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Rev Neurosci. 2007;18(2):137-48.

Interleukin-1beta and caspase-1: players in the regulation of age-related cognitive dysfunction.

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Center of Excellence for Aging and Brain Repair, Department of Neurosurgery, University of South Florida College of Medicine, Tampa, FL 33612, USA.


Scientific research on the unprecedented and growing number of older adults in the United States and other industrialized countries has focused much attention on the health consequences of aging. Over the last few decades, inflammation in the brain and its implication in the progression of aging and age-related cognitive dysfunction has been an area of increasing importance to neuroscientists and is now considered as one of the most interesting and promising topics for aging research. One of the critical aspects of inflammatory processes is that the activation of one upstream inflammatory molecule initiates a cascade of self-sustaining inflammatory events which leads to the activation of a number of different downstream functions. Recently, a great deal of attention has been given to the interplay between inflammatory and apoptotic processes and the regulation of these processes by the caspases. The caspase family of proteases can be divided into proapoptotic and pro-inflammatory members. The present review summarizes recent observations of the interactions between the inflammatory cytokine interleuldn-1 (IL-1) beta and the inflammatory/apoptotic caspase-1 and their involvement in age-related impairments in cognition. A comprehensive understanding of these mechanisms could potentially lead to the development of preventive or protective therapies that reduce or inhibit the cognitive decline associated with aging and age-related neurodegenerative disease.

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