In aging, a series of unchecked inflammatory events can lead to exaggerated proin-flammatory cytokine levels; such as, increases in interleukin 1 (IL-1), IL-1 receptor agonists, tumor necrosis factor (TNF), and transforming growth factor-^ .1>2 When functioning correctly, cytokines send the appropriate amount of the correct signal to assist in resolving the immune stimulus; such as, IL-4, IL-10, and IL-13, which act to suppress inflammation, or IL-1, IL-6, IL-8, IL-11, and IL-12, which act to stimulate inflammation. In a healthily immune system both pro- and anti-inflammatory cytokine are used to acutely handle the immune stimulus. In the aged system, the profile of cytokine activation does not resemble acute activation; instead a chronic inflammation state is seen. This chronic pattern of activation can change the microenvironment within the CNS leading to detrimental outcomes. A growing body of evidence has linked age-dependent alterations in cognitive ability with an altered inflammatory response in the brain.3'4 Increased levels of the proinflammatory cytokine IL-1^ have been correlated with natural aging and with the development of cognitive dysfunction.5-7 A great deal of evidence suggests that IL-1^ plays an important role in neuronal plasticity' as revealed by the fact that this cytokine is implicated in the age-related impairment in long-term potentiation (LTP), a model system for the neural mechanism underlying hippocampus-dependent memory.2,8 Consistent with this finding it has been demonstrated that, IL-1^ inhibits LTP in dentate gyrus,9 CA1, and CA310'11 and that such effect is associated with a decrease in glutamate release, a neurotransmitter that mediates LTP.11 In addition, intraperitoneal injection of lipo-polysaccride (LPS) also leads to an inhibition of glutamate release and a compromise in LTP, which is accompanied by increases in IL-1^ concentration in hippocampus.12 In spite of a general agreement concerning the impairment in the maintenance of LTP in aged rats, it is still questioned whether or not the induction of LTP is impaired in aged rats. Induction of LTP in vitro and in vivo caused a long lasting increase in IL-1^ gene expression, which was prevented by blockade of potentiation with N-methyl-D-aspartate (NMDA) receptor antagonist.13 NMDA receptor binding and density have been reported to decrease with increasing age.14,15 We have recently shown that the nonsteroidal anti-inflammatory drug (NSAID) sulindac reversed age-related deficits in radial arm water maze performance and contextual fear conditioning and attenuated age-related decreases in hippocampal NMDA receptor subunits NR1 and NR2B at the same time we observed a decline in IL-1^.16 A recent study using a genome-scale screening has shown a distinct temporal gene expression profile associated with spatial learning and memory of rats in Morris water maze in young rats. Among other changes the authors have shown a reduction in IL-1^ gene expression in water maze trained animals, and this data was consistent with the finding that central administration of IL-1^ impairs the consolidation of memories that depend on the hippocampal formation.17
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