The neuroprotective effect of vitamin E on chronic sleep deprivation-induced memory impairment: The role of oxidative stress

Alzoubi, Karem H.; Khabour, Omar F.; Rashid, Baraa Abu; Damaj, Imad; Salah, Heba

doi:10.1016/j.bbr.2011.09.017

Cited by 162 publications

(105 citation statements)

References 64 publications

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“…Earlier findings have reported that TSD and CPSR can decrease the activity of the antioxidant enzyme, ie, superoxide dismutase, in the brainstem and hippocampus (20). Based on this, it was hypothesized that these conditions, which activate the reactive oxygen species, can trigger cascade of events that facilitate the release of proinflammatory factors such as TNF-α and interleukins (IL-1 and IL-6) in different brain areas including the hippocampal region.…”

Section: Discussionmentioning

confidence: 98%

“…This is proposed to be at least partly due to the SD-resultant oxidative stress and meanwhile, is attributed to excessive corticosteroid levels, arguably, and the depression-like symptoms. SD is shown to considerably reduce the hippocampal antioxidant markers including glutathione, catalase, and superoxide dismutase (20,39), which negatively affect synaptic plasticity (20). On cellular level, sleep loss is shown to deleteriously affect synaptic plasticity (10,37).…”

Section: Discussionmentioning

confidence: 99%

“…Based on this, it was hypothesized that these conditions, which activate the reactive oxygen species, can trigger cascade of events that facilitate the release of proinflammatory factors such as TNF-α and interleukins (IL-1 and IL-6) in different brain areas including the hippocampal region. These are shown to attenuate the secretion of BDNF, which is a neuroprotective factor (9,20,22). Based on the established positive correlation between the circulating BDNF level and its secretion in various brain regions (51), we measured the serum BDNF.…”

Section: Discussionmentioning

confidence: 99%

“…Cognitive impairments can be seen following a chronic and continued exposure to an oxidative stress such as sleep loss. Some evidence have supported the SD-induced oxidative stress to the brain (19,20); however, the challenging question that should be addressed through molecular and genetic approaches is "how are sleep duration, sleep fragmentation, oxidative stress, and aging related?" It must determine whether the correlation between SD and neurodegenerative processes is indeed a causal one, and if it is, which mechanisms are involved.…”

Section: Introductionmentioning

confidence: 99%

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Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

et al. 2014

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Background: Sleep deprivation (SD) is emerging as a hot topic due to its health concerns. There are compelling reasons for a tremendous interest in neuroscience of sleep in recent years. Objectives: We aimed to evaluate how total sleep deprivation (TSD) and chronic partial sleep restriction (CPSR) might affect memory, anxiety-related behaviors, and the serum level of neurochemical markers such as brain-derived neurotrophic factor (BDNF) and corticosterone in a rat model. Materials and Methods:The disk-over-water (DOW) apparatus was employed to induce TSD and CPSR in male Wistar rats. The six study arms were as follows: cage control, 48 hours; cage control, seven days; DOW control, 48 hours; DOW control, seven days, TSD, and CPSR. Elevated plus-maze (EPM) was used to measure parameters (percentage of OAT, percentage of OAE, and locomotor activity) corresponding to anxiety and aversive memory. To measure serum BDNF and corticosterone levels using the ELISA method, blood samples were drawn from all rats on the fourth day at 5 P.M. Results: Our results demonstrated that TSD (P < 0.001) and CPSR (P < 0.001) induce memory impairment while exert anxiolytic-like effects in comparison with controls. Data showed that CPSR causes more memory impairment and anxiolytic-like effect in comparison to TSD (P < 0.001).These interventions however, did not alter the locomotor activity. Serum corticosterone level raised dramatically in CPSR rats in comparison to TSD and controls. Although the difference in serum BDNF level between TSD and CPSR arms was insignificant, it was markedly decreased in comparison to corresponding controls (P < 0.001). Conclusions: Our findings suggest the more pronounced effect of CPSR rather than TSD in impairing aversive memory and reducing anxiety. Decreased BDNF and peaked corticosterone level in TSD and CPSR suggest the probable inflammatory processes involved in possible insults to the brain caused by SD.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

et al. 2014

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“…Research has shown that vitamin E deficiency in cases such as aging, negatively affects learning and memory (32). Vitamin E, through its antioxidant activity in the hippocampus, inhibits memory loss and enhances learning (33)(34)(35). It has also been shown that ascorbic acid has positive effects on learning and memory (36,37).…”

Section: Discussionmentioning

confidence: 99%

Effect of the hydroalcoholic extract of pistachio on avoidance learning in male Wistar rats

Salari

Baloochi

Ali

et al. 2014

JOHE

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Received: December 2015, Accepted: January 2016Background: Pistachio is a plant that has long been cultivated in different parts of Iran. Pistachios are very nutritious and contain vitamins E and B, flavonoids, antioxidants, and carotenoids. Since the pistachio is effective in the treatment of some neurological disorders and is indigenous to Iran and considering the substantial use of this nut, it is necessary to investigate its effects on cognitive functions of the brain. This study aimed to investigate the effect of the hydroalcoholic extract of the pistachio on avoidance learning in rats. Materials and Methods: In this experimental study, 40 male Wistar rats (200-250 g body weight and 2-3 months of age) were divided into 4 groups. Dimethyl sulfoxide (DMSO) 2.5% (vehicle) and hydroalcoholic extract of the pistachio (10, 50, and 100 mg/kg/day) were administered by gavage for 14 days. Avoidance learning test was performed using the shuttle box. Results:The results of this study indicated a significant increase in the latency to enter the dark room in the groups receiving different doses of pistachio extract compared to vehicle treated group. Moreover, in the treated groups, time spent in the dark room was decreased compared to the vehicle group. The comparison of different doses of pistachio extract demonstrated that 100 mg/kg was more effective than 10 and 50 mg/kg of the extract. Conclusions:The results of this study indicated that treatment of rats with pistachio extract, which is rich in vitamins, flavonoids, and antioxidant compounds, can improve learning and memory.

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Vitamin E for Alzheimer's dementia and mild cognitive impairment

Farina

Isaac

Clark

et al. 2012

Cochrane Database of Systematic Reviews

101

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Background Vitamin E is a dietary compound that functions as an antioxidant scavenging toxic free radicals. Evidence that free radicals may contribute to the pathological processes of cognitive impairment including Alzheimer's disease has led to interest in the use of vitamin E in the treatment of mild cognitive impairment (MCI) and Alzheimer's dementia (AD). Objectives To assess the efficacy of vitamin E in the treatment of AD and prevention of progression of MCI to dementia. Search methods The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (ALOIS), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS as well as many trials databases and grey literature sources were searched on 25 June 2012 using the terms: "Vitamin E", vitamin-E, alpha-tocopherol. Selection criteria All unconfounded, double-blind, randomised trials in which treatment with vitamin E at any dose was compared with placebo for patients with AD and MCI. Data collection and analysis Two review authors independently applied the selection criteria and assessed study quality and extracted and analysed the data. For each outcome measure data were sought on every patient randomised. Where such data were not available an analysis of patients who completed treatment was conducted. It was not possible to pool data between studies owing to a lack of comparable outcome measure. Main results Only three studies met the inclusion criteria: two in an AD population and one in an MCI population. In the first of the AD studies (Sano 1996) the authors reported some benefit from vitamin E (2000 IU/day) with fewer participants reaching an end point of death, institutionalisation, change to a Clinical Dementia Rating (CDR) of three, or loss of two basic activities of daily living within two years. Of patients completing treatment, 58% (45/77) on vitamin E compared with 74% (58/78) on placebo reached one of the end 1 Vitamin E for Alzheimer's dementia and mild cognitive impairment (Review)

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The neuroprotective effect of vitamin E on chronic sleep deprivation-induced memory impairment: The role of oxidative stress

Cited by 162 publications

References 64 publications

Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

Effect of the hydroalcoholic extract of pistachio on avoidance learning in male Wistar rats

Vitamin E for Alzheimer's dementia and mild cognitive impairment

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