ArticleHandbook of experimental pharmacology2021
WNT Signaling Is a Key Player in Alzheimer's Disease.
Article in Handbook of experimental pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
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- Unraveling novel mechanisms of ATP-Binding cassette (ABC) transporter in insulin Resistance-induced amyloidogenesis.Metabolic brain disease · 2025Review
- Formulating Treatment to Cure Alzheimer's Dementia: Approach #2.International journal of molecular sciences · 2024Review
- Mitochondrial unfolded protein response (UPRFrontiers in cell and developmental biology · 2024Review
- Review
- Exercise Intervention for Alzheimer's Disease: Unraveling Neurobiological Mechanisms and Assessing Effects.Life (Basel, Switzerland) · 2023Review
- Analysis of Why Alzheimer's Dementia Never Spontaneously Reverses, Suggests the Basis for Curative Treatment.Journal of clinical medicine · 2023Article
- Microglial Expression of the Wnt Signaling ModulatoreNeuro · 2023Article
- Menopause and development of Alzheimer's disease: Roles of neural glucose metabolism and Wnt signaling.Frontiers in endocrinology · 2022Review
- Protective effect of chlorogenic acid on cognitive impairment in rats with early Alzheimer's disease via Wnt signaling pathway.Journal of Alzheimer's disease reportsArticle
- Elevated sclerostin levels in cerebrospinal fluid are associated with cognitive impairment in the Alzheimer's disease continuum.Alzheimer's & dementia (Amsterdam, Netherlands)Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular processes regulated by WNT signaling have been mainly studied during embryonic development and cancer. In the last two decades, the role of WNT in the adult central nervous system has been the focus of interest in our laboratory. In this chapter, we will be summarized β-catenin-dependent and -independent WNT pathways, then we will be revised WNT signaling function at the pre- and post-synaptic level. Concerning Alzheimer's disease (AD) initially, we found that WNT/β-catenin signaling activation exerts a neuroprotective mechanism against the amyloid β (Αβ) peptide toxicity. Later, we found that WNT/β-catenin participates in Tau phosphorylation and in learning and memory. In the last years, we demonstrated that WNT/β-catenin signaling is instrumental in the amyloid precursor protein (APP) processing and that WNT/β-catenin dysfunction results in Aβ production and aggregation. We highlight the importance of WNT/β-catenin signaling dysfunction in the onset of AD and propose that the loss of WNT/β-catenin signaling is a triggering factor of AD. The WNT pathway is therefore positioned as a therapeutic target for AD and could be a valid concept for improving AD therapy. We think that metabolism and inflammation will be relevant when defining future research in the context of WNT signaling and the neurodegeneration associated with AD.
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