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Figure 14.9. Summary of the role of glutamate, p-amyloid and pro-inflammatory cytokines such as tumour necrosis factor (TNF) in the production of reactive oxygen species leading to neuronal death.

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Figure 14.9. Summary of the role of glutamate, p-amyloid and pro-inflammatory cytokines such as tumour necrosis factor (TNF) in the production of reactive oxygen species leading to neuronal death.

Direct evidence for the role of inflammatory processes in the progression of AD has been provided by the study of IL-6 mRNA expression in the hippocampus. Thus a positive correlation has been found between the progression of the symptoms from the moderate to the severe form of the disease and the increase in IL-6 mRNA expression. From these observations it can be concluded that the increase in inflammatory mediators in the brain plays an important, but not the only, part in the development and progression of AD. Thus the deposition of Ab plaques in the cortex, an essential feature of the disease, may precede the changes in neurotrans-mitter function and the increase in inflammatory mediators. Whichever of these changes is eventually found to be of primary importance, it is now evident that AD is not due to a random failure of neuronal pathways but is the consequence of a systematic and progressive degeneration of different neuronal systems within the brain.

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