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Multi-factorial evidence supports the concept that chronic inflammation contributes to the progression of Alzheimer's disease. NF-kB is a key component in a major signaling cascade mediating inflammation, but NF-kB activation also supports neuronal survival in certain contexts. An important avenue of drug development lies in understanding the balance between attenuating NF-kB-mediated inflammatory processes that contribute to Alzheimer's disease progression while maintaining its closely linked pro-survival signaling. This review discusses evidence supporting a contributory role for NF-kB-mediated inflammation in Alzheimer's pathogenesis, and pharmacological strategies that suppress this pathway. Also reviewed is evidence that development of agents that engage the pro-survival/neuroprotective arm of the NF-kB signaling pathway could prove beneficial in Alzheimer's disease therapy.

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