The effects of glucagon-like peptide 1 receptor agonist (exenatide) on memory impairment, and anxiety- and depression-like behavior induced by REM sleep deprivation

TURAN, İnci; Özaçmak, Hale Sayan; Özaçmak, Veysel Haktan; ERGENÇ, Meryem; Bayraktaroğlu, Taner

doi:10.1016/j.brainresbull.2021.06.011

Cited by 23 publications

(12 citation statements)

References 61 publications

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“…Previous reports have shown that acute SD lasting 72 h or 2 months of CSD could induce anxiety‐like behaviors in mice. [ 31,32 ] We thought that depression‐like behavior in our study might have been delayed, as previously demonstrated. [ 33 ]…”

Section: Resultsmentioning

confidence: 55%

Farnesol Exerts Protective Effects against Chronic Sleep Deprivation‐Induced Cognitive Impairment via Activation SIRT1/Nrf2 Pathway in the Hippocampi of Adult Mice

Xie

Luo

et al. 2023

Molecular Nutrition Food Res

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Scope: Sleep deprivation (SD) negatively affects all aspects of health, with one serious consequence being impaired cognition. Farnesol (FOL) is a sesquiterpene synthesized by plants and mammals that has antioxidant, anti-inflammatory, and neuroprotective properties. This study investigates the mechanism underlying the neuroprotective effect of FOL on SD-induced cognitive impairment. Methods and results: Administration of FOL dramatically ameliorates chronic sleep deprivation (CSD)-induced cognitive impairment. In addition, FOL notably attenuates oxidative stress damage, pro-inflammatory cytokines activation, and microglial activation in the hippocampi of the CSD-exposed mice. Further examination indicates that administration of FOL after the CSD significantly increases the protein expressions of silent information regulator factor 2-related enzyme 1 (Sirt1), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and glutathione peroxidase 4 (Gpx4) in the hippocampi. Sirt1 agonist resveratrol (RES) has a similar neuroprotective effect, indicating that FOL could exert neuroprotective effects through the activation of the Sirt1/Nrf2 signaling pathway. Conclusion: The results reveal that FOL could protect against CSD-induced cognitive impairment by activating the Sirt1/Nrf2 signaling pathway.

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Section: Resultsmentioning

confidence: 55%

Farnesol Exerts Protective Effects against Chronic Sleep Deprivation‐Induced Cognitive Impairment via Activation SIRT1/Nrf2 Pathway in the Hippocampi of Adult Mice

Xie

Luo

et al. 2023

Molecular Nutrition Food Res

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“…Overall, only a limited number of studies (11.1%, n = 6/54) reported a lack of significant changes in any of the evaluated parameters compared to their respective control group [ 26 , 27 , 28 , 29 , 30 , 31 ]. Conversely, the overwhelming majority of results point to either increases or decreases in at least one parameter associated with oxidative stress.…”

Section: Resultsmentioning

confidence: 99%

Sleep Deprivation-Induced Oxidative Stress in Rat Models: A Scoping Systematic Review

et al. 2023

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Sleep deprivation is highly prevalent in the modern world, possibly reaching epidemic proportions. While multiple theories regarding the roles of sleep exist (inactivity, energy conservation, restoration, brain plasticity and antioxidant), multiple unknowns still remain regarding the proposed antioxidant roles of sleep. The existing experimental evidence is often contradicting, with studies pointing both toward and against the presence of oxidative stress after sleep deprivation. The main goals of this review were to analyze the existing experimental data regarding the relationship between sleep deprivation and oxidative stress, to attempt to further clarify multiple aspects surrounding this relationship and to identify current knowledge gaps. Systematic searches were conducted in three major online databases for experimental studies performed on rat models with oxidative stress measurements, published between 2015 and 2022. A total of 54 studies were included in the review. Most results seem to point to changes in oxidative stress parameters after sleep deprivation, further suggesting an antioxidant role of sleep. Alterations in these parameters were observed in both paradoxical and total sleep deprivation protocols and in multiple rat strains. Furthermore, the effects of sleep deprivation seem to extend beyond the central nervous system, affecting multiple other body sites in the periphery. Sleep recovery seems to be characterized by an increased variability, with the presence of both normalizations in some parameters and long-lasting changes after sleep deprivation. Surprisingly, most studies revealed the presence of a stress response following sleep deprivation. However, the origin and the impact of the stress response during sleep deprivation remain somewhat unclear. While a definitive exclusion of the influence of the sleep deprivation protocol on the stress response is not possible, the available data seem to suggest that the observed stress response may be determined by sleep deprivation itself as opposed to the experimental conditions. Due to this fact, the observed oxidative changes could be attributed directly to sleep deprivation.

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“…A recent study investigated the possible effects of EXE (0.5 μg/kg as a single dose for 9 days) in 40 male, rapid eye movement (REM) sleep-deprived Wistar rats; data for memory performance, anxiety/depression like behaviour, markers of oxidative stress, and synaptic protein levels were evaluated [75]. Memory performance was significantly reduced after REM sleep deprivation for 24 h. EXE administration improved memory performance for 24 and 48 h after REM sleep deprivation.…”

Section: Exenatidementioning

confidence: 99%

GLP-1 receptor agonists, SGLT-2 inhibitors, and obstructive sleep apnoea: can new allies face an old enemy?

Papaetis¹

2023

Arch Med Sci Atheroscler Dis

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Obstructive sleep apnoea (OSA) is the most common form of abnormal sleep pattern (ASP). It is characterized by narrowing of the upper airways (complete or partial) during sleep. Although continuous positive airway pressure is recognized as the gold standard treatment of OSA, unfortunately treatment adherence is often suboptimal and does not address the pathophysiological mechanisms governing its pathogenesis. Weight gain is an important risk factor for the development and worsening of OSA both in adults and in children. Meaningful and sustained weight reduction using lifestyle modifications alone remains difficult and challenging. Novel therapeutic strategies are vital because currently there are no approved pharmacological therapies. This paper explores thoroughly both preclinical and clinical studies that investigated the possible role of GLP-1 receptor agonists and SGLT-2 inhibitors in individuals with ASP and especially OSA. It also discusses their future role in order to ameliorate the global burden of OSA.

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The effects of glucagon-like peptide 1 receptor agonist (exenatide) on memory impairment, and anxiety- and depression-like behavior induced by REM sleep deprivation

Cited by 23 publications

References 61 publications

Farnesol Exerts Protective Effects against Chronic Sleep Deprivation‐Induced Cognitive Impairment via Activation SIRT1/Nrf2 Pathway in the Hippocampi of Adult Mice

Farnesol Exerts Protective Effects against Chronic Sleep Deprivation‐Induced Cognitive Impairment via Activation SIRT1/Nrf2 Pathway in the Hippocampi of Adult Mice

Sleep Deprivation-Induced Oxidative Stress in Rat Models: A Scoping Systematic Review

GLP-1 receptor agonists, SGLT-2 inhibitors, and obstructive sleep apnoea: can new allies face an old enemy?

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