Otros/as autores/as

Institut Català de la Salut

[Coccia E, Solé M, Comella JX] Grup de Recerca en Senyalització Cel·lular i Apoptosi, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED), ISCIII, Madrid, Spain. Departament de Bioquímica i Biologia Molecular, Facultat de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain

Vall d'Hebron Barcelona Hospital Campus

Fecha de publicación

2023-01-09T12:27:26Z

2023-01-09T12:27:26Z

2022-01-10



Resumen

Alzheimer's disease; Axon remodeling; Synaptic plasticity


Malaltia d'Alzheimer; Remodelació axònica; Plasticitat sinàptica


Enfermedad de Alzheimer; Remodelación axónica; Plasticidad sináptica


Apoptosis is crucial for the correct development of the nervous system. In adulthood, the same protein machinery involved in programmed cell death can control neuronal adaptiveness through modulation of synaptic pruning and synaptic plasticity processes. Caspases are the main executioners in these molecular pathways, and their strict regulation is essential to perform neuronal remodeling preserving cell survival. FAIM-L and SIVA-1 are regulators of caspase activation. In this review we will focus on FAIM-L and SIVA-1 as two functional antagonists that modulate non-apoptotic caspase activity in neurons. Their participation in long-term depression and neurite pruning will be described in base of the latest studies performed. In addition, the association of FAIM-L non-apoptotic functions with the neurodegeneration process will be reviewed.

Tipo de documento

Artículo


Versión publicada

Lengua

Inglés

Publicado por

Frontiers Media

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Frontiers in Cell and Developmental Biology;9

https://doi.org/10.3389/fcell.2021.826037

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Derechos

Attribution 4.0 International

http://creativecommons.org/licenses/by/4.0/

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