Restoring Wnt/β-catenin signaling is a promising therapeutic strategy for Alzheimer’s disease
Open accessAbstract
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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Wnt/β-catenin signaling is greatly suppressed in AD brains.
“restoring Wnt/β-catenin signaling, which is greatly suppressed in AD brains, is a promising therapeutic strategy”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [14]
Wnt/β-catenin signaling is crucial for neuronal survival and neurogenesis and plays important roles in regulating synaptic plasticity and blood-brain barrier integrity and function.
“Wnt/β-catenin signaling is not only crucial for neuronal survival and neurogenesis but also plays important roles in regulating synaptic plasticity and blood–brain barrier integrity and function [14].”
From CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease (2026) · cites this paper as [14]
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Expression of tiRNA and tRF in APP/PS1 transgenic mice and the change of related proteins expression
Lu, H., Liu, L., Han, S., Wang, B., Qin, J., Bu, K., Zhang, Y. N., Li, Z., Ma, L., Tian, J., et al. (2021) · Annals of Translational Medicine · doi:10.21037/atm-21-4318 · Cited by 17 · see citing works
- Authors
- Jia, L., Piña-Crespo, J., & Li, Y.
- Affiliations
- Mayo Clinic (US)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Corresponding author
- Li, Yonghe
- Venue
- Molecular Brain
- Published
- 2019-12
- Volume
- 12
- Issue
- 1
- Pages
- 104-104
- ISSN
- 1756-6606 (ISSN-L)
- PMC
- PMC6894260
- OpenAlex
- W2992486783
- Cited by
- 288
- References
- 187
- Citations by year
- 2026: 31 · 2025: 42 · 2024: 48 · 2023: 48 · 2022: 57 · 2021: 45 · 2020: 16 · 2018: 1
- FWCI
- 3.47
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecular Brain (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- The Ed and Ethel Moore Alzheimer’s Disease Research Program Pilot Grant from the Florida Department of Health (9AZ09)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, Wnt/β-catenin signaling, therapeutic target, synaptic plasticity, blood-brain barrier, amyloid-beta production, tau hyperphosphorylation, neuronal survival, neurogenesis, synaptic loss
- MeSH terms
- Alzheimer Disease, Animals, Brain, Humans, Neuronal Plasticity, Neurogenesis, Molecular Targeted Therapy, Wnt Signaling Pathway
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