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Senile neurodegeneration: Pathogenic role of microglia-derived free radicals

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Part of the book series: Molecular and Cell Biology Updates ((MCBU))

Summary

At present, the diagnosis of Alzheimer’s disease (AD) dementia prompts a pessimistic prognosis of loss of memory and cognitive function. However, studies into the disease have provided significant insights into the aetiopathogenesis of the neurodegenerative processes, although prospects of effective therapy remain uncertain. The activated microglial cell — the brain macrophage is an important cellular component of the characteristic senile plaque in AD brains, and a potent generator of free radical and related reactive oxygen metabolites (ROM). The proposed capacity of aluminosilicate/amyloid particulate and fibrillar aggregate deposits to induce a chronic inflammatory production of microglia-derived and neuronal-injurious ROM provides a plausible rationale for the understanding of the role of oxidative stress in the pathogenesis of AD dementia. Futhermore, it offers a feasible target cellular process for beneficial nutritional and pharmacological antioxidant intervention to combat deleterious cognitive decline.

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Evans, P.H., Peterhans, E., Bürge, T., Klinowski, J., Yano, E. (1995). Senile neurodegeneration: Pathogenic role of microglia-derived free radicals. In: Cutler, R.G., Packer, L., Bertram, J., Mori, A. (eds) Oxidative Stress and Aging. Molecular and Cell Biology Updates. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7337-6_30

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