scholarly journals Jiao-Tai-Wan Improves Cognitive Dysfunctions through Cholinergic Pathway in Scopolamine-Treated Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-16
Author(s):  
Xin-Chen Wang ◽  
Yu-Min Xu ◽  
Hong-Ying Li ◽  
Chun-Ying Wu ◽  
Ting-Ting Xu ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Neuroprotective Effect ◽  
Learning Ability ◽  
Behavioral Experiments ◽  
Deficit Model ◽  
Y Maze ◽  
Medicine Prescription ◽  
Learning And Memory Deficit

Cognitive dysfunction is characterized as the gradual loss of learning ability and cognitive function, as well as memory impairment. Jiao-tai-wan (JTW), a Chinese medicine prescription including Coptis chinensis and cinnamon, is mainly used for the treatment of insomnia, while the effect of JTW in improving cognitive function has not been reported. In this study, we employed a scopolamine- (SCOP-) treated learning and memory deficit model to explore whether JTW could alleviate cognitive dysfunction. In behavioral experiments, Morris water maze, Y-maze, fearing condition test, and novel object discrimination test were conducted. Results showed that oral administration of JTW (2.1 g/kg, 4.2 g/kg, and 8.4 g/kg) can effectively promote the ability of spatial recognition, learning and memory, and the memory ability of fresh things of SCOP-treated mice. In addition, the activity of acetylcholinesterase (AChE) was effectively decreased; the activity of choline acetyltransferase (ChAT) and concentration of acetylcholine (Ach) were improved after JTW treatment in both hippocampus and cortex of SCOP-treated mice. JTW effectively ameliorated oxidative stress because of decreased the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) and increased the activities of superoxide dismutase (SOD) and catalase (CAT) in hippocampus and cortex. Furthermore, JTW promotes the expressions of neurotrophic factors including postsynaptic density protein 95 (PSD95) and synaptophysin (SYN) and brain-derived neurotrophic factor (BDNF) in both hippocampus and cortex. Nissl’s staining shows that the neuroprotective effect of JTW was very effective. To sum up, JTW might be a promising candidate for the treatment of cognitive dysfunction.

Curcumin Reduces Neuroinflammation and Improves the Impairments of Anesthetics on Learning and Memory by Regulating the Expression of miR-181a-5p

2021 ◽  
pp. 1-9
Author(s):  
Guizhen Liu ◽  
Yuchuan Sun ◽  
Fei Liu
Keyword(s):  
Cognitive Impairment ◽  
Protective Effect ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Inflammatory Cytokines ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Sprague Dawley Rats

<b><i>Objective:</i></b> The purpose of this study was to explore the role of curcumin (Cur) in isoflurane (ISO)-induced learning and memory dysfunction in Sprague-Dawley rats and further elucidate the mechanism of the protective effect produced by Cur. <b><i>Methods:</i></b> Rat models of cognitive impairment were established by inhaling 3% ISO. The Morris water maze test was used to assess the cognitive function of rats. ELISA and qRT-PCR were used to analyze the protein levels of pro-inflammatory cytokines and expression levels of miR-181a-5p, respectively. <b><i>Results:</i></b> Cur significantly improved the ISO-induced cognitive dysfunction in rats and alleviated the ISO-induced neuroinflammation. miR-181a-5p was overexpressed in ISO-induced rats, while Cur treatment significantly reduced the expression of miR-181a-5p. Overexpression of miR-181a-5p promoted the cognitive impairment and the release of inflammatory cytokines and reversed the neuroprotective effect of Cur. <b><i>Conclusion:</i></b> Cur has a protective effect on ISO-induced cognitive dysfunction, which may be achieved by regulating the expression of miR-181a-5p.

scholarly journals PENGARUH TRITERPEN TOTAL PEGAGAN (Centella asiatica (L) Urban) TERHADAP FUNGSI KOGNITIF BELAJAR DAN MENGINGAT PADA MENCIT JANTAN ALBINO (Mus musculus) YANG DIHAMBAT DENGAN SKOPOLAMIN

Molekul ◽  
2010 ◽  
Vol 5 (2) ◽  
pp. 89
Author(s):  
Herlina Herlina
Keyword(s):  
Cognitive Function ◽  
Learning And Memory ◽  
Mus Musculus ◽  
Memory Performance ◽  
Centella Asiatica ◽  
Positive Control ◽  
Negative Control ◽  
Learning Ability ◽  
Control Group ◽  
Albino Mice

Pegagan (Centella asiatica (L) Urban) has been described to posses CNS effects such as improving cognitive function, learning and memory. The aim of the research was to evaluate the effects of total triterpen’s pegagan extract on cognitive functions as the learning and memory performance in male albino mice (Mus musculus) inhibited by scopolamine. The research design was Complete Randomized Design (RAL) – factorial on thirty six mice divided into 4 groups. One control group received only aquabidest (negative control). Three treatment groups received total triterpen 16 mg/kg BW, 32 mg/kg BW orally and piracetam 500 mg/kg BW by intra peritoneally (positive control) for 21 days. Data indicating learning and memory process of all subjects were obtained from one-trial passive avoidance test. Data were analyzed by two way ANOVA and BNT (p<0,05). Result showed that total triterpen 32 mg/kg BW had significantly prolonged the retention time compared to control group indicating improvement in cognitive function (505,03 second vs -18,53 second) (p<0,05) and it was not significantly different to piracetam 500 mg/kg BW group (505,03 second vs 522,48 second) (p>0,05). In conclusion, total triterpen from pegagan (Centella asiatica (L) Urban) improved learning ability and memory of male albino mice (Mus musculus) even though, it was inhibited by scopolamine.

scholarly journals CZYH Alleviates β-Amyloid-Induced Cognitive Impairment and Inflammation Response via Modulation of JNK and NF-κB Pathway in Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Yuanyuan Deng ◽  
Lianzhi Ye ◽  
Cheng Yu ◽  
Caixia Yin ◽  
Jingshan Shi ◽  
...  
Keyword(s):  
Protein Expression ◽  
Learning And Memory ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Nissl Staining ◽  
Neuroinflammatory Response ◽  
Neuron Loss ◽  
Pharmacological Mechanism ◽  
Β Amyloid ◽  
Learning And Memory Deficit

Cu-Zhi-Yi-Hao (CZYH), an empirical formula of traditional Chinese medicine (TCM), has been used for amnesia treatment in clinical practice. However, its underlying pharmacological mechanism has not been fully illuminated. The current study was designed to investigate the neuroprotective effect of CZYH on a β-amyloid 25-35- (Aβ25-35-) induced learning and memory deficit rat model. CZYH (200, 400, or 800 mg/kg), donepezil (1.0 mg/kg), or distilled water was given to Aβ25-35-stimulated animals for 17 days consecutively. The Morris water maze test revealed that CZYH (400 or 800 mg/kg) administration improved the Aβ25-35-induced cognitive impairments in rats, and Nissl staining demonstrated that CZYH mitigated the Aβ-caused neuron loss. In addition, CZYH treatment markedly inhibited the activation of microglia as evidenced by a decreased level of IBA-1 and increased YM-1/2 protein expression. The protein expression levels of TNF-α, IL-1β, and COX-2 were also repressed by CZYH. Besides, CZYH treatment alleviated Aβ-induced IκB-α degradation and NF-κB p65 phosphorylation, as well as reduced the JNK phosphorylation level. In conclusion, the present study suggests that CZYH could improve learning and memory abilities and relieve neuron loss in Aβ25-35-induced rats, at least partly through inhibition of the neuroinflammatory response via inhibiting the JNK-dependent NF-κB activation, indicating that CZYH might be a promising formula for the treatment of AD.

scholarly journals Lentivirus-Carried microRNA-195 Rescues Memory Deficits of Alzheimer’s Disease Transgenic Mouse by Attenuating the Generation of Amyloid Plaques

2021 ◽  
Vol 12 ◽  
Author(s):  
Dan Su ◽  
Yani Chai ◽  
Junkai Yang ◽  
Xuqiao Wang ◽  
Ying Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Learning And Memory ◽  
Transgenic Mouse ◽  
New Drugs ◽  
Learning Ability ◽  
Gain Of Function ◽  
Memory Ability ◽  
Bace1 Level

Although lots of new drugs are developed to treat Alzheimer’s disease (AD), many clinical trials of monotherapy have failed to affect disease progression or symptoms compared with placebo. Recently, scientists believe that combination treatment is more promising than monotherapy. Previous studies found that microRNA-195 (miR-195) was down-regulated in the hippocampi and cortices of chronic brain hypoperfusion (CBH) rats and ApoE4(+/+) mice, and up-regulation of miR-195 can improve the declined cognitive function of ApoE4(+/+) mice and CBH rats by targeting multi-genes that are related to AD pathology, including amyloid precursor protein (APP) and β-site APP cleaving enzyme 1 (BACE1) genes. However, whether the gain-of-function of miR-195 could improve the impaired learning and memory ability of APP/PS1 transgenic mouse has not been reported. In this study, we stereotaxically injected lentiviral-carried miR-195 into the bilateral hippocampus of 4-month-old (4M) APP/PS1 mice. Morris water maze (MWM) was performed to detect the effect of miR-195 on the cognitive function of APP/PS1 mice after 1M, 2M, and 3M treatment. Western blot was used to detect the expression of APP, BACE1, and AT8. Aβ plagues were quantitatively assessed by immunofluorescence technique. We found that the declined cognitive phenotype of APP/PS1 mice occurred at the age of 6M, not at the age of 5M. And treatment of Lv-pre-miR-195 to APP/PS1 mice for 1M did not achieve any changes. Although Lv-pre-miR-195 treatment for 2M improved the declined learning ability of APP/PS1 mice, it did not affect the memory functions. However, Lv-pre-miR-195 treatment in APP/PS1 mice for 3M can effectively improve both the learning and memory ability of APP/PS1 mice at the age of 7M. Further studies demonstrated that gain-of-function of miR-195 by Lv-pre-miR-195 injection could inhibit the increased APP and AT8 expression of APP/PS1 mice but did not affect BACE1 level that was not changed in both hippocampus and cortex. By counting the number of Aβ plaques of different sizes, we found that Lv-pre-miR-195 treatment mainly reduced the number of Aβ plaques of less than 20 μm, but did not affect the number of Aβ plaques of greater than 50 μm. Taken together, the gain-of -function of miR-195 in the hippocampus can improve the cognition of APP/PS1 mice, probably by blocking the formation of Aβ plagues rather than clearing those that have already formed Aβ plagues.

Abstract TP118: Activation of Alpha-7 Nicotinic Acetylcholine Receptor Improved Long-Term Cognitive Function of Mice With Long-Bone Fracture and Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Kang Hou ◽  
Meng Wei ◽  
Meng Zhang ◽  
Zhanqiang Wang ◽  
Sonali Shaligram ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Dentate Gyrus ◽  
Acetylcholine Receptor ◽  
Cognitive Dysfunction ◽  
Nicotinic Acetylcholine Receptor ◽  
Neuronal Damage ◽  
Neuronal Injury ◽  
Nicotinic Acetylcholine ◽  
Y Maze

Introduction: Tibia fracture (BF) enhances stroke injury and when occurring 6 hrs before stroke (BF6+Stroke) causes long-lasting cognitive dysfunction in mouse. Activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) reduced neuroinflammation, neuronal injury and sensorimotor dysfunction in mice with BF one day after stroke (Stroke+1BF). Hypothesis: Activation of α-7 nAchR improves long-term cognitive function of BF6+Stroke mice. Methods: BF6+Stroke mice were randomly assigned to saline, PHA-568487 (α-7 nAchR agonist) and MLA (α-7 nAchR antagonist) treatment groups. The sensorimotor function were tested by adhesive removal and corner tests at 3 days, the cognitive function was tested by Y-maze weekly for 8 weeks and Novel Objective Recognition (NOR) at 8 weeks post-injuries. The neuronal damage, neuroinflammaiton, neurogenesis were analyzed 3 and/or 8 weeks post-injuries. Results: Similar to Stroke+1BF mice, PHA reduced and MLA enhanced neuronal injury, neuroinflammation, and sensorimotor dysfunction of BF6+Stroke mice. Further, PHA reduced and MLA enhanced their long-term cognitive dysfunction. In Y maze test, all mice made fewer alternations 1-week post-surgeries than baseline; PHA group recovered to baseline at week 5 post-surgeries; saline and MLA groups continuously made fewer alternations throughout the 8-weeks. In NOR test, PHA group spent more time, MLA group spent less time than saline group on novel objects. Injection of BrdU in the 2 nd week post-surgeries labeled more neurons in the contralateral than in the ipsilateral dentate gyrus in all groups; PHA group had the most, MLA group had the least BrdU + neurons. Injection BrdU in the 7th week post-surgeries did not labeled any neuron. Conclusion: Activation of α-7 nAchR decreased neuronal damage and neuroinflammation, increased neurogenesis at the dentate gyrus of BF6+Stroke mice; and improved their sensorimotor and long-term cognitive function.

scholarly journals Fucoidan-Rich Substances from Ecklonia cava Improve Trimethyltin-Induced Cognitive Dysfunction via Down-Regulation of Amyloid β Production/Tau Hyperphosphorylation

Marine Drugs ◽  
2019 ◽  
Vol 17 (10) ◽  
pp. 591 ◽  
Author(s):  
Seon Kyeong Park ◽  
Jin Yong Kang ◽  
Jong Min Kim ◽  
Seul Ki Yoo ◽  
Hye Ju Han ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Cognitive Dysfunction ◽  
Memory Function ◽  
Amyloid Β ◽  
Inhibitory Effect ◽  
Ecklonia Cava ◽  
Mitochondrial Activity ◽  
Tau Hyperphosphorylation ◽  
Y Maze ◽  
Improvement Effect

Ecklonia cava (E. cava) was investigated to compare the effect of polyphenol and fucoidan extract and mixture (polyphenol:fucoidan = 4:6) on cognitive function. The ameliorating effect of E. cava was evaluated using the Y-maze, passive avoidance and Morris water maze tests with a trimethyltin (TMT)-induced cognitive dysfunction model, and the results showed that the fucoidan extract and mixture (4:6) had relatively higher learning and memory function effects than the polyphenol extract. After a behavioral test, the inhibitory effect of lipid peroxidation and cholinergic system activity were examined in mouse brain tissue, and the fucoidan extract and mixture (4:6) also showed greater improvements than the polyphenol extract. Mitochondrial activity was evaluated using mitochondrial reactive oxygen species (ROS) content, mitochondrial membrane potential (MMP, ΔΨm), adenosine triphosphate (ATP) content, and mitochondria-mediated protein (BAX, cytochrome C) analysis, and these results were similar to the results of the behavioral tests. Finally, to confirm the cognitive function-related mechanism of E. cava, the amyloid-β production and tau hyperphosphorylation-medicated proteins were analyzed. Based on these results, the improvement effect of E. cava was more influenced by fucoidan than polyphenol. Therefore, our study suggests that the fucoidan-rich substances in E. cava could be a potential material for improving cognitive function by down-regulating amyloid-β production and tau hyperphosphorylation.

scholarly journals Reversal of Trimethyltin-Induced Learning and Memory Deficits by 3,5-Dicaffeoylquinic Acid

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Jin Yong Kang ◽  
Seon Kyeong Park ◽  
Tian Jiao Guo ◽  
Jeong Su Ha ◽  
Du Sang Lee ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Neuroprotective Effect ◽  
Memory Deficits ◽  
Behavioral Tests ◽  
Dicaffeoylquinic Acid ◽  
Artemisia Argyi ◽  
Y Maze ◽  
Mda Content ◽  
Learning And Memory Deficits ◽  
Total Superoxide Dismutase

The antiamnesic effect of 3,5-dicaffeoylquinic acid (3,5-diCQA) as the main phenolic compound in Artemisia argyi H. extract on cognitive dysfunction induced by trimethyltin (TMT) (7.1 μg/kg of body weight; intraperitoneal injection) was investigated in order to assess its ameliorating function in mice. In several behavioral tests, namely, the Y-maze, passive avoidance, and Morris water maze (MWM) test, 3,5-diCQA significantly ameliorated learning and memory deficits. After the behavioral tests, brain tissues from the mice were analyzed to characterize the basis of the neuroprotective effect. Acetylcholine (ACh) levels increased, whereas the activity of acetylcholinesterase (AChE) decreased upon administration of 3,5-diCQA. In addition, 3,5-diCQA effectively protected against an increase in malondialdehyde (MDA) content, an increase in the oxidized glutathione (GSH) ratio, and a decline of total superoxide dismutase (SOD) level. 3,5-diCQA may prevent neuronal apoptosis through the protection of mitochondrial activities and the repression of apoptotic signaling molecules such as p-Akt, BAX, and p-tau (Ser 404).

scholarly journals Effects of Non-Spatial Pre-Training on Learning and Memory Impairment Detection in the Morris Water Maze

2016 ◽  
Vol 15 (2) ◽  
pp. 169-177
Author(s):  
Phanit KOOMHIN ◽  
Apsorn SATTAYAKHOM ◽  
Sarawoot PALIPOCH ◽  
Chuchard PUNSAWAD ◽  
Sompol TAPECHUM
Keyword(s):  
Learning And Memory ◽  
Morris Water Maze ◽  
Rat Model ◽  
Water Maze ◽  
Memory Impairment ◽  
Memory Deficit ◽  
Learning Ability ◽  
Vessel Occlusion ◽  
Training Strategy ◽  
Learning And Memory Deficit

One of the most popular learning and memory tests is the Morris water maze. The Morris water maze is a circular pool filled with water with a hidden platform under the water surface. The test is appropriate for rodents, especially rats and mice. The testing protocol comprises 2 parts that evaluate learning ability and memory retention. When animals are placed in the pool, they experience stress, which is the driving force for discovery of a strategy to leave the water. In the experiment, animals use environmental cues to find the location of the hidden platform in the pool. After consecutive training days, animals can more quickly locate the hidden platform. The last day of the task involves a memory test without the platform. It shows a limitation of the test in mild learning and memory deficit models such as 2-vessel occlusion. Differences between the normal and memory impairment models are expressed only in a narrow range. So, we tried to modify the original protocol for mild learning and memory impairment models. We used an albino rat strain for the experiment. A pre-training strategy of 3 days of swimming in the pool with a visible platform prior to the ordinary task was used. The results suggest that this pre-training strategy improved learning and memory in the rat model. When compared to normal rats and 2-vessel occlusion rats (a rat model for vascular dementia), those that participated in the pre-training strategy showed an increase in the percent difference of area under the curve for learning trials. In conclusion, the pre-training strategy increases ability to discriminate learning and memory impairment in the rat model, especially for the mild learning and memory deficit models.

Cognitive Impairment in Patients with Multiple Myeloma Undergoing Autologous Hematopoietic Stem Cell Transplantation

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 603-603
Author(s):  
Desiree Jones ◽  
Elisabeth G Vichaya ◽  
Jeffrey S Wefel ◽  
Melissa S.Y. Thong ◽  
Tito R Mendoza ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Cognitive Deficits ◽  
Hematopoietic Stem ◽  
Post Induction ◽  
Objective Tests ◽  
Md Anderson

Abstract Abstract 603 Background and Objectives: Cancer or aggressive cancer therapy induced cognitive dysfunction is receiving increased attention as a survivorship issue due to its potential to impact occupational, social, and scholastic activities. Neuropsychological functioning has been investigated previously in patients with hematological malignancies undergoing Autologous Hematopoietic Stem Cell Transplantation (AuHSCT); however, only a couple of studies have had samples that included patients specifically with multiple myeloma (MM). The objectives of this study were to: 1) report the incidence of cognitive deficits in patients with MM post-induction (pre- AuHSCT) and post-AuHSCT; 2) present changes in deficits based on patients' performance on a battery of key cognitive tests 1 month and 3 months post-AuHSCT; 3) identify sub-groups of patients that may be vulnerable to cognitive decline, and 4) present a comparative evaluation of patient's objective performance with their subjective self-appraisal of cognitive function pre- and post-AuHSCT. Methods: Patients were recruited from the University of Texas MD Anderson Cancer Center, Houston, Texas if they: 1) had a confirmed diagnosis of MM; 2) were ≥ 18 years old, and 3) had received induction therapy and been approved to receive AuHSCT. Neuropsychological tests designed to measure multiple cognitive domains were administered pre-AuHSCT and at 1 and 3 months post-AuHSCT. Tests included the evaluation of attention, psychomotor speed, learning and memory, language, and executive function. Patients' symptoms were assessed using the MD Anderson Symptom Inventory Multiple Myeloma Module (MDASI-MM). Results: Approximately 46% of patients exhibited cognitive impairment post induction (pre-AuHSCT) (n =48), 37.8% at 1 month post-AuHSCT (n =37), and 32.4% at 3 months post-AuHSCT (n = 34). Pre-AuHSCT, impairments were higher in learning and memory, language, and executive function relative to other domains. Older patients, minorities, those with less education, and those with more comorbidities were significantly more likely to have cognitive deficits (all P's <.05). Pearson correlations were significant between patients' self-appraisal of cognitive function and performance on objective tests (P <.05). One month post-AuHSCT, the majority of patients exhibited stable/improving cognitive function; however, decline was observed for a subset of patients in the learning and memory, psychomotor speed, and motor function domains. Patient reported “difficulty paying attention” rather than “difficulty remembering,” was better correlated with performance on objective tests 1 month post-AuHSCT. At 3 months post-AuHSCT, most patients appeared to remain stable/improve from pre-AuHSCT levels. Conclusions: Nearly half of the patient sample exhibited cognitive impairment pre-AuHSCT indicating that cognitive dysfunction is high in patients post-induction. However, cognitive function remains stable or improves for most patients1 month and 3 months post-AuHSCT. Older patients, minorities, those with less education, and those with more comorbidities may be more vulnerable to cognitive decline. Knowledge and awareness of the incidence, patterns and predictors of cognitive dysfunction is critical for patients undergoing acute therapy as well as for clinicians. Disclosures: Wefel: AstraZeneca: Research Funding.

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