scholarly journals Time-restricted feeding alters isoflurane-induced memory deficits

2020 ◽  
Vol 11 (1) ◽  
pp. 341-355
Author(s):  
Jia Song ◽  
Shuaishuai Chu ◽  
Xin Fang ◽  
Fangxia Xu ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Cognitive Dysfunction ◽  
Food Access ◽  
Memory Deficits ◽  
Daily Rhythm ◽  
Control Group ◽  
Restricted Feeding ◽  
Isoflurane Anaesthesia ◽  
Feeding Group ◽  
Night Feeding

AbstractFood consumption during the rest phase promotes circadian desynchrony, which is corrected with harmful physiological and mental disorders. Previously, we found that circadian desynchrony was involved in isoflurane-induced cognitive impairment. Here, we scheduled food access to modulate daily rhythm to examine its impact on isoflurane-induced cognitive impairments. Mice were randomly transferred to restricted feeding (RF) time groups: Control group (Zeitgeber time (ZT) 0–ZT24, ad libitum feeding), Day-Feeding group (ZT0–ZT12, misaligned feeding), and Night-Feeding group (ZT12–ZT24, aligned feeding). Then, some of them were subjected to 5 h of 1.3% isoflurane anaesthesia from ZT14 to ZT19 and were divided into the Control + Anes group, the Day-Feeding + Anes group, and the Night-Feeding + Anes group. Mini-Mitter was used to monitor the daily rhythm. Fear conditioning system was conducted to assess cognition of mice. We observed that the Night-Feeding group adapted to RF gradually, whereas the Day-Feeding group exhibited a disturbed daily rhythm. The Night-Feeding + Anes group exhibited a partially enhanced daily rhythm, whereas the Day-Feeding + Anes group exhibited sustained phase advances and diurnality score increase 7 days after isoflurane anaesthesia. Notably, in tests of hippocampus-dependent contextual memory, the Night-Feeding + Anes group demonstrated decreased deficits; the Day-Feeding + Anes group showed prolonged post-anaesthetic deficits 14 days after isoflurane anaesthesia. However, amygdala-dependent cued-fear conditioning post-anaesthesia was not altered by the RF schedule. In conclusion, we demonstrated that misaligned feeding disturbed the daily rhythm and led to persistent post-anaesthetic cognitive dysfunction. Aligned feeding enhanced the daily rhythm partially and improved post-anaesthetic cognitive dysfunction.

scholarly journals Neuronal damage and memory deficits after seizures are reversed by ascorbic acid?

2010 ◽  
Vol 68 (4) ◽  
pp. 579-585 ◽  
Author(s):  
Adriana da Rocha Tomé ◽  
Chistiane Mendes Feitosa ◽  
Rivelilson Mendes de Freitas
Keyword(s):  
Ascorbic Acid ◽  
Cognitive Dysfunction ◽  
Neuronal Damage ◽  
Memory Task ◽  
Memory Deficits ◽  
Reference Memory ◽  
Control Group ◽  
Hippocampal Region ◽  
Neuroprotective Effects ◽  
Epileptic Patients

The objective of the present study was to evaluate the neuroprotective effects of ascorbic acid (AA) in rats, against the neuronal damage and memory deficit caused by seizures. Wistar rats were treated with 0.9% saline (i.p., control group), ascorbic acid (500 mg/kg, i.p., AA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of ascorbic acid (500 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before of administration of ascorbic acid (AA plus pilocarpine group). After the treatments all groups were observed for 24 h. Pilocarpine group presented seizures which progressed to status epilepticus in 75% of the animals. Pretreatment with AA led to a reduction of 50% of this rate. Results showed that pretreatment with AA did not alter reference memory when compared to a control group. In the working memory task, we observed a significant day's effect with important differences between control, pilocarpine and AA plus pilocarpine groups. Pilocarpine and AA plus pilocarpine groups had 81 and 16% of animals with brain injury, respectively. In the hippocampus of pilocarpine animals, it was detected an injury of 60%. As for the animals tested with AA plus pilocarpine, the hippocampal region of the group had a reduction of 43% in hippocampal lesion. Our findings suggest that seizures caused cognitive dysfunction and neuronal damage that might be related, at least in part, to the neurological problems presented by epileptic patients. AA can reverse cognitive dysfunction observed in rats with seizures as well as decrease neuronal injury in rat hippocampus.

scholarly journals Amantadine Alleviates Postoperative Cognitive Dysfunction Possibly by Increasing Glial Cell Line-derived Neurotrophic Factor in Rats

2014 ◽  
Vol 121 (4) ◽  
pp. 773-785 ◽  
Author(s):  
Junfeng Zhang ◽  
Hongying Tan ◽  
Wei Jiang ◽  
Zhiyi Zuo
Keyword(s):  
Fear Conditioning ◽  
Cell Line ◽  
Glial Cell ◽  
Cognitive Dysfunction ◽  
Neurotrophic Factor ◽  
Postoperative Cognitive Dysfunction ◽  
Control Group ◽  
Intracerebroventricular Injection ◽  
Barnes Maze ◽  
Surgery Group

Abstract Background: Postoperative cognitive dysfunction is a clinical entity that is associated with poor outcome. We determined the effectiveness of amantadine in reducing surgery-induced cognitive impairment and the role of glial cell line-derived neurotrophic factor (GDNF) in this effect. Methods: Four-month old male Fischer 344 rats were subjected to right carotid exposure under intravenous anesthesia. Some rats received intraperitoneal injection of 25 mg/kg/day amantadine for 3 days with the first dose at 15 min before the surgery or intracerebroventricular injection of GDNF or an anti-GDNF antibody at the end of surgery. One week later, rats were started to be tested by Barnes maze and fear conditioning. Hippocampus was harvested at 6 h, 24 h or 10 days after the surgery for biochemical analysis. C8-B4 cells, a microglial cell line, were pretreated with 1 ng/ml GDNF for 30 min before being exposed to 5 ng/ml lipopolysaccharide for 2 h. Results: Surgery increased the time to identify the target box in the Barnes maze when tested 1 day [22 (median) (11–66) (interquartile range) of control group vs. 158 (29–180) of surgery group, n = 15, P = 0.022) or 8 days after the training sessions and reduced context-related freezing behavior in the fear conditioning test. These effects were attenuated by amantadine (25 (14–90), n = 15, P = 0.029 compared with surgery group at 1 day after the training sessions in Barnes maze) and intracerebroventricular GDNF. Amantadine increased GDNF that was co-localized with glial fibrillary acidic protein, an astrocytic marker, in the hippocampus. Intracerebroventricular injection of an anti-GDNF antibody but not the denatured antibody blocked the effects of amantadine on cognition. Surgery induced neuroinflammation that was inhibited by amantadine. Lipopolysaccharide increased interleukin 1β production from C8-B4 cells. This effect was inhibited by GDNF. Conclusions: Our results suggest that amantadine attenuated surgery-induced learning and memory impairment. This effect may be mediated by GDNF via inhibition of neuroinflammation.

scholarly journals Time-restricted feeding improves blood glucose and insulin sensitivity in overweight patients with type 2 diabetes: a randomised controlled trial

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Tingting Che ◽  
Cheng Yan ◽  
Dingyuan Tian ◽  
Xin Zhang ◽  
Xuejun Liu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Control Group ◽  
Model Assessment ◽  
Restricted Feeding ◽  
Feeding Group

Abstract Background Time-restricted feeding is an emerging dietary intervention that is becoming increasingly popular. There are, however, no randomised clinical trials of time-restricted feeding in overweight patients with type 2 diabetes. Here, we explored the effects of time-restricted feeding on glycaemic regulation and weight changes in overweight patients with type 2 diabetes over 12 weeks. Methods Overweight adults with type 2 diabetes (n = 120) were randomised 1:1 to two diet groups: time-restricted feeding (n = 60) or control (n = 60). Sixty patients participated in a 10-h restricted feeding treatment program (ad libitum feeding from 8:00 to 18:00 h; fasting between 18:00 and 8:00 h) for 12 weeks. Results Haemoglobin A1c and body weight decreased in the time-restricted feeding group (− 1.54% ± 0.19 and − 2.98 ± 0.43 kg, respectively) relative to the control group over 12 weeks (p < 0.001). Homeostatic model assessment of β-cell function and insulin resistance changed in the time-restricted feeding group (0.73 ± 0.21, p = 0.005; − 0.51 ± 0.08, p = 0.02, respectively) compared with the control group. The medication effect score, SF-12 score, and the levels of triglycerides, total cholesterol and low-density lipoprotein cholesterol were improved in the time-restricted feeding group (− 0.66 ± 0.17, p = 0.006; 5.92 ± 1.38, p < 0.001; − 0.23 ± 0.08 mmol/L, p = 0.03; − 0.32 ± 0.07 mmol/L, p = 0.01; − 0.42 ± 0.13 mmol/L, p = 0.02, respectively) relative to the control group. High-density lipoprotein cholesterol was not significantly different between the two groups. Conclusion These results suggest that 10-h restricted feeding improves blood glucose and insulin sensitivity, results in weight loss, reduces the necessary dosage of hypoglycaemic drugs and enhances quality of life. It can also offer cardiovascular benefits by reducing atherosclerotic lipid levels. Trial registration: This study was registered with the Chinese Clinical Trial Registry (ChiCTR-IPR-15006371).

The effect of 4-h versus 6-h time restricted feeding on sleep quality, duration, insomnia severity and obstructive sleep apnea in adults with obesity

2021 ◽  
pp. 026010602110023
Author(s):  
Sofia Cienfuegos ◽  
Kelsey Gabel ◽  
Faiza Kalam ◽  
Mark Ezpeleta ◽  
Vicky Pavlou ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Quality ◽  
Sleep Onset ◽  
Control Group ◽  
Sleep Onset Latency ◽  
Restricted Feeding ◽  
Wake Time ◽  
Obstructive Sleep ◽  
Insomnia Severity

Background: Time restricted feeding (TRF) involves deliberately restricting the times during which energy is ingested. Preliminary findings suggest that 8–10-h TRF improves sleep. However, the effects of shorter TRF windows (4–6 h) on sleep, remain unknown. Aims: This study compared the effects of 4-h versus 6-h TRF on sleep quality, duration, insomnia severity and the risk of obstructive sleep apnea. Methods: Adults with obesity ( n = 49) were randomized into one of three groups: 4-h TRF (eating only between 3 and 7 p.m.), 6-h TRF (eating only between 1 and 7 p.m.), or a control group (no meal timing restrictions) for 8 weeks. Results: After 8 weeks, body weight decreased ( p < 0.001) similarly by 4-h TRF (–3.9 ± 0.4 kg) and 6-h TRF (–3.4 ± 0.4 kg), versus controls. Sleep quality, measured by the Pittsburgh Sleep Quality Index (PSQI), did not change by 4-h TRF (baseline: 5.9 ± 0.7; week 8: 4.8 ± 0.6) or 6-h TRF (baseline: 6.4 ± 0.8; week 8: 5.3 ± 0.9), versus controls. Wake time, bedtime, sleep duration and sleep onset latency also remained unchanged. Insomnia severity did not change by 4-h TRF (baseline: 4.4 ± 1.0; week 8: 4.7 ± 0.9) or 6-h TRF (baseline: 8.3 ± 1.2; week 8: 5.5 ± 1.1), versus controls. Percent of participants reporting obstructive sleep apnea symptoms did not change by 4-h TRF (baseline: 44%; week 8: 25%) or 6-h TRF (baseline: 47%; week 8: 20%), versus controls. Conclusion: These findings suggest that 4- and 6-h TRF have no effect on sleep quality, duration, insomnia severity, or the risk of obstructive sleep apnea.

scholarly journals Study of cognitive functions in major idiopathic interstitial pneumonias

2020 ◽  
Vol 14 (1) ◽  
Author(s):  
Mohamed W. Zakaria ◽  
Reem I. El-Korashy ◽  
Mostafa O. Shaheen ◽  
Samah Selim ◽  
Kwashi J. Amum
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Cognitive Dysfunction ◽  
Mini Mental State Examination ◽  
Mmse Score ◽  
Control Group ◽  
Healthy Individuals ◽  
Co Morbidity ◽  
Impaired Lung Function ◽  
State Examination

Abstract Background Cognitive dysfunction in idiopathic interstitial pneumonia (IIP) is an important clinical co-morbidity that is associated with impaired lung function. The aim of the work is to assess cognitive function in major IIP and to find out the relation between cognitive dysfunction and the oxygenation parameters. Results Fifty individuals were involved in the study; 30 patients with major IIP and 20 healthy individuals. Patients with IIP had significantly lower mini mental state examination (MMSE) score compared to the control group (P < 0.001). Wechsler Deterioration Index (WDI) revealed that 33.3% (n = 10) of the patients with IIP had sure cognitive impairment and 26.6% (n = 8) had ongoing cognitive deterioration. Patients with idiopathic pulmonary fibrosis (IPF) had lower cognitive function than other IIP. Conclusion There is an impairment of cognitive function in patients with major IIP, particularly in IPF, as measured by WDI and MMSE. Further large studies are needed to assess the possible predictors of cognitive impairment and their effects on the patients’ outcome.

A cAMP analog reverses contextual and tone memory deficits induced by a PKA inhibitor in Pavlovian fear conditioning

2013 ◽  
Vol 105 ◽  
pp. 177-182 ◽  
Author(s):  
Ehsan Nassireslami ◽  
Parmida Nikbin ◽  
Borna Payandemehr ◽  
Elham Amini ◽  
Mojdeh Mohammadi ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Memory Deficits ◽  
Pavlovian Fear Conditioning ◽  
Camp Analog

Combined Memory Training: An Approach for Episodic Memory Deficits in Traumatic Brain Injury

2021 ◽  
Vol 30 (2S) ◽  
pp. 920-932
Author(s):  
Elisabeth Cochran D'Angelo ◽  
Beth A. Ober ◽  
Gregory K. Shenaut
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Treatment Group ◽  
Episodic Memory ◽  
Semantic Memory ◽  
Memory Deficits ◽  
Control Group ◽  
Wait List ◽  
Wait List Control Group ◽  
Wait List Control

Purpose The study aimed to test a combination of semantic memory and traditional episodic memory therapies on episodic memory deficits in adults with traumatic brain injury. Method Twenty-five participants who had been diagnosed with traumatic brain injury and had episodic memory deficits were randomly assigned either to a combined memory treatment group ( n = 16) or to a wait-list control group ( n = 9). Before and after treatment, they completed standardized neuropsychological testing for episodic memory and related cognitive domains, including the California Verbal Learning Test–Second Edition, the Controlled Oral Word Association Test, the University of Southern California Repeatable Episodic Memory Test, the Wechsler Abbreviated Scale of Intelligence–Second Edition Matrices, the Test of Everyday Attention, the Memory Assessment Clinics Self-Rating Scale, the Expressive Vocabulary Test–Second Edition, and the Story Recall subtest from the Rivermead Behavioural Memory Test. In addition to a traditional episodic memory therapy, the treatment group received a novel semantic memory–focused therapy, which involved participants finding meaningful connections between diverse concepts represented by sets of two or three words. Results The treatment group demonstrated statistically significant improvement in memory for list learning tasks, and there was a significant difference from pretest to posttest between the treatment group and the wait-list control group. Clinical significance was demonstrated for the treatment group using minimally important difference calculations. Conclusion Combined memory therapy resulted in significant improvements in episodic memory, semantic memory, and attention, in comparison to no treatment. Supplemental Material https://doi.org/10.23641/asha.14049968

scholarly journals Effects of L-655,708 on expression changes of GABA, glutamate, and beta-endorphin induced by propofol anesthesia in rats

2018 ◽  
Vol 16 ◽  
pp. 205873921879670
Author(s):  
Jin Wang ◽  
Xinyi Li ◽  
Huisheng Wu ◽  
Jianjuan Ke ◽  
Zongze Zhang ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Cognitive Dysfunction ◽  
Sham Group ◽  
Postoperative Cognitive Dysfunction ◽  
Expression Level ◽  
Control Group ◽  
Beta Endorphin ◽  
Anesthetized Rats ◽  
Significant Difference ◽  
Dentate Gyrus Region

Anesthetics are considered to be one of the important inducing factors of postoperative cognitive dysfunction (POCD). The hippocampal region of the rat is one of the action sites of general anesthesia drugs. L 655,708, a reverse agonist of gamma aminobutyric acid (GABA) receptor, can significantly improve short-term memory dysfunction in mice after anesthetized with isoflurane. So the purpose of this study is to investigate the effects of L-655,708 on expression of GABA, glutamate (GLU), and beta-endorphin (β-EP) in the dentate gyrus region of the hippocampus and cognition of rats anesthetized with propofol. In all, 30 male Sprague–Dawley (SD) rats were randomly allocated into the control group, sham group, and L-655,708 group, with 10 in each group. The cognitive function of rats was measured by Morris water maze before and 1 h after administration. Then the rats were sacrificed for brain tissues. Immunohistochemistry was used to study the expression of GABA, GLU, and β-EP in the hippocampus of anesthetized rats in each group. Compared with the control group, the latency of the sham group and L-655,708 group were significantly prolonged after administration ( P < 0.05). However, L-655,708 could shorten the prolonged latency ( P < 0.05). There was no significant difference in times of accessing original platform area between the three groups before and after medication ( P > 0.05). The expression level of GABA in the dentate gyrus region of hippocampus of rats in the sham group was significantly higher than that in the control group ( P < 0.05), while the expression level in the L-655,708 group was significantly lower than that in the sham group ( P < 0.05). No significant difference was found in the expression of GLU in the dentate gyrus region of hippocampus of rats in each group ( P > 0.05). Compared with the control group, the expression of β-EP was significantly lower in the dentate gyrus region of the hippocampus of sham group rats ( P < 0.05). However, the expression of β-EP in the L-655,708 group was significantly higher than that in the sham group ( P < 0.05). Cognitive dysfunction in rats anesthetized with propofol may be related to high expression of GABA and low expression of β-EP in the hippocampus. The mechanism of L-655,708 in reducing the cognitive impairment in propofol anesthetized rats may be bound up with down-regulating the expression of GABA and increasing the expression of β-EP in the hippocampus.

scholarly journals Cognitive dysfunction in children with sleep disorders

2004 ◽  
Vol 62 (2a) ◽  
pp. 212-216 ◽  
Author(s):  
Luciane Bizari Coin de Carvalho ◽  
Lucila Bizari Fernandes do Prado ◽  
Luciana Silva ◽  
Marilaine Medeiros de Almeida ◽  
Tatiana Almeida e Silva ◽  
...  
Keyword(s):  
Sleep Disorders ◽  
Cognitive Dysfunction ◽  
Screening Test ◽  
Total Sample ◽  
Control Group ◽  
Lower Prevalence ◽  
Control Groups ◽  
Similar Frequency ◽  
Visual Motor ◽  
And Control

Sleep is basic for physical and cognitive development and some studies have suggested that there may be an association between sleep disorders (SD) and cognitive dysfunction (CD) in children. Little is known, however, about SD and cognition in 7-10-year-old children, a fact that motivated the present study. METHOD: We applied an SD questionnaire in 1180 children, 547 with SD and 633 without SD (CG), to assess cognition with a screening test (Bender Visual Motor Gestalt Test - BT). RESULTS: We observed a similar frequency of CD in the children with SD (39%) and that ot the CG (40%). The 8-year-old children with SD presented a lower prevalence of CD than the CG (SD=6%, n=6; CG=13%, n=16; p=0.04). CONCLUSION: The frequency of children with CD was equal in the study and control groups when considering the total sample (7- to 10-year-old children). In contrast to our expectations, the SD group of 8-year-old children presented a lower frequency of CD than the control group.

scholarly journals Acute transient cognitive dysfunction and acute brain injury induced by systemic inflammation occur by dissociable IL-1-dependent mechanisms

2017 ◽  
Author(s):  
Donal T. Skelly ◽  
Éadaoin W. Griffin ◽  
Carol L. Murray ◽  
Sarah Harney ◽  
Conor O’Boyle ◽  
...  
Keyword(s):  
Working Memory ◽  
Brain Injury ◽  
Cognitive Dysfunction ◽  
Systemic Inflammation ◽  
De Novo ◽  
Hippocampal Slices ◽  
Memory Deficits ◽  
Acute Brain Injury ◽  
Contextual Fear Conditioning

AbstractSystemic inflammation can impair cognition with relevance to dementia, delirium and post-operative cognitive dysfunction. Acute episodes of delirium also contribute significantly to rates of long-term cognitive decline, implying that de novo pathology occurs during these acute episodes. Whether systemic inflammation-induced acute dysfunction and acute brain injury occur by overlapping or discrete mechanisms has not been investigated. Here we show that systemic inflammation, induced by bacterial LPS, produces both working memory deficits and acute brain injury in the degenerating brain and that these occur by dissociable IL-1-dependent processes. In normal C57BL/6 mice, LPS (100μg/kg) did not affect working memory but robustly impaired contextual fear conditioning (CFC). However prior hippocampal synaptic loss left mice selectively vulnerable to LPS-induced working memory deficits. Systemically administered IL-1 receptor antagonist (IL-1RA) was protective against, and systemic IL-1β replicated, these working memory deficits. Although LPS-induced deficits still occured in IL-1RI-/- mice, systemic TNF-α was sufficient to induce similar deficits, indicating redundancy among these cytokines. Dexamethasone abolished systemic cytokine synthesis and was protective against working memory deficits despite failing to block brain IL-1β synthesis. Direct application of IL-1β to ex vivo hippocampal slices induced non-synaptic depolarisation and irrevesible loss of membrane potential in CA1 neurons from diseased animals and systemic LPS increased apoptosis in the degenerating brain, in an IL-1RI-/- dependent-fashion. The data suggest that LPS induces working memory dysfunction via circulating IL-1β but dysfunction leading to neuronal death is mediated by hippocampal IL-1β. The data suggest that acute systemic inflammation produces both reversible cognitive deficits, resembling delirium, and acute brain injury that may lead to long-term cognitive impairment but that these events are mechanistically dissociable. This would have significant implications for management of cognitive dysfunction and decline during acute illness.

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