Herbal Extracts Alter Amyloid Beta Levels in SH-SY5Y Neuroblastoma Cells
(1) Ridge High School, Basking Ridge, New Jerseyhttps://doi.org/10.59720/19-092
Alzheimer’s disease (AD) is a type of dementia that affects more than 5.5 million Americans. It is characterized by progressive memory loss and impairment of other cognitive abilities that affect daily life. Unfortunately, there are no approved treatments that can delay the advancement of the disease. However, it is known that factors such as amyloid beta (Aβ) plaques and tau neurofibrillary tangles disrupt connections between neurons, leading to the eventual death of neurons that are responsible for memory. For this investigation, we focused on the neurotoxic Aβ1-40 peptide, which is formed by the amyloidogenic cleavage and processing of amyloid precursor protein (APP), a crucial component in the development of AD. Neuroinflammatory cytokines have also been shown to reduce the efflux transport of Aβ from the brain, leading to increased Aβ concentrations. The objective of the experiment was to test the effects of various herbal extracts (bugleweed, hops, sassafras, and white camphor) on Aβ1-40 peptide levels in human neuroblastoma cells that were transfected to overexpress APP. Due to the herbal extracts’ common anti-inflammatory property, the experiment determined whether or not this property had the potential to change Aβ1-40 concentrations. Prior to the quantification of Aβ1-40 peptide with an enzyme-linked immunosorbent assay (ELISA), we determined the cytotoxicity of the extracts using an MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, assay to discern whether decreases in Aβ1-40 concentrations were the result of cell death. The results indicated that white camphor was toxic to neuroblastoma cells and resulted in decreased Aβ1-40 levels; sassafras was not toxic and resulted in slightly elevated Aβ1-40 levels; hops was not toxic and resulted in increased Aβ1-40 levels; and bugleweed was not toxic, yet resulted in decreased Aβ1-40 levels. Thus, only bugleweed may have the potential to reduce Aβ1-40 levels through its anti-inflammatory properties.
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