Neuroinflammation, Nuclear Factor kappa B and Memory Impairment Induced by Lipopolysaccharides | ||||
| Aswan Science and Technology Bulletin | ||||
| Articles in Press, Accepted Manuscript, Available Online from 07 August 2025 PDF (755.14 K) | ||||
| Document Type: Review article | ||||
| DOI: 10.21608/astb.2025.385925.1023 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Ola A Mohamed 1; Eatemad Awadalla  1; Ahmed Abdelsadik1; Hoda S Sherkawy2; Abd El-Kader M Abd El-Kader1
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| 1Department of Zoology, Faculty of Science, Aswan University | ||||
| 2Department of Medical Biochemistry, Faculty of Medicine, Aswan University | ||||
| Abstract | ||||
| The transcription factor Nuclear Factor kappa B (NF-κB) controls several cellular signaling pathways, including inflammatory ones. In mammals, Gram-negative bacteria's cell wall contains a chemical called lipopolysaccharide (LPS), which is commonly used to induce inflammation of the nervous system. LPS can trigger NF-κB, Leading to an inflammatory response. This stimulation is part of the body's defense mechanism, incontrast to bacterial infection, but can also contribute to chronic inflammation if not regulated. So, LPS increases the expression of interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor (TNF-α) via attaching to immune cells, as aresult of stimulating NF κB. Following the production of cytokines, the central nervous system (CNS)'s microglia and macrophages also generate these cytokines, which guide neuronal substrates and cause inflammation inside neurons. In addition to increasing amyloid precursor protein (APP) expression and the production of amyloid plaques, which cause Alzheimer's disease, these cytokines can also increase β-secretase mRNA, protein, and enzymatic activity. | ||||
| Keywords | ||||
| Lipopolysaccharide; Neuroinflammation; Nuclear factor kappa B; Alzheimer’s disease | ||||
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