Chapter 21: Targeting NF-κB Inflammatory and Prosurvival Signalling in Alzheimer's Disease Check Access
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Published:07 May 2010
S. Keslacy and M. L. Vallano, in Emerging Drugs and Targets for Alzheimer's Disease: Volume 2: Neuronal Plasticity, Neuronal Protection and Other Miscellaneous Strategies, ed. A. Martinez and A. Martinez, The Royal Society of Chemistry, 2010, vol. 2, ch. 21, pp. 129-152.
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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.