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Background: In Ayurvedic medicine, herbal, metallic, and herbometalic preparations gain recognition for treating physiological maladies. Aurothioglucose serves as a pharmaceutical intervention for the management of rheumatoid arthritis and can be potential as a potential pharmacological agent for mitigating neuronal toxicity. Objective: The current study was planned to explore the neuroprotective potential of aurothioglucose-loaded poly (lactic-co-glycolic acid) nanoparticles against aluminum chloride (AlCl3) induced Alzheimer's Disease. Method: In the in vivo study, AlCl3 (100 mg/kg, 21 days) was orally administered to rats, while, Aurothioglucose (ATG) and ATG NPs (Nanoparticles) (5, 10 mg/kg and 2.5 and 5 mg/kg, s.c.) were administered sub-cutaneous for a duration of 2 weeks. Following the treatment regimen, neurobehavioral evaluations were conducted utilizing the Open Field Test (OFT), Morris Water Maze (MWM), and Object Recognition Test (ORT). Subsequently, the rats were euthanized, and hippocampal tissue samples were procured for the assessment of biochemical and neuroinflammatory markers. Results: In the in-vivo experiment, the administration of both ATG and ATGNPs elicited a noteworthy reversal of cognitive impairments, biochemical perturbations, and neuroinflammatory markers induced by AlCl3. These observations suggest that ATG NPs demonstrate superior neuroprotective capabilities compared to ATG alone. Conclusion: The observed therapeutic outcomes imply that ATG and ATG NPs conferred amelioration against AlCl3-induced neurotoxicity in rats through mechanisms involving antioxidative and anti-inflammatory effects. Hence, ATG NPs could be a potential drug for correcting Alzheimer’s disease.
Background: In Ayurvedic medicine, herbal, metallic, and herbometalic preparations gain recognition for treating physiological maladies. Aurothioglucose serves as a pharmaceutical intervention for the management of rheumatoid arthritis and can be potential as a potential pharmacological agent for mitigating neuronal toxicity. Objective: The current study was planned to explore the neuroprotective potential of aurothioglucose-loaded poly (lactic-co-glycolic acid) nanoparticles against aluminum chloride (AlCl3) induced Alzheimer's Disease. Method: In the in vivo study, AlCl3 (100 mg/kg, 21 days) was orally administered to rats, while, Aurothioglucose (ATG) and ATG NPs (Nanoparticles) (5, 10 mg/kg and 2.5 and 5 mg/kg, s.c.) were administered sub-cutaneous for a duration of 2 weeks. Following the treatment regimen, neurobehavioral evaluations were conducted utilizing the Open Field Test (OFT), Morris Water Maze (MWM), and Object Recognition Test (ORT). Subsequently, the rats were euthanized, and hippocampal tissue samples were procured for the assessment of biochemical and neuroinflammatory markers. Results: In the in-vivo experiment, the administration of both ATG and ATGNPs elicited a noteworthy reversal of cognitive impairments, biochemical perturbations, and neuroinflammatory markers induced by AlCl3. These observations suggest that ATG NPs demonstrate superior neuroprotective capabilities compared to ATG alone. Conclusion: The observed therapeutic outcomes imply that ATG and ATG NPs conferred amelioration against AlCl3-induced neurotoxicity in rats through mechanisms involving antioxidative and anti-inflammatory effects. Hence, ATG NPs could be a potential drug for correcting Alzheimer’s disease.
Alzheimer disease (AD) chronic neurodegenerative disease. Beta amyloid and tau neuropathy associated with this disease. New drug therapy deals with AREA, DIED etc. The in vitro and in vivo study shows Aducanumab was the first treatment to address an underlying cause of the disease. This removes sticky depositions of amyloid plaques. Alzheimer's neuropathology the superfrontal cortex suffer from atrophy and loss of neurones, which occurs inflammation and deposition of amyloid plaques and bundles of connective tissue and abnormal set of protein fragments. The monoclonal part of the drug attacks the aggregated depositions. Gantenerumab & Solanezumab also are tested for curing for this disease. There much model like 2D and 3D and various cultural model by which the AD cure process can be reached. A neuron is unit of the brain function, which contains an excess amount of polyunsaturated (fatty) acids. It can react with ROS, which can deals with lipid peroxidation response and cell apoptosis, in addition, low glutathione to neurons and is major causes of oxidative stress injure Modelling has been formed by stem cells, vascularised organ. Advanced models are used to understand better neurodegeneration, and potential therapies. In this review we can say that the current progress of new therapeutics like lipid metabolism, inflammation, and disease customize genes to AD in preclinical and clinical research. It’seeming that higher dose are worked in AD patients but lower dose causes AREA. ARIA can successfully cured in most of the patients who engaged themselves in important tests without stopping the treatment.
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