Abstract
The concept of a neuroinflammatory etiology in Alzheimer’s disease continues to gain increasing credibility since its inception in the McGeer labs over a decade ago. In this brief review, we compare and contrast the published findings for inflammatory mediators in the neocortex, a brain region with extensive neuronal losses, and those in the cerebellum, a brain region with minimal or no neuronal cell death. The basic hypothesis that evolves from this review of the literature is that neuroinflammation is a widespread phenomenon in the brains of Alzheimer’ s patients, but that in the case of the cerebellum, this is an inflammatory process that is either halted at a critical step or buffered sufficiently by endogenous protective mechanisms to prevent the cascade of events that results in neuronal losses. This hypothesis, therefore, has the corollary that pharmacological treatments that interfere with the neuroinflammatory cascade in the neocortex of Alzheimer’ s patients should slow the progression of the disease and/or prevent the onset of the disease, if implemented prior to the neuronal degeneration that results from sustained neuroinflammation.
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© 2003 Humana Press Inc., Totowa, NJ
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Wood, P.L. (2003). The Cerebellum in AD. In: Wood, P.L. (eds) Neuroinflammation. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-297-5_15
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DOI: https://doi.org/10.1007/978-1-59259-297-5_15
Publisher Name: Humana Press, Totowa, NJ
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