Abstract
One of the early events in Alzheimer’s disease (AD) is the extracellular deposition of amyloid-beta peptide (An), a 39- to 43- amino acid cleavage product of the transmembrane glycoprotein, amyloid precursor protein. Excess A13 within the brain has long been thought to play a major role in AD pathogenesis, however, the mechanisms of its actions are highly debatable. Recent evidence suggests that inflammation may be the pathogenetic link between AP deposition and neuronal death (Halliday et al., 2000).
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Bilunas, M.H., Moore, S.A. (2002). Cyclooxygenase-2 Expression and Activity are Induced by Amyloid-Beta 1-42 in Brain-Derived Cells. In: Honn, K.V., Marnett, L.J., Nigam, S., Dennis, E., Serhan, C. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 5. Advances in Experimental Medicine and Biology, vol 507. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0193-0_15
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DOI: https://doi.org/10.1007/978-1-4615-0193-0_15
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