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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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“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]
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“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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Metadata
- 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
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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