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CNS & Neurological Disorders - Drug Targets

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ISSN (Print): 1871-5273
ISSN (Online): 1996-3181

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Review Article

NF-κB as a Key Mediator of Brain Inflammation in Alzheimer’s Disease

Author(s): Chul Ju Hwang, Dong-Young Choi, Mi Hee Park and Jin Tae Hong*

Volume 18, Issue 1, 2019

Page: [3 - 10] Pages: 8

DOI: 10.2174/1871527316666170807130011

Price: $65

Abstract

Alzheimer’s disease is the most common form of dementia. It is characterized by betaamyloid peptide fibrils which are extracellular deposition of a specific protein, accompanied by extensive neuroinflammation. Various studies show the presence of a number of inflammation markers in the AD brain: elevated inflammatory cytokines and chemokines, and an accumulation of activated microglia in the damaged regions. NF-κB is a family of redox sensitive transcriptional factors, and it is known that NF-κB has binding sites in the promoter region of the genes involved in amyloidogenesis and inflammation. Long-term use of non-steroidal anti-inflammatory drugs prevents progression of AD and delays its onset, suggesting that there is a close correlation between NF-κB and AD pathogenesis. This study aims to (1) assess the association between NF-κB activity and AD through discussion of a variety of experimental and clinical studies on AD and (2) review treatment strategies designed to treat or prevent AD with NF-κB inhibitors.

Keywords: Alzheimer's disease, amyloidogenesis, Beta-amyloid, neuroinflammation, nuclear factor kappa B, nuclear factor kappa B inhibitor.

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