c-Abl kinase at the crossroads of healthy synaptic remodeling and synaptic dysfunction in neurodegenerative diseases

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dc.catalogadoraba
dc.contributor.authorGutiérrez García, Daniela A.
dc.contributor.authorChandía Cristi, América Valeska
dc.contributor.authorYanez, Maria Jose
dc.contributor.authorZanlungo Matsuhiro, Silvana
dc.contributor.authorÁlvarez Rojas, Alejandra
dc.date.accessioned2024-06-10T21:25:33Z
dc.date.available2024-06-10T21:25:33Z
dc.date.issued2023
dc.description.abstractOur ability to learn and remember depends on the active formation, remodeling, and elimination of synapses. Thus, the development and growth of synapses as well as their weakening and elimination are essential for neuronal rewiring. The structural reorganization of synaptic complexes, changes in actin cytoskeleton and organelle dynamics, as well as modulation of gene expression, determine synaptic plasticity. It has been proposed that dysregulation of these key synaptic homeostatic processes underlies the synaptic dysfunction observed in many neurodegenerative diseases. Much is known about downstream signaling of activated N-methyl-D-aspartate and a-amino-3-hydroxy5-methyl-4-isoazolepropionate receptors; however, other signaling pathways can also contribute to synaptic plasticity and long-lasting changes in learning and memory. The non-receptor tyrosine kinase c-Abl (ABL1) is a key signal transducer of intra and extracellular signals, and it shuttles between the cytoplasm and the nucleus. This review focuses on c-Abl and its synaptic and neuronal functions. Here, we discuss the evidence showing that the activation of c-Abl can be detrimental to neurons, promoting the development of neurodegenerative diseases. Nevertheless, c-Abl activity seems to be in a pivotal balance between healthy synaptic plasticity, regulating dendritic spines remodeling and gene expression after cognitive training, and synaptic dysfunction and loss in neurodegenerative diseases. Thus, c-Abl genetic ablation not only improves learning and memory and modulates the brain genetic program of trained mice, but its absence provides dendritic spines resiliency against damage. Therefore, the present review has been designed to elucidate the common links between c-Abl regulation of structural changes that involve the actin cytoskeleton and organelles dynamics, and the transcriptional program activated during synaptic plasticity. By summarizing the recent discoveries on c-Abl functions, we aim to provide an overview of how its inhibition could be a potentially fruitful treatment to improve degenerative outcomes and delay memory loss.
dc.fechaingreso.objetodigital
dc.format.extent7 páginas
dc.fuente.origenWOS
dc.fuente.origenORCID
dc.identifier.doi10.4103/1673-5374.346540
dc.identifier.eissn1876-7958
dc.identifier.issn1673-5374
dc.identifier.urihttps://doi.org/10.4103/1673-5374.346540
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/86720
dc.identifier.wosidWOS:000834672700001
dc.information.autorucFacultad de Ciencias Biológicas; Gutiérrez García, Daniela A.; S/I; 1030646
dc.information.autorucFacultad de Ciencias Biológicas; Chandía Cristi, América Valeska; S/I; 237253
dc.information.autorucEscuela de Medicina; Zanlungo Matsuhiro, Silvana; 0000-0001-8383-9829; 72650
dc.information.autorucFacultad de Ciencias Biológicas; Álvarez Rojas, Alejandra; 0000-0002-8129-9280; 83681
dc.issue.numero2
dc.language.isoen
dc.nota.accesocontenido completo
dc.pagina.final243
dc.pagina.inicio237
dc.revistaNeural Regeneration Research
dc.rightsacceso abierto
dc.rights.licenseATTRIBUTION 4.0 INTERNATIONAL
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.en
dc.subjectActin cytoskeleton
dc.subjectActivity-dependent plasticity
dc.subjectAlzheimer's disease
dc.subjectc-Abl
dc.subjectDendritic spines
dc.subjectLearning
dc.subjectSynapse
dc.subjectSynaptic plasticity
dc.subjectTranscription
dc.subjectTyrosine kinase
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.titlec-Abl kinase at the crossroads of healthy synaptic remodeling and synaptic dysfunction in neurodegenerative diseases
dc.typereseña
dc.volumen18
sipa.codpersvinculados1030646
sipa.codpersvinculados237253
sipa.codpersvinculados72650
sipa.codpersvinculados83681
sipa.trazabilidadORCID;2024-06-03
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