 4 h, or 8 h post-injury, followed by five boosters at 24 h intervals | 50 mg/kg, i.p | MWM | Improved working memory |
Swan et al. [34] | Male Sprague–Dawley Rat | TBI | NAM | Single dose after CCI | 500 mg/kg or 50 mg/kg, i.p | MWM | NAM (50 mg/kg) appeared to have no effect, 500-mg/kg dose worsened performance, not reduce reactive gliosis and edema |
Haar et al. [35] | Male Sprague–Dawley Rat | TBI | NAM | 30 days | 50 mg/kg s.c | MWM | Improved reference memory and decreased lesion size |
Haar et al. [36] | Male Long-Evans Rat | TBI | NAM | Starting at 2Â h post-surgery and then at 12, 24, 36, 48, 60 and 72Â h | 150Â mg/kg, i.p | MWM | Improved retraining on the discrimination task |
Shear et al. [37] | Male Sprague–Dawley Rat | TBI | NAM | 15 min and 24 h after injury | 50 or 500 mg/kg i.v | MWM | Reduced GFAP levelsand improve working memory |
Hoane et al. [38] | Sprague–Dawley Rat | TBI | NAM | 15 min and 24 h post-FPI | 500 or 50 mg/kg; i.p | MWM | High dose prevented of behavioral deficits and decreased GFAP expression |
Hao et al. [39] | Wistar Rat | Schizophrenia | NAM | 30 days | 100 mg/kg, i.p | NOR and Barnes maze test | IL-1β, TNF-α, and IL-6 expression, and microglial activation↓ |
Hao et al. [40] | Wistar Rat | Schizophrenia | NAM | 30 days | 100 mg/kg gavage | NOR and Barnes maze test | Neuronal apoptosis and microglial over-activation ↓ and cognition function↑ |
Hee Jae Lee and Soo Jin Yang. [19] | ICR Male Mice | Diabetes | NR | Six weeks | 400 mg/kg, gavage | Y-Maze | Brain inflammation ↓ and Cognitive function↑ |
Jangra et al. [41] | Sprague–Dawley Rat | Diabetes | NAM | 14 days | 300 and 1000 mg/kg, s.c | Passive avoidance and open field | Oxidative stress–PARP overactivation ↓, Glutamate levels ↑, GABA levels ↓, ameliorated the reduction in hippocampal AChE level |
Chandrasekaran et al. [14] | Male Sprague–Dawley Rat | Diabetes | NMN | 3 months | 100 mg/kg i.p | Y-Maze test | Memory impairment and hippocampal neurodegeneration ↓ and NAD+ levels↑ |
Wang et al. [42] | Male Sprague–Dawley Rat | Hypoglycemia | NMN | 7 days | 500 mg/kg, i.p | MWM | Reduced neuronal cell death, cognitive impairment, ROS, PARP-1 activation, and increased NAD+ and ATP levels |