Interaction of NF-κB and Wnt/β-catenin Signaling Pathways in Alzheimer's Disease and Potential Active Drug Treatments.

Abstract

The most important neuropathological features of Alzheimer's disease (AD) are extracellular amyloid-β protein (Aβ) deposition, tau protein hyperphosphorylation and activation of neurometabolic reaction in the brain accompanied by neuronal and synaptic damage, and impaired learning and memory function. According to the amyloid cascade hypothesis, increased Aβ deposits in the brain to form the core of the senile plaques that initiate cascade reactions, affecting the synapses and stimulating activation of microglia, resulting in neuroinflammation. A growing number of studies has shown that NF-κB and Wnt/β-catenin pathways play important roles in neurodegenerative diseases, especially AD. In this review, we briefly introduce the connection between neuroinflammation-mediated synaptic dysfunction in AD and elaborated on the mechanism of these two signaling pathways in AD-related pathological changes, as well as their interaction. Based on our interest in natural compounds, we also briefly introduce and conduct preliminary screening of potential therapeutics for AD.

• Authors: Xiao Liu, Kaiyue Wang, Xing Wei, Tian Xie, Bin Lv, Qian Zhou, Xiaoying Wang
• Journal: Neurochemical research (Neurochem Res) Vol. 46 Issue 4 Pg. 711-731 (Apr 2021) ISSN: 1573-6903 [Electronic] United States
• PMID: 33523396 (Publication Type: Journal Article, Review)

Chemical References

• Biological Products
• Drugs, Chinese Herbal
• NF-kappa B p50 Subunit
• NFKB1 protein, human

Topics

• Alzheimer Disease (drug therapy, physiopathology)
• Animals
• Biological Products (therapeutic use)
• Drugs, Chinese Herbal (therapeutic use)
• Humans
• Inflammation (drug therapy, physiopathology)
• Microglia (metabolism)
• NF-kappa B p50 Subunit (metabolism)
• Synapses (metabolism)
• Wnt Signaling Pathway (drug effects, physiology)