Science Discovery Design and Optimization of Myric

Type: Article
Price: $5.00
 

Description

Science Discovery

Design and Optimization of Myricetin Encapsulated Nanostructured Lipid Carriers: In-Vivo Assessment Against Cognitive Impairment in Amyloid Beta (1-42) Intoxicated Rats

Review: Dr. Ghuncha Ambrin and Prof. Bal Ram Singh

Halder, T., Patel, B., & Acharya, N. (2022). Design and optimization of myricetin encapsulated nanostructured lipid carriers: In-Vivo assessment against cognitive impairment in amyloid beta (1-42) intoxicated rats. Life Sciences, 297, 120479. doi: https://doi.org/10.1016/j.lfs.2022.120479

Type of Study:

Alzheimer's disease is a form of dementia identified by impairment of cognitive functions by AB (amyloid b peptide of about 37-48 amino acid, that is a proteolytic product of amyloid precursor protein of APP), neurofibrillary tangles, phosphorylated tau and plaque depostitions. AB are the main factors causing senile plaques in hippocampus and the neocortex as well as in the cerebrovascular. There are only limited treatments of neurogenerative diseases, and with increase life expectancy it is becoming a major social and economic burden in the society. Myricetin (MY) has been recognized as a potential therapeutic, playing a protective role in the treatment of neurodegenerative diseases like Alzheimer's Disease (AD), Parkinson's disease (PD), Huntington's disease etc. Because of hydrophobic nature, MY has low solubility in aqueous solution, that may in fact be responsible for its cellular toxicity. The study accessed the bioavailability of MY encapsulated nanostructured lipid carriers (mY-NCLs) in the brain. Cellular toxicity and internalization of MY-NCLs were performed with an in vitro model, using SHSY5Y neuroblastoma cells. Furthermore, the study also reports neuroprotective role of MY against AB induced cytotoxicity and prevents AB induced caspase-3 activation and apoptosis. The study demonstrated significant reduction of AB levels in the brain with MY treatment exhibiting marked improvement in memory recognition in AB1-42induced AD rat model.

 

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