Restoring Wnt/β-catenin signaling is a promising therapeutic strategy for Alzheimer's disease

被引：209
|
作者：
Jia, Lin [1 ,2 ]
Pina-Crespo, Juan [3 ]
Li, Yonghe [1 ]
机构：
[1] Mayo Clin, Dept Neurosci, Jacksonville, FL 32224 USA
[2] Xiamen Univ, Coll Med, Fujian Prov Key Lab Neurodegenerat Dis & Aging Re, Inst Neurosci, Xiamen 361102, Peoples R China
[3] Sanford Burnham Prebys Med Discovery Inst, Neurosci Initiat, La Jolla, CA 92037 USA
来源：
MOLECULAR BRAIN | 2019年 / 12卷 / 01期
关键词：
Wnt; Alzheimer's disease; Neuronal survival; Neurogenesis; Synaptic plasticity; Drug target; BLOOD-BRAIN-BARRIER; AMYLOID PRECURSOR PROTEIN; BETA-CATENIN; HIPPOCAMPAL NEUROGENESIS; NERVOUS-SYSTEM; COGNITIVE DEFICITS; ADULT NEUROGENESIS; GENETIC SCREEN; SYNAPSE LOSS; WNT PATHWAY;
D O I：
10.1186/s13041-019-0525-5
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Alzheimer's disease (AD) is an aging-related neurological disorder characterized by synaptic loss and dementia. Wnt/beta-catenin signaling is an essential signal transduction pathway that regulates numerous cellular processes including cell survival. In brain, Wnt/beta-catenin signaling is not only crucial for neuronal survival and neurogenesis, but it plays important roles in regulating synaptic plasticity and blood-brain barrier integrity and function. Moreover, activation of Wnt/beta-catenin signaling inhibits amyloid-beta production and tau protein hyperphosphorylation in the brain. Critically, Wnt/beta-catenin signaling is greatly suppressed in AD brain via multiple pathogenic mechanisms. As such, restoring Wnt/beta-catenin signaling represents a unique opportunity for the rational design of novel AD therapies.
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收藏
页数：11
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