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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.

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


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.


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

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