Possible mechanism involved in sleep deprivation-induced memory
dysfunction

Kalonia, Harikesh; Bishnoi, Mahendra; Kumar, Awanish

doi:10.1358/mf.2008.30.7.1186074

Cited by 13 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, from this first experiment, we can also hypothesize that values stored in reference memory are impaired by sleep deprivation. This would be congruent with data reporting that sleep deprivation impairs reference memory in rats (Kalomia, Bishnoi, & Kular, 2008;Smith, Conway, & Rose, 1998) as well as data from insomniacs who often complain of memory deficits, both suggesting that insomnia severity is related to a decrement in delayed recall (Schmidt, Richter, Gendolla, & Van Der Linden, 2010).…”

Section: Discussionsupporting

confidence: 89%

How does one night of sleep deprivation affect the internal clock?

Casini¹,

Ramdani-Beauvir²,

Burle³

et al. 2013

Neuropsychologia

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 89%

How does one night of sleep deprivation affect the internal clock?

Casini¹,

Ramdani-Beauvir²,

Burle³

et al. 2013

Neuropsychologia

View full text Add to dashboard Cite

“…While many factors may contribute to the mechanism for the observed changes during sleep eprivation [98], increased noradrenaline levels [99, 100] may play a role in reducing glymphatic fluid transport, as reported [27]. The causes of sleep deprivation are complex and multifactorial, which involves many biological factors, including metabolic and neurotransmitter changes [101, 102]. We use a milder procedure to induce sleep deprivation to minimize major changes.…”

Section: Discussionmentioning

confidence: 99%

Glymphatic distribution of CSF-derived apoE into brain is isoform specific and suppressed during sleep deprivation

Achariyar

Peng

et al. 2016

Mol Neurodegeneration

200

137

View full text Add to dashboard Cite

BackgroundApolipoprotein E (apoE) is a major carrier of cholesterol and essential for synaptic plasticity. In brain, it’s expressed by many cells but highly expressed by the choroid plexus and the predominant apolipoprotein in cerebrospinal fluid (CSF). The role of apoE in the CSF is unclear. Recently, the glymphatic system was described as a clearance system whereby CSF and ISF (interstitial fluid) is exchanged via the peri-arterial space and convective flow of ISF clearance is mediated by aquaporin 4 (AQP4), a water channel. We reasoned that this system also serves to distribute essential molecules in CSF into brain. The aim was to establish whether apoE in CSF, secreted by the choroid plexus, is distributed into brain, and whether this distribution pattern was altered by sleep deprivation.MethodsWe used fluorescently labeled lipidated apoE isoforms, lenti-apoE3 delivered to the choroid plexus, immunohistochemistry to map apoE brain distribution, immunolabeled cells and proteins in brain, Western blot analysis and ELISA to determine apoE levels and radiolabeled molecules to quantify CSF inflow into brain and brain clearance in mice. Data were statistically analyzed using ANOVA or Student’s t- test.ResultsWe show that the glymphatic fluid transporting system contributes to the delivery of choroid plexus/CSF-derived human apoE to neurons. CSF-delivered human apoE entered brain via the perivascular space of penetrating arteries and flows radially around arteries, but not veins, in an isoform specific manner (apoE2 > apoE3 > apoE4). Flow of apoE around arteries was facilitated by AQP4, a characteristic feature of the glymphatic system. ApoE3, delivered by lentivirus to the choroid plexus and ependymal layer but not to the parenchymal cells, was present in the CSF, penetrating arteries and neurons. The inflow of CSF, which contains apoE, into brain and its clearance from the interstitium were severely suppressed by sleep deprivation compared to the sleep state.ConclusionsThus, choroid plexus/CSF provides an additional source of apoE and the glymphatic fluid transporting system delivers it to brain via the periarterial space. By implication, failure in this essential physiological role of the glymphatic fluid flow and ISF clearance may also contribute to apoE isoform-specific disorders in the long term.Electronic supplementary materialThe online version of this article (doi:10.1186/s13024-016-0138-8) contains supplementary material, which is available to authorized users.

show abstract

“…It re ects the function of hippocampus [18]. Some studies have shown that the decline of memory function in mice may be related to the decrease of CAT and LPO content in brain [19].…”

Section: Discussionmentioning

confidence: 99%

Effect of Noni on memory impairment induced by hydrocortisone in mice

Zhang¹,

Liu²,

Hou³

et al. 2021

Preprint

View full text Add to dashboard Cite

Background Oxidative stress and memory impairment have been implicated, a common functional brain disease. Nuclear factor E2-related factor 2 (Nrf2) is highly induced in oxidative stress, indicating that Nrf2 is an emerging target of memory therapy. This study aimed to investigate the effect of Noni on brain memory impairment induced by hydrocortisone and its protection mechanism in mice. Methods Male Kuming mice were (n = 8/group) given hydrocortisone by gastric gavage for 14 consecutive days to establish the memory impairment model except for those in the control group. At the same day, the corresponding drugs were given by gastric gavage. The changes in ethology were examined. Brains were extracted and subjected to western blot analysis and biochemical analyses to assess the activities of oxidative stress. Results The middle and high-dose Noni groups ameliorated the ethology and the high-dose Noni group increased cerebral protein expressions of Nrf2, kelch-like ECH-associated protein 1 (KEAP1) and heme oxygenase-1 (HO-1), as compared to the model group. The arrangement of CA3 vertebral cells in hippocampus of mice was slightly compact and hyperchromatic and pyknosis were alleviated. Furthermore, the biochemical analyses showed the activities of related enzymes of oxidative stress in high-dose Noni group were increased. Conclusions Noni might be a powerful antioxidant that can protect nerve cell and may possess as a potential benefit for the treatment of memory impairment.

show abstract

Possible mechanism involved in sleep deprivation-induced memory dysfunction

Cited by 13 publications

References 0 publications

How does one night of sleep deprivation affect the internal clock?

How does one night of sleep deprivation affect the internal clock?

Glymphatic distribution of CSF-derived apoE into brain is isoform specific and suppressed during sleep deprivation

Effect of Noni on memory impairment induced by hydrocortisone in mice

Contact Info

Product

Resources

About