scholarly journals Effects of Memantine in a Mouse Model of Postoperative Cognitive Dysfunction

2019 ◽  
Vol 9 (3) ◽  
pp. 24 ◽  
Author(s):  
Ahmad Almahozi ◽  
Mohamed Radhi ◽  
Suja Alzayer ◽  
Amer Kamal
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Dysfunction ◽  
Animal Studies ◽  
Postoperative Cognitive Dysfunction ◽  
Tail Suspension Test ◽  
Morris Water Maze Test ◽  
Neuroinflammatory Response ◽  
Plus Maze

Persistent impairment in cognitive functioning postoperatively is reported by clinical and animal studies, and is labeled as postoperative cognitive dysfunction (POCD). Evidence points to an exaggerated neuroinflammatory response resulting from peripheral systemic inflammation after surgery, with subsequent cytokine-induced glutamatergic excitotoxicity and synaptic impairment. These immunological changes, among many others, are also observed in Alzheimer’s disease. Memantine is an N-methyl-D-aspartate receptor (NMDAR) antagonist commonly used to treat Alzheimer’s disease. Surprisingly, little research exists on the role of memantine in preventing POCD. The purpose of this study is to investigate the effects of memantine on a spectrum of cognitive functions postoperatively. Mice were divided into 3 groups and each received treatment for 4 weeks. Placebo groups received a placebo then underwent either a sham procedure or a laparotomy procedure. The memantine group received memantine hydrochloride then underwent a laparotomy procedure. Cognitive tests were performed on postoperative days (POD) 1 and 7. Compared to sham-operated mice, placebo groups that underwent a laparotomy procedure showed impaired memory in the Morris water maze test, higher anxiety-like behavior in the open field and the elevated plus maze tests, increased depression-like behavior in the tail suspension test, and lack of preference for social novelty in the three-chamber test. On the other hand, memantine-treated mice that underwent a laparotomy procedure showed enhanced memory on POD7, improved depression-like behavior on POD1 and POD7, enhanced preference for social novelty on POD1, and no improvement in anxiety-like behavior. These findings suggest a potential protective effect of memantine in mice postoperatively on memory, depression-like behavior, and preference for social novelty.

scholarly journals Coffee polyphenols prevent cognitive dysfunction and suppress amyloid β plaques in APP/PS2 transgenic mouse

2018 ◽  
Author(s):  
Keiko Ishida ◽  
Masaki Yamamoto ◽  
Koichi Misawa ◽  
Noriyasu Ota ◽  
Akira Shimotoyodome
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mouse ◽  
Cognitive Dysfunction ◽  
Amyloid Β ◽  
Morris Water Maze Test ◽  
Dependent Manner ◽  
Chlorogenic Acids ◽  
Caffeoylquinic Acid ◽  
Model Of Alzheimer’S Disease

AbstractEpidemiological studies have found that habitual coffee consumption may reduce the risk of Alzheimer’s disease. Coffee contains numerous phenolic compounds (coffee polyphenols) such as chlorogenic acids. However, evidence demonstrating the contribution of chlorogenic acids in preventing cognitive dysfunction induced by Alzheimer’s disease is limited. In this study, we investigated the effect of chlorogenic acids on prevention of cognitive dysfunction in APP/PS2 transgenic mouse model of Alzheimer’s disease. Five-week-old APP/PS2 mice were administered a diet supplemented with coffee polyphenols daily for 5 months. The memory and cognitive function of mice was determined using the novel object recognition test, the Morris water maze test, and the step-through passive avoidance test. We found that chronic treatment with coffee polyphenols prevented cognitive dysfunction and significantly reduced hippocampal Aβ deposition. We then determined the effect of 5-caffeoylquinic acid, one of the primary components of coffee polyphenols, on Aβ formation. 5-Caffeoylquinic acid did not inhibit Aβ fibrillation, but degraded Aβ fibrils in a dose-dependent manner. In conclusion, these results demonstrate that coffee polyphenols prevented cognitive deficits and alleviated Aβ plaque deposition via disaggregation of Aβ in APP/PS2 mouse.

Bilberry anthocyanins improve neuroinflammation and cognitive dysfunction in APP/PSEN1 mice via the CD33/TREM2/TYROBP signaling pathway in microglia

2020 ◽  
Vol 11 (2) ◽  
pp. 1572-1584 ◽  
Author(s):  
Jing Li ◽  
Runtian Zhao ◽  
Yuhan Jiang ◽  
Yi Xu ◽  
Huan Zhao ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathway ◽  
Cognitive Dysfunction ◽  
Beta Amyloid ◽  
Amyloid Protein ◽  
Neuroinflammatory Response ◽  
Beta Amyloid Protein

Bilberry anthocyanins reversed Alzheimer's disease-induced cognitive disfunction, reduced neuroinflammatory response and induced phagocytosis to beta-amyloid protein plaques via activating microglia.

Oligodendrocyte generation and maturation in the hippocampus may be a target of fluoxetine for delaying cognitive dysfunction during early Alzheimer’s disease

2020 ◽  
Author(s):  
Yi Zhang ◽  
Feng-lei Chao ◽  
Lei Zhang ◽  
Chun-ni Zhou ◽  
Lin Jiang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Dysfunction ◽  
Laser Scanning ◽  
Morris Water Maze Test ◽  
Spatial Learning And Memory ◽  
Abnormal Increase ◽  
Early Alzheimer’S Disease ◽  
Expression And Activity ◽  
Novel Therapeutic

Abstract Background In the central nervous system, the myelin sheath and the cells that form it—oligodendrocytes—are associated with cognitive function. Oligodendrocyte abnormalities is an important early pathogenic factor of Alzheimer’s disease (AD). However, it is unclear how the hippocampal oligodendrocytes change during early AD and whether early hippocampal oligodendrocyte pathology in AD can be regarded as a novel therapeutic target.Methods To address these questions, we subjected APP/PS1 transgenic mice and nontransgenic littermates to fluoxetine interventions for 2 months. After intervention, the behaviors were assessed with open field test and Morris water maze test, the changes in hippocampal oligodendrocytes were studied using immunohistochemistry, immunofluorescence, unbiased stereological techniques, laser scanning confocal microscope and molecular biotechnology.Results AD mice had an abnormally high number of oligodendrocyte lineage cells (Olig2 + cells) but lower expressions of CNPase and MBP and fewer mature oligodendrocytes (CNPase + cells) in the hippocampus than nontransgenic littermates. Among the oligodendrocyte lineage cells in the hippocampus of AD mice, fewer were mature oligodendrocytes and more were immature oligodendrocytes. Furthermore, decreased expression of SOX10, increased expression of LINGO1 and its ligands, and increased expression and activity of GSK3β might work together to induce oligodendrocyte maturation disorder in the hippocampus of AD mice. Fluoxetine treatment not only delayed the deficiencies in spatial learning and memory ability but also rescued the decrease in mature oligodendrocytes and reversed the abnormal increase in oligodendrocyte lineage cells in the hippocampus of AD mice, potentially by inhibiting the expression of LINGO1 and its ligands, inhibiting the expression and activity of GSK3β, reducing the levels of soluble Aβ40 and Aβ42, reducing β-amyloid plaques, reducing the ratio of oligodendrocytes expressing p16, promoting the expression of SOX10 in oligodendrocytes and promoting the maturation of newborn oligodendrocytes, and then increasing the number of mature oligodendrocytes in the hippocampus of AD mice.Conclusion There is oligodendrocyte maturation disorder in the hippocampus during early AD mice. Fluoxetine exposure during early AD may delay cognitive dysfunction by affecting hippocampal oligodendrocyte generation and maturation. Early hippocampal oligodendrocyte generation and maturation in AD might be regarded as a novel therapeutic target.

scholarly journals Verum- versus Sham-Acupuncture on Alzheimer’s Disease (AD) in Animal Models: A Preclinical Systematic Review and Meta-Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-21 ◽  
Author(s):  
Fei-Yi Zhao ◽  
Qiang-Qiang Fu ◽  
Zhen Zheng ◽  
Li-Xing Lao ◽  
Hua-Ling Song ◽  
...  
Keyword(s):  
Systematic Review ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Animal Studies ◽  
Memory Performance ◽  
Meta Analysis ◽  
Sham Acupuncture ◽  
Health Condition ◽  
Morris Water Maze Test

Background. Alzheimer’s disease (AD) is a common health condition affecting senile people and leads to severe cognitive dysfunctions. Acupuncture has been shown to be a possible alternative natural remedy for AD in some animal studies. Objective. To perform a systematic review to identify the effect of verum-acupuncture compared with sham-acupuncture on learning and memory performance among animal models of AD. Methods. Experimental animal studies of treating AD via verum- and sham- acupuncture were searched in nine electronic databases, including Sciverse ScienceDirect, PubMed, Springer, Ebsco Medline, AMED, EMBASE (Elsevier), Scopus (Elsevier), PsycINFO (ProQuest), and OVID from the dates of the databases’ inception to June 2019. The Morris water maze test was considered as an outcome measure. The software Revman 5.3 and Stata 16.0 were used to conduct the meta-analysis. Heterogeneity was examined by using I2 statistics. The publication bias was assessed via Begg’s test by Stata 16.0. Results. Twelve studies involving 229 animals met the inclusion criteria. Most of the studies had a moderate quality according to SYRCLE's risk of bias tool for animal studies. The results of the meta-analysis indicated that verum-acupuncture could reduce the escape latency (MD = −12.90, 95% CI (−17.08, −8.71), p<0.001) and increase the time spent in the original platform quadrant (MD = 7.28, 95% CI (4.23, 10.33), p<0.001) and frequency of the crossing former platform (MD = 2.01, 95% CI (1.53, 2.50), p<0.001) compared with the sham-acupuncture. Conclusions. Acupuncture is effective in improving cognitive functions in AD animal models, and this benefit is more than just a placebo effect. Further clinical trials are needed to confirm the findings.

scholarly journals Alzheimer’s disease and cytokine IL-10 gene polymorphisms: is there an association?

2017 ◽  
Vol 75 (9) ◽  
pp. 649-656 ◽  
Author(s):  
Carolina Antunes Magalhães ◽  
Maria das Graças Carvalho ◽  
Lirlândia Pires de Sousa ◽  
Paulo Caramelli ◽  
Karina Braga Gomes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Dysfunction ◽  
Current Literature ◽  
Gene Polymorphisms ◽  
Inflammatory Mediator ◽  
Interleukin 10 ◽  
Inflammatory Biomarkers ◽  
Inflammatory Molecule

ABSTRACT Alzheimer’s disease (AD) is the most common form of dementia. In the last 15 years, a new theory has proposed the autoimmune mechanism as a trigger for AD. Studies on the association between AD and inflammatory biomarkers have yielded controversial results. Interleukin-10 (IL-10), an anti-inflammatory mediator, has been pointed out as one of the main cytokines associated with the occurrence of AD. Moreover, treatment that increases IL-10 levels could be a potential therapy for AD, since this cytokine acts on amyloid and pro-inflammatory molecule reduction. Based on the current literature, this study reviews evidence regarding the role of IL-10 polymorphisms in the context of AD, which has been shown to be of paramount importance for attenuating neuroinflammation, cognitive dysfunction and neurodegeneration.

scholarly journals Role of Scavenger Receptors in Glia-Mediated Neuroinflammatory Response Associated with Alzheimer’s Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Francisca Cornejo ◽  
Rommy von Bernhardi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Degeneration ◽  
Scavenger Receptor ◽  
Scavenger Receptors ◽  
Immune Functions ◽  
Neuroinflammatory Response ◽  
Disease Therapy ◽  
The Brain

It is widely accepted that cells serving immune functions in the brain, namely, microglia and astrocytes, are important mediators of pathological phenomena observed in Alzheimer’s disease. However, it is unknown how these cells initiate the response that results in cognitive impairment and neuronal degeneration. Here, we review the participation of the immune response mediated by glial cells in Alzheimer’s disease and the role played by scavenger receptors in the development of this pathology, focusing on the relevance of class A scavenger receptor (SR-A) for Aβclearance and inflammatory activation of glial cell, and as a potential target for Alzheimer’s disease therapy.

scholarly journals 18F-florbetapir Positron Emission Tomography–determined Cerebral β-Amyloid Deposition and Neurocognitive Performance after Cardiac Surgery

2018 ◽  
Vol 128 (4) ◽  
pp. 728-744 ◽  
Author(s):  
Rebecca Y. Klinger ◽  
Olga G. James ◽  
Salvador Borges-Neto ◽  
Tiffany Bisanar ◽  
Yi-Ju Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Cognitive Dysfunction ◽  
Postoperative Cognitive Dysfunction ◽  
Amyloid Deposition ◽  
Emission Tomography ◽  
Amyloid Burden ◽  
Neurocognitive Performance ◽  
Positron Emission

Abstract Background Amyloid deposition is a potential contributor to postoperative cognitive dysfunction. The authors hypothesized that 6-week global cortical amyloid burden, determined by 18F-florbetapir positron emission tomography, would be greater in those patients manifesting cognitive dysfunction at 6 weeks postoperatively. Methods Amyloid deposition was evaluated in cardiac surgical patients at 6 weeks (n = 40) and 1 yr (n = 12); neurocognitive function was assessed at baseline (n = 40), 6 weeks (n = 37), 1 yr (n = 13), and 3 yr (n = 9). The association of 6-week amyloid deposition with cognitive dysfunction was assessed by multivariable regression, accounting for age, years of education, and baseline cognition. Differences between the surgical cohort with cognitive deficit and the Alzheimer’s Disease Neuroimaging Initiative cohorts (normal and early/late mild cognitive impairment) was assessed, adjusting for age, education, and apolipoprotein E4 genotype. Results The authors found that 6-week abnormal global cortical amyloid deposition was not associated with cognitive dysfunction (13 of 37, 35%) at 6 weeks postoperatively (median standard uptake value ratio [interquartile range]: cognitive dysfunction 0.92 [0.89 to 1.07] vs. 0.98 [0.93 to 1.05]; P = 0.455). In post hoc analyses, global cortical amyloid was also not associated with cognitive dysfunction at 1 or 3 yr postoperatively. Amyloid deposition at 6 weeks in the surgical cohort was not different from that in normal Alzheimer’s Disease Neuroimaging Initiative subjects, but increased over 1 yr in many areas at a rate greater than in controls. Conclusions In this study, postoperative cognitive dysfunction was not associated with 6-week cortical amyloid deposition. The relationship between cognitive dysfunction and regional amyloid burden and the rate of postoperative amyloid deposition merit further investigation.

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