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.

Tannoid principles ofEmblica officinalisrenovate cognitive deficits and attenuate amyloid pathologies against aluminum chloride induced rat model of Alzheimer's disease

2015 ◽  
Vol 19 (6) ◽  
pp. 269-278 ◽  
Author(s):  
Arokiasamy Justin Thenmozhi ◽  
Mathiyazahan Dhivyabharathi ◽  
Tharsius Raja William Raja ◽  
Thamilarasan Manivasagam ◽  
Musthafa Mohamed Essa
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficits ◽  
Rat Model ◽  
Aluminum Chloride ◽  
Model Of Alzheimer’S Disease

Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease

Nature ◽  
2000 ◽  
Vol 408 (6815) ◽  
pp. 982-985 ◽  
Author(s):  
Dave Morgan ◽  
David M. Diamond ◽  
Paul E. Gottschall ◽  
Kenneth E. Ugen ◽  
Chad Dickey ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Memory Loss ◽  
Aβ Peptide ◽  
Peptide Vaccination ◽  
Model Of Alzheimer’S Disease

Protective Effect of Kaempferol on the Transgenic Drosophila Model of Alzheimer’s Disease

2018 ◽  
Vol 17 (6) ◽  
pp. 421-429 ◽  
Author(s):  
Tanveer Beg ◽  
Smita Jyoti ◽  
Falaq Naz ◽  
Rahul ◽  
Fahad Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Neuronal Damage ◽  
Natural Antioxidants ◽  
Acetylcholinesterase Activity ◽  
Model Of Alzheimer’S Disease ◽  
Climbing Ability ◽  
Transgenic Drosophila

Background: Alzheimer’s disease (AD) is characterized by the accumulation and deposition of β-amyloid peptides leading to a progressive neuronal damage and cell loss. Besides several hypotheses for explaining the neurodegenerative mechanisms, oxidative stress has been considered to be one of them. Till date, there is no cure for AD, but the pathogenesis of the disease could be delayed by the use of natural antioxidants. In this context, we decided to study the effect of kaempferol against the transgenic Drosophila expressing human amyloid beta-42. Method: The AD flies were allowed to feed on the diet having 10, 20, 30 and 40µM of kaempferol for 30 days. After 30 days of exposure, the amyloid beta flies were studied for their climbing ability and Aversive Phototaxis Suppression assay. Amyloid beta flies head homogenate was prepared for estimating the oxidative stress markers, Caspase and acetylcholinesterase activity. Results: The results of the present study reveal that the exposure of AD flies to kaempferol delayed the loss of climbing ability, memory, reduced the oxidative stress and acetylcholinesterase activity. Conclusion: Kaempferol could be used as a possible therapeutic agent against the progression of the Alzheimer’s disease.

scholarly journals Suppression of the dihydrolipoamide dehydrogenase gene (dld-1) protects against the toxicity of human amyloid beta in C. elegans model of Alzheimer’s disease

2017 ◽  
Author(s):  
Waqar Ahmad
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Energy Metabolism ◽  
Mitochondrial Enzymes ◽  
Aβ Peptide ◽  
Dihydrolipoamide Dehydrogenase ◽  
Gene Suppression ◽  
C Elegans ◽  
Model Of Alzheimer’S Disease ◽  
Enzyme Complexes

AbstractDeclines in energy metabolism and associated mitochondrial enzymes are linked to the progression of Alzheimer’s disease (AD). Dihydrolipoamide dehydrogenase (dld) and two of its enzyme complexes namely, pyruvate dehydrogenase and α-ketoglutarate dehydrogenase are associated with AD and have a significant role in energy metabolism. Interestingly, dld gene variants are genetically linked to late-onset AD; and reduced activity of DLD-containing enzyme complexes has been observed in AD patients. To understand how energy metabolism influences AD progression, we suppressed the dld-1 gene in C. elegans expressing the human Aβ peptide. dld-1 gene suppression improved many aspects of vitality and function directly affected by Aβ pathology in C. elegans. This includes protection against paralysis, improved fecundity and improved egg hatching rates. Suppression of the dld-1 gene restores normal sensitivity to aldicarb, levamisole and serotonin, and improves chemotaxis. Suppression of dld-1 does not decrease levels of the Aβ peptide, but does reduce the formation of toxic Aβ oligomers. The mitochondrial uncoupler, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) acts synergistically with Aβ to overcome the protective effect of dld-1 gene suppression. Another metabolic toxin, phosphine, acted additively with Aβ. Our work supports the hypothesis that lowering energy metabolism may protect against Aβ pathogenicity, but that this may increase susceptibility to other metabolic disturbances.

Sign in / Sign up

Export Citation Format

Share Document