WNT signaling in neuronal maturation and synaptogenesis
Open accessAbstract
The Wnt signaling pathway plays a role in the development of the central nervous system and growing evidence indicates that Wnts also regulates the structure and function of the adult nervous system. Wnt components are key regulators of a variety of developmental processes, including embryonic patterning, cell specification, and cell polarity. In the nervous system, Wnt signaling also regulates the formation and function of neuronal circuits by controlling neuronal differentiation, axon outgrowth and guidance, dendrite development, synaptic function, and neuronal plasticity. Wnt factors can signal through three very well characterized cascades: canonical or β-catenin pathway, planar cell polarity pathway and calcium pathway that control different processes. However, divergent downstream cascades have been identified to control neuronal morphogenesis. In the nervous system, the expression of Wnt proteins is a highly controlled process. In addition, deregulation of Wnt signaling has been associated with neurodegenerative diseases. Here, we will review different aspects of neuronal and dendrite maturation, including spinogenesis and synaptogenesis. Finally, the role of Wnt pathway components on Alzheimer's disease will be revised.
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PI3K/AKT, RAS/ERK, WNT and β-catenin pathways control soma size, dendritic arborization, axon generation, spine development and synapse function.
“These pathways control soma size, dendritic arborization, axon generation, spine development and synapse function [184–188].”
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- Authors
- Rosso, S. B., & Inestrosa, N. C.
- Affiliations
- National University of Rosario (AR)
- Pontificia Universidad Católica de Chile (CL)
- Corresponding author
- Rosso, Silvana B.
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2013
- Volume
- 7
- Pages
- 103-103
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC3701138
- OpenAlex
- W2161428975
- Cited by
- 272
- References
- 120
- Citations by year
- 2026: 14 · 2025: 29 · 2024: 24 · 2023: 20 · 2022: 31 · 2021: 20 · 2020: 22 · 2019: 16 · 2018: 15 · 2017: 18 · 2016: 17 · 2015: 21 · 2014: 24 · 2013: 1
- FWCI
- 9.40
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Repositorio Hipermedial UNR (Universidad Nacional de Rosario) (publishedVersion, cc-by)
- Americanae (AECID Library) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-sa)
- Greater South Information System
- Funders
- Consejo Nacional de Investigaciones Científicas y Técnicas (PIP-2012)
- Comisión Nacional de Investigación Científica y Tecnológica (12/2007, PFB12/2007)
- Agencia Nacional de Promoción Científica y Tecnológica (CONICET)
- Fondo para la Investigación Científica y Tecnológica
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- Wnt signaling, neuronal maturation, synaptogenesis, dendrite formation, neuronal differentiation, axon guidance, neuroplasticity, canonical Wnt/β-catenin pathway, planar cell polarity pathway, calcium signaling, neuronal morphogenesis, neurodegenerative diseases, Alzheimer's disease, spinogenesis
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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.
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