scholarly journals EVALUATION OF ANTI-ALZHEIMER ACTIVITY OF ETHANOLIC AND METHANOLIC EXTRACTS OF POLYGONUM GLABRUM AGAINST ALUMINUM CHLORIDE-INDUCED ALZHEIMER’S IN EXPERIMENTAL RATS

2021 ◽  
pp. 118-125
Author(s):  
SUNEESHA Y ◽  
VINAY KUMAR T
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Aluminum Chloride ◽  
Methanolic Extract ◽  
Ethanolic Extract ◽  
Morris Water Maze Test ◽  
Methanolic Extracts ◽  
Maze Test ◽  
Behavioral Parameters ◽  
Acetylcholinesterase Enzyme

Objective: The current study aimed at the investigation of the effectiveness of ethanolic and methanolic extract of Polygonum glabrum in aluminum chloride-induced Alzheimer’s disease in experimental rats. Methods: The behavioral parameters evaluated by following methods such as Morris water maze test, radial arm maze test, and active avoidance test. Biochemical parameters were also estimated such as acetylcholine and acetylcholine esterase. Results: Polygonum glabrum extract was instituted to be neuroprotective against AlCl3-induced toxicity. Enhanced learning and memory were allied to the ingestion of extract in rats. Al overload, acetylcholinesterase enzyme hyperactivity is responsible for Alzheimer’s disease which is neutralized or reduced with treatment of extract, which might be due to the synergistic action of its active constituents. Ethanolic extract was shown slightly higher efficacy as compared to methanolic extract. Conclusion: Based on these current findings, it is suggested that lowering Aβ is an unproven strategy, and it may be time to refocus on other targets for the treatment of this disease, including pathological forms of tau.

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 Effect of Piper betel leaf extract on learning and memory in Aluminium chloride induced Alzheimer’s disease in Wistar rats

2019 ◽  
Vol 12 (3) ◽  
pp. 1425-1431
Author(s):  
Shreeraksha Upadhyaya ◽  
Shivaprakash Gangachannaiah ◽  
Pallavi Lakshmi Chandrashekar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Wistar Rats ◽  
Treated Group ◽  
Aluminium Chloride ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Betel Leaf ◽  
Maze Test ◽  
Piper Betel Leaf

Alzheimer's disease is a common neurological disorder affecting a significant proportion of the elderly population.There are only a few drugs which can be used safely to treat it. We sought to investigate for the first time Piper betel leaf, a postmeal mouth freshener for its potential use in Alzheimer's disease. Five groups of male Wistar rats with six rats in each group aged 10-12 weeks were used. The control group received the distilled water, aluminium chloride (AlCl3) group was treated with AlCl3, the standard group was treated with rivastigmine with AlCl3, and the two test groups received piper betel leaf extract (PBE) at doses of 400mg/kg and 500mg/kg body weight with AlCl3. AlCl3 was administered orally for 42 days in all the treated groups. Memory and learning were evaluated by Morris water maze test and Passive avoidance test.The results of the Morris water maze test showed reduced mean escape latency period in all the groups on trial day three (P≤0.05) and on trial day four (P ≤0.01) compared to AlCl3 group. The retention of spatial memory by probe trial showed that PBE and rivastigmine treated group spent more time in the target (platform) quadrant when compared to AlCl3 group (P≤0.01). The passive avoidance test showed a significant increase in step through latency in standard and test groups compared to the AlCl3 treated group. The weight of the rats treated with AlCl3 and PBE was reduced at the end of the treatment period while increased in standard and control group. The study shows the beneficial effects of Piper betel leaves in Alzheimer’s disease by significantly improving the learning and memory functions in rats.

scholarly journals Protective effect of Picrorhiza kurroa on Alzheimer’s disease induced by aluminium chloride in rats

2017 ◽  
Vol 6 (3) ◽  
pp. 602 ◽  
Author(s):  
Somasekhar K. Reddy ◽  
Sudheer A. ◽  
Arunamma M. ◽  
Likitha Sree P. ◽  
Jyothirmayi E.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Aluminum Chloride ◽  
Neurodegenerative Disorder ◽  
Ethanolic Extract ◽  
Aluminium Chloride ◽  
Control Group ◽  
Picrorhiza Kurroa ◽  
Group I ◽  
Brain Acetylcholinesterase

Background: Alzheimer’s disease is a progressive neurodegenerative disorder characterized by cognitive deterioration together with declining activities of daily living and behavioural changes. The present work is aimed to investigate the effect of methanolic extract of rhizomes of Picrorhiza kurroa against aluminum chloride induced Alzheimer’s disease.Methods: Wistar rats were selected in this study and were divided into 5 groups (6 each). Group I served as normal control. Group II received aluminum chloride (300mg/kg, P.O.). Group III and IV received ethanolic extract of Picrorhiza kurroa (200mg/kg, 400mg/kg, P.O. respectively) and inducing agent (AlCl3 300mg/kg, P.O.). Group V received rivastigmine (0.3mg/kg, I.P.) and inducing agent (AlCl3 300mg/kg, P.O.). The rats were given respective treatment for 20 days and behavioural parameters were determined on 20th day. After 20th day rats were sacrificed and anti-oxidant parameters, brain acetylcholinesterase content were determined.Results: Oral administration of ethanolic extract of Picrorhiza kurroa at doses 200, 400mg/kg body weight showed improve in behavioural parameters when compared to AlCl3 induced rats, showed increase in superoxide dismutase, catalase, reduced glutathione and decreased levels of malondialdehyde and showed decrease in brain acetylcholinesterase content when compared to AlCl3 induced rats.Conclusions: The study clearly demonstrated the beneficial effects of Picrorhiza kurroa by improving biochemical and behavioural parameters.

scholarly journals High Methionine Diet-Induced Alzheimer’s Disease like Symptoms Are Accompanied by 5-Methylcytosine Elevated Levels in the Brain

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Tingting Pi ◽  
Shenjiao Wei ◽  
Yongxuan Jiang ◽  
Jing-Shan Shi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Food Intake ◽  
Amyloid Β ◽  
The Body ◽  
Morris Water Maze Test ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ability Test ◽  
Maze Test ◽  
Related Proteins

Background. Excessive or insufficient intake of methionine (Met) causes neuronal dysfunction, neurodegeneration, cerebrovascular dysfunction, vascular leakage, and short-term memory loss, which result in the occurrence of Alzheimer’s disease- (AD-) like symptoms. Objective. To determine the relationship between high methionine diets (HMD) induced AD-like symptoms and 5-methylcytosine (5-mC) level. Methods. C57BL/6J mice were randomly divided into two groups: the control group (Maintain diets) and the model group (2% HMD). Mice were fed with 2% HMD for 9 weeks. Animals were weighed and food intake was recorded weekly. Open field test, nesting ability test, Y maze test, new object recognition test, and Morris water maze test were used to detect the motor, learning, and memory ability. Hematoxylin-eosin (HE) staining was used to observe the damage of cells in hippocampus and cortex. Immunofluorescence (IF) staining was used to detect the expression and distribution of amyloid-β 1-40 (Aβ1-40), amyloid-β 1-42 (Aβ1-42), and 5-methylcytosine (5-mC) in hippocampus and cortex. Western blotting (WB) was used to determine the expression of Aβ and DNA methyltransferases- (DNMTs-) related proteins in the cortex. Enzyme-linked immunosorbent assay (ELISA) was performed to detect homocysteine (Hcy) level (ELISA). Results. Feeding of HMD decreased the body weight and food intake of mice. Behavioral testing revealed that HMD caused learning, memory, and motor ability impairment in the mice. HE staining results showed that HMD feeding caused damage of hippocampal and cortical neurons, along with disordered cell arrangement, and loss of neurons. Furthermore, HMD increased the contents of Aβ1-40, Aβ1-42, and 5-mC in the hippocampus and cortex. WB results showed that HMD increased the expression of Aβ production-related proteins, such as amyloid precursor protein (APP) and beta-secretase 1 (BACE1), and decreased the expression of Aβ metabolism-related protein in the cortex, including insulin-degrading enzyme (IDE) and neprilysin (NEP). Additionally, the decreased expression of DNA methyltransferase1 (DNMT1) was observed in HMD-treated mice, but there was no significant change of DNMT3a level. ELISA results showed that HMD increased the levels of Hcy in serum. Conclusion. Our result suggested that the HMD can cause neurotoxicity, leading to AD-like symptoms in mice, which may be related to 5-mC elevated.

scholarly journals miR-485-5p alleviates Alzheimer’s disease progression by targeting PACS1

2021 ◽  
Vol 12 (1) ◽  
pp. 335-345
Author(s):  
Chuan He ◽  
Caixia Su ◽  
Wentong Zhang ◽  
Qi Wan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Biological Function ◽  
Neurological Diseases ◽  
Flow Cytometric Analysis ◽  
Immunofluorescent Staining ◽  
Luciferase Reporter ◽  
Morris Water Maze Test ◽  
Flow Cytometric ◽  
Maze Test

Abstract Alzheimer’s disease (AD) is a common dementia and a heterogeneous disease. Previous research has validated that microRNAs (miRNAs) are pivotal regulators in the initiation and development of tremendous diseases including AD. MicroRNA-485-5p (miR-485-5p) was reported to be an important participant implicated in several neurological diseases, but its role in AD still needs to be further investigated. In this research, we explored the biological function of miR-485-5p in AD. RT-qPCR revealed that miR-485-5p expression was downregulated in the hippocampus of APP/PS1 mice. Additionally, miR-485-5p overexpression facilitated the learning and memory capabilities of APP/PS1 mice according to Morris water maze test, fear conditioning test, and immunofluorescent staining. Moreover, CCK-8 assay, flow cytometric analysis, and western blot analysis suggested that miR-485-5p overexpression promoted pericyte viability and prohibited pericyte apoptosis in APP/PS1 mice. Mechanistically, miR-485-5p directly targeted PACS1 in pericytes, as shown in a luciferase reporter assay. In rescue assays, PACS1 overexpression countervailed the effect of miR-485-5p overexpression on pericyte viability and apoptosis. In conclusion, miR-485-5p ameliorates AD progression by targeting PACS1.

scholarly journals Neuroprotective Effect of Garcinia Mangostana on Streptozotocin Induced Sporadic Type Alzheimer’s Disease in Mice

2016 ◽  
Vol 1 (01) ◽  
pp. 8-15 ◽  
Author(s):  
Vasudha Bakshi ◽  
Avinash P ◽  
Arun Reddy R ◽  
Nazia Begum
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuroprotective Effect ◽  
Ethanolic Extract ◽  
Garcinia Mangostana ◽  
Y Maze ◽  
Study Results ◽  
Behavioral Parameters ◽  
Pre Treatment ◽  
Dose Dependent

Objectives: The main objective of the study is to determine the neuroprotective potential of ethonolic extract of Garcinia mangostana (EEGM) in mouse against Intracerebroventricular- Streptozotocin (ICV –STZ) induced sporadic type Alzheimer's disease. Methods: Neurotoxicity was induced by ICV injection of STZ (0.5 mg/kg/b.w) as a first dose then the second dose after the 48 hours and the animals were pre-treated with ethanolic extract of Garcinia mangostana for 28 days. To assess the behavioral parameters learning and memory, open field and Y-maze were employed. Acetylcholinesterase, antioxidant enzymes (superoxide dismutase, glutathione peroxidise, reduced glutathione and catalase) were estimated in brain tissue. Results: Pre-treatment with EEGM (200 and 400 mg/kg/b.w) exhibited a dose dependent reduction of AChE levels and increased habituation memory and percentage alteration which are indicative of the enhanced cognitive function. The extract showed significant increase in the antioxidant parameter. Conclusion: The study results suggested that the neuroprotective potentiality of EEGM against ICV STZ induced neurotoxicity. The extract of EEGM proved to have a potential therapeutic action in preventing or decreasing the progression of sporadic Alzheimer‟s disease due to aging and oxidative stress.

Taurine and Camel Milk Modulate Neurobehavioral and Biochemical Changes in Aluminum Chloride-Induced Alzheimer’s Disease in Rats

2021 ◽  
pp. 1-12
Author(s):  
Teslim S. Abdulkadir ◽  
Fatima A. Dawud ◽  
Ahmed Sherif Isa ◽  
Joseph O. Ayo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Superoxide Dismutase ◽  
Aluminum Chloride ◽  
Motor Coordination ◽  
Acetylcholinesterase Activity ◽  
Camel Milk ◽  
Aβ Peptide ◽  
Model Of Alzheimer’S Disease ◽  
Female Wistar Rats

Background: Alzheimer’s disease (AD) is a neurodegenerative disease associated with deficiency in motor coordination, cognitive impairment, and excessive reactive oxygen species production in the brain. Objective: The study evaluated effects of taurine and camel milk (CM) on neurobehavior, amyloid-beta peptide 1–42 (Aβ) expression, acetylcholinesterase, and superoxide dismutase activities in aluminum chloride (AlCl3) model of Alzheimer’s disease in rats. Methods: Thirty-five female Wistar rats were divided into seven groups (n = 5): Normal saline (0.2 mL/kg body weight); AlCl3 (100 mg/kg) (AD); CM (33 mL/kg); Taurine (50 mg/kg); AlCl3 (100 mg/kg) + CM (33 mL/kg); AlCl3 (100 mg/kg) + Taurine (50 mg/kg); and AlCl3 (100 mg/kg) + CM (33 mL/kg) + Taurine (50 mg/kg). The administration lasted for eight weeks via oral gavage. After the eighth week, neurobehavior assessments were performed. Rats were sacrificed, and brain and blood samples collected for analysis. Results: There was a significant (p <  0.0001) increase in the duration of motor endurance in AD + CM rats, compared to AD rats. Duration of forced swimming time was lowest (p <  0.0001) in AlCl3 + Taurine rats, compared to that of AD rats. Concentration of Aβ peptide decreased (p <  0.05) in AD rats, treated with CM and/or combination. In taurine-treated rats, superoxide dismutase activity was significantly (p <  0.05) higher than in AD rats. Treatment with taurine + CM increased (p <  0.05) acetylcholinesterase activity compared to controls. Conclusion: Taurine and CM enhanced cognition and sensorimotor activity by decreasing Aβ peptide concentration and increasing superoxide dismutase and acetylcholinesterase activities in AD rats.

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