The Role of Galanin, Conjugated Linoleic Acid, 12-O-Tetradecanoylphorbol-13-acetate and Molecular Docking of Treatments on Beta- Secretase 1 Enzyme: Effects of Inflammation on Alzheimer's Disease

Obese Alzheimer patients are at double the risk for memory loss compared to non-obese Alzheimer patients. Therefore a correlation between obesity and neuronal function as it correlates to memory loss pathology was investigated. This study also investigated the role of inflammation by exacerbating this pathology. MTT assay was used on 3T3 differentiated and undifferentiated cells treated with galanin, and its antagonist, M40, conjugated linoleic acid, and lipopolysaccharide to determine percent survival. LDH assay was used on 3T3 differentiated cells treated with Aβ40 and tetradecanoylphorbol acetate to determine cell cytotoxicity. Oil red staining of immune cells treated with galanin, M40, and conjugated linoleic acid were used to enhance cell imaging of lipid accumulation. 3T3 differentiated cells treated with conjugated linoleic acid in MTT assay had a 23.20% greater cell survival than 3T3 undifferentiated cells. In the LDH assay, there were 653.63 cells treated with Aβ40 and 652.63 cells treated with tetradecanoylphorbol acetate. Galanin treated cells in oil red staining had 6.18% fat which indicated cell accumulation and an inflammatory response of cells which is similar to the response in the brain. M40, toll-like receptor 4, and somatostatin were molecularly docked to the beta-secretase 1 enzyme and results indicated that somatostatin had the greatest ligand efficiency. Somatostatin had a ligand efficiency of -0.13 and a binding energy of -14.9986. Compared to the other treatments, the results suggested that somatostatin had the greatest binding effects and had the most significant role on the binding to the Alzheimer’s disease enzyme. To further evaluate Alzheimer’s disease and obesity, testing ginseng, berberine, and polychlorinated biphenyls on Aβ40 is pertinent. This will help elucidate how other dietary supplements and environmental contaminants that can affect the human body when ingested, influence the risk of Alzheimer’s disease. This study provided a potential method in minimizing the risk of Alzheimer’s disease in which future research would also be conducted.


Chloe Liu1* and Wei Zhu2

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