scholarly journals Analysis of Learning and Memory Ability in an Alzheimer's Disease Mouse Model using the Morris Water Maze

10.3791/60055 ◽  
2019 ◽  
Author(s):  
Huiling Tian ◽  
Ning Ding ◽  
Mengwei Guo ◽  
Shun Wang ◽  
Zidong Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Ability

scholarly journals Musical Electroacupuncture May Be a Better Choice than Electroacupuncture in a Mouse Model of Alzheimer’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jing Jiang ◽  
Gang Liu ◽  
Suhua Shi ◽  
Zhigang Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Frontal Lobe ◽  
Morris Water Maze ◽  
Water Maze ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Model Of Alzheimer’S Disease ◽  
Samp8 Mice

Objectives. To compare musical electroacupuncture and electroacupuncture in a mouse model of Alzheimer’s disease.Methods. In this study, 7.5-month-old male senescence-accelerated mouse prone 8 (SAMP8) mice were used as an Alzheimer’s disease animal model. In the normal control paradigm, 7.5-month-old male SAMR1 mice were used as the blank control group (N group). After 15 days of treatment, using Morris water maze test, micro-PET, and immunohistochemistry, the differences among the musical electroacupuncture (MEA), electroacupuncture (EA), Alzheimer’s disease (AD), and normal (N) groups were assessed.Results. The Morris water maze test, micro-PET, and immunohistochemistry revealed that MEA and EA therapies could improve spatial learning and memory ability, glucose metabolism level in the brain, and Aβamyloid content in the frontal lobe, compared with the AD group (P<0.05). Moreover, MEA therapy performed better than EA treatment in decreasing amyloid-beta levels in the frontal lobe of mice with AD.Conclusion. MEA therapy may be superior to EA in treating Alzheimer’s disease as demonstrated in SAMP8 mice.

scholarly journals Protective Effect of Recombinant Ganoderma Lucidum Immunomodulatory Protein (rLZ-8) Against Scopolamine-Induced Alzheimer's Disease in Rats

2020 ◽  
Author(s):  
Haotian Wang ◽  
Jun Fu ◽  
Huan Tang ◽  
Yan Li ◽  
Liping Song ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protective Effect ◽  
Learning And Memory ◽  
Ganoderma Lucidum ◽  
Water Maze ◽  
The Elderly ◽  
Model Group ◽  
Memory Ability ◽  
Maze Test

Abstract Backgroud: Alzheimer's disease (AD) is one of the most common neurodegenerative diseases in the elderly, seriously threatening the health of the elderly. In this study, the protective effect of recombinant Ganoderma lucidum immunomodulatory protein (rLZ-8) against the scopolamine-induced Alzheimer's disease (AD) in rats was studied for the first time. Methods: Male Wistar rats in rLZ-8-treated groups were intraperitoneally injected with 56 μg/kg, 112 μg/kg, and 224 μg/kg rLZ-8, respectively, those in donepezil group were intraperitoneally injected with 1.0mg/kg donepezil, and those in the normal saline group were intraperitoneally injected with an equal volume of normal saline, successively for 14 days. On the 7th day after the administration, the learning and memory ability of rats was observed by Morris water maze test, and the biochemical indexes and cytokines in the serum and brain tissues of the rats were detected after the behaviour test for investigating the protective mechanism of rLZ-8 against the scopolamine-induced AD in rats. Results: In the water maze test, compared with that in the model group, the escape latency and the swimming distance of rats on the 5th and 6th day were significantly shortened in the three rLZ-8-treated groups. In the space exploration test, compared with that in the model group, the number of passing through the location of original platform was significantly increased and the time of rats’ staying in the second quadrant was significantly prolonged in the three rLZ-8-treated groups, and furthermore, the detectionresults related to Alzheimer's disease in the serum, hippocampus and cerebral cortex of ratsindicated that rLZ-8 could improve the contents or activities of the related indexes. Conclusion: In rlZ-8 could significantly improve the learning and memory ability of AD rats, and the possible mechanism was to improve the learning and memory ability by protecting the cholinergic system.

scholarly journals Electroacupuncture Treatment Improves Learning-Memory Ability and Brain Glucose Metabolism in a Mouse Model of Alzheimer’s Disease: Using Morris Water Maze and Micro-PET

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jing Jiang ◽  
Kai Gao ◽  
Yuan Zhou ◽  
Anping Xu ◽  
Suhua Shi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Normal Control ◽  
Uptake Rate ◽  
Water Maze ◽  
Control Group ◽  
Male Mice ◽  
Memory Ability ◽  
Electroacupuncture Treatment

Introduction. Alzheimer’s disease (AD) causes progressive hippocampus dysfunctions leading to the impairment of learning and memory ability and low level of uptake rate of glucose in hippocampus. What is more, there is no effective treatment for AD. In this study, we evaluated the beneficial and protective effects of electroacupuncture in senescence-accelerated mouse prone 8 (SAMP8).Method. In the electroacupuncture paradigm, electroacupuncture treatment was performed once a day for 15 days on 7.5-month-old SAMP8 male mice. In the normal control paradigm and AD control group, 7.5-month-old SAMR1 male mice and SAMP8 male mice were grabbed and bandaged while electroacupuncture group therapy, in order to ensure the same treatment conditions, once a day, 15 days.Results. From the Morris water maze (MWM) test, we found that the treatment of electroacupuncture can improve the spatial learning and memory ability of SAMP8 mouse, and from the micro-PET test, we proved that after the electroacupuncture treatment the level of uptake rate of glucose in hippocampus was higher than normal control group.Conclusion. These results suggest that the treatment of electroacupuncture may provide a viable treatment option for AD.

scholarly journals AAV2/1 CD74 Gene Transfer Reduces β-amyloidosis and Improves Learning and Memory in a Mouse Model of Alzheimer's Disease

2015 ◽  
Vol 23 (11) ◽  
pp. 1712-1721 ◽  
Author(s):  
Tomomi Kiyota ◽  
Gang Zhang ◽  
Christine M Morrison ◽  
Megan E Bosch ◽  
Robert A Weir ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gene Transfer ◽  
Mouse Model ◽  
Learning And Memory ◽  
Model Of Alzheimer’S Disease

SPINGOSINE-1-PHOSPHATE RECEPTOR 5 AGONIST α-971432 IMPROVES LEARNING AND MEMORY IN THE SAMP8 MOUSE MODEL OF ALZHEIMER’S DISEASE

2017 ◽  
Vol 13 (7) ◽  
pp. P949
Author(s):  
Susan A. Farr ◽  
Elizabeth Louise van der Kam ◽  
Jordan W. Brown ◽  
Michael L. Niehoff ◽  
John E. Morley
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Learning And Memory ◽  
Samp8 Mouse ◽  
Model Of Alzheimer’S Disease

scholarly journals Caspase-1/IL-1β represses membrane transport of GluA1 by inhibiting the interaction between Stargazin and GluA1 in Alzheimer’s disease

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Xunhu Gu ◽  
Hanjun Wu ◽  
Yuqin Xie ◽  
Lijun Xu ◽  
Xu Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Membrane Transport ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Senile Plaque ◽  
Spatial Learning And Memory ◽  
Memory Ability ◽  
Caspase 1 ◽  
Plaque Deposition

Abstract Background Alzheimer's disease is a neurodegenerative disease. Previous study has reported that caspase-1/IL-1β is closely associated with Alzheimer's disease. However, the biological role of caspase-1/IL-1β in Alzheimer's disease has not been fully elucidated. This study aimed to explore the mechanism of action of caspase-1/IL-1β in Alzheimer's disease. Methods Mouse hippocampal neurones were treated with Aβ1-42 to induce Alzheimer's disease cell model. APP/PS1 mice and Aβ1-42-induced hippocampal neurones were treated with AC-YVAD-CMK (caspase-1 inhibitor). Spatial learning and memory ability of mice were detected by morris water maze. Flow cytometry, TUNEL staining, Thioflavin S staining and immunohistochemistry were performed to examine apoptosis and senile plaque deposition. Enzyme linked immunosorbent assay and western blot were performed to assess the levels of protein or cytokines. Co-Immunoprecipitation was performed to verify the interaction between Stargazin and GluA1. Results AC-YVAD-CMK treatment improved spatial learning and memory ability and reduced senile plaque deposition of APP/PS1 mice. Moreover, AC-YVAD-CMK promoted membrane transport of GluA1 in APP/PS1 mice. In vitro, Aβ1-42-induced hippocampal neurones exhibited an increase in apoptosis and a decrease in the membrane transport of GluA1, which was abolished by AC-YVAD-CMK treatment. In addition, Stargazin interacted with GluA1, which was repressed by caspase-1. Caspase-1/IL-1β inhibited membrane transport of GluA1 by inhibiting the interaction between Stargazin and GluA1. Conclusions Our data demonstrate that caspase-1/IL-1β represses membrane transport of GluA1 by inhibiting the interaction between Stargazin in Alzheimer's disease. Thus, caspase-1/IL-1β may be a target for Alzheimer's disease treatment.

Protective Effects of Dendrobium nobile Lindl. Alkaloids on Alzheimer's Disease-like Symptoms Induced by High-methionine Diet

2021 ◽  
Vol 19 ◽  
Author(s):  
Tingting Pi ◽  
Guangping Lang ◽  
Bo Liu ◽  
Jingshan Shi
Keyword(s):  
Alzheimer’S Disease ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Cpg Island ◽  
Morris Water Maze Test ◽  
Dendrobium Nobile ◽  
Maze Test ◽  
Neuron Damage ◽  
Cpg Island Methylation

Background: High methionine-diet (HMD) causes Alzheimer's disease (AD)-like symptoms. Previous studies have shown that Dendrobium nobile Lindle. alkaloids (DNLA) had potential benefits for AD. Object: Whether DNLA can improve AD-like symptoms induced by HMD is to be explored. Method: Mice were fed with 2% HMD diet for 11 weeks, the DNLA20 control group (20 mg/kg), DNLA10 group (10 mg/kg), and DNLA20 group (20 mg/kg) were administrated with DNLA for 3 months. Morris water maze test was used to detect learning and memory ability. Neuron damage was evaluated by HE and Nissl stainings. Levels of homocysteine (Hcy), beta-amyloid 1-42 (Aβ1-42), S-adenosine methionine (SAM), and S-adenosine homocysteine (SAH) were detected by ELISA. Immunofluorescence and western blotting (WB) were used to determine the expression of proteins. CPG island methylation. Results: Morris water maze test revealed that DNLA improved learning and memory dysfunction. HE, Nissl, and immunofluorescence stainings showed that DNLA alleviated neuron damage and reduced the 5-methylcytosine (5-mC), Aβ1-40, and Aβ1-42 levels. DNLA also decreased the levels of Hcy and Aβ1-42 in the serum, along with decreased SAM/SAH levels in the liver tissue. WB results showed that DNLA down-regulated the expression of the amyloid-precursor protein (APP), presenilin-1 (PS1), beta-secretase-1 (BACE1), DNA methyltransferase1 (DNMT1), Aβ1-40, and Aβ1-42 proteins. DNLA also up-regulated the expression of the protein of insulin-degrading enzyme (IDE), neprilysin (NEP), DNMT3a, and DNMT3b. Meanwhile, DNLA increased CPG island methylation levels of APP and BACE1 genes. Conclusions: DNLA alleviated AD-like symptoms induced by HMD via the DNA methylation pathway.

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