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Mol Brain. 2019 Dec 4;12(1):104. doi: 10.1186/s13041-019-0525-5.

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

Author information

1
Department of Neuroscience, Mayo Clinic, Jacksonville, FL, 32224, USA.
2
Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, 361102, China.
3
Neuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, 92037, USA.
4
Department of Neuroscience, Mayo Clinic, Jacksonville, FL, 32224, USA. Li.Yonghe@mayo.edu.

Abstract

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.

KEYWORDS:

Alzheimer’s disease; Drug target; Neurogenesis; Neuronal survival; Synaptic plasticity; Wnt

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