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Titlebook: Interaction Between Neurons and Glia in Aging and Disease; João O. Malva,Ana Cristina Rego,Catarina R. Olivei Book 2007 Springer-Verlag US

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Neuroinflammation and Mitochondrial Dysfunction in Alzheimer’s and Prion’s Diseasesmyloidogenic proteins, amyloid-beta (A ), and pathogenic scrapie prion (PrPSc), respectively. In both disorders, cerebral amyloid deposits are associated with a local inflammatory response, which is initiated by the activation of microglia and recruitment of astrocytes. Activated microglia, particul
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athology.Includes supplementary material: .Interactions Between Neurons and Glia in Aging and Disease is a source of "reference reviews" and "concise overviews" of the functional cross-talk between neurons and glial cells, with a focus on microglia and inflammation in the aging brain and in neurolog
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Book 2007tween neurons and glial cells, with a focus on microglia and inflammation in the aging brain and in neurological disorders. The scientific area covered by this book may be considered of key interest, and it is recognized, by the scientific community, as a major competitive area with critical implica
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Aging and Cognitive Decline: Neuroprotective Strategiesy phenomena in dementia, especially in Alzheimer’s disease (AD), is impressive, and the role of inflammatory cells and mediators has been extensively studied. Furthermore, anti-inflammatory drugs (specially the nonsteroidal anti-inflammatory drugs (NSAIDs)) have been shown to attenuate these phenomena in preclinical studies.
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Neuroinflammation and Mitochondrial Dysfunction in Alzheimer’s and Prion’s Diseasesarly those in the vicinity of amyloid deposits can produce and release proinflammatory cytokines, chemokines, complement proteins, acute-phase proteins, and reactive oxygen and nitrogen species that can damage the neighboring neurons.
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The Impact of an Imbalance Between Proinflammatory and Anti-inflammatory Influences on Synaptic funct it is an imbalance between proinflammatory and anti-inflammatory cytokines that leads to age-related deficits in synaptic function and that strategies that restore the balance are likely to be beneficial in reducing the deterioration of function that accompanies age.
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