The Effects of Novel Anti-Inflammatory Drugs on LPS-Induced Cytokine Gene Expression in BV2 Cells
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2025-05-19
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Alzheimer's Disease (AD), the most common form of dementia, currently impacts almost seven million people in the United States over the age of 65. It is predicted that by 2060 over 13 million people in the United States will be affected by AD, which is why there is a growing demand for treatments. Amyloid B plaques and phosphorylated tau proteins are both associated with the progression of the AD pathology since they play a role in the disruption of neuronal integrity. These aggregated proteins along with other molecules, such as lipopolysaccharide (LPS), lead to increased inflammation by activating the NFkB pathway. The NFkB pathway regulates the production of pro-inflammatory cytokines, such as Interleukin-1 Beta (IL-1B) and tumor necrosis factor-alpha (TNFa); however, if it is overactive, it can lead to harmful inflammation. The company P2D Biosciences provides novel compounds designed to reduce inflammation, but the exact mode of action of these compounds is unknown. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) can be utilized to measure cytokine mRNA from BV2 cells that have been pretreated with the drugs and then with LPS. In this project we screened multiple compounds (PD340 and PD2244) provided by P2D Biosciences to evaluate their use as anti-inflammatory agents to treat AD. It was concluded that PD340 reduced IL-1B and TNFa gene expression while PD2244 reduced IL-1B gene expression. Further testing needs to be conducted to find the exact mechanism of the compounds.
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Biology