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

被引:0
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作者
Lin Jia
Juan Piña-Crespo
Yonghe Li
机构
[1] Mayo Clinic,Department of Neuroscience
[2] Institute of Neuroscience,Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research
[3] Medical College,undefined
[4] Xiamen University,undefined
[5] Neuroscience Initiative,undefined
[6] Sanford Burnham Prebys Medical Discovery Institute,undefined
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关键词
Wnt; Alzheimer’s disease; Neuronal survival; Neurogenesis; Synaptic plasticity; Drug target;
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摘要
Alzheimer’s disease (AD) is an aging-related neurological disorder characterized by synaptic loss and dementia. Wnt/β-catenin signaling is an essential signal transduction pathway that regulates numerous cellular processes including cell survival. In brain, Wnt/β-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/β-catenin signaling inhibits amyloid-β production and tau protein hyperphosphorylation in the brain. Critically, Wnt/β-catenin signaling is greatly suppressed in AD brain via multiple pathogenic mechanisms. As such, restoring Wnt/β-catenin signaling represents a unique opportunity for the rational design of novel AD therapies.
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