Convergent mechanisms between autophagia and axonal function and metabolic influence in the regulation of neurodegenerative diseases. (Q3144266): Difference between revisions
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(Created claim: summary (P836): Axonal degeneration or axonopathy is a very common feature in many neurodegenerative diseases such as Parkinson’s Disease (PD), Alzheimer’s disease (AD) or X-associated Adrenoleucodystrophy (X-ALD). However, the molecular pathways that regulate this process are unknown. We have recently shown in C. elegans that the activity of Rac1 in phagocytosis of apoptotic cells, intimately related to autophagia, is regulated by proteasome [1]. Besides, we a...) |
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Convergent mechanisms between autophagia and axonal function and metabolic influence in the regulation of neurodegenerative diseases. | |||
Revision as of 14:01, 12 October 2021
Project Q3144266 in Spain
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | Convergent mechanisms between autophagia and axonal function and metabolic influence in the regulation of neurodegenerative diseases. |
Project Q3144266 in Spain |
Statements
12,250.0 Euro
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24,500.0 Euro
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50.0 percent
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1 January 2016
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16 December 2018
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UNIVERSIDAD AUTONOMA DE BARCELONA
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41°29'27.71"N, 2°8'15.00"E
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08266
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La degeneración axonal o axonopatía es un rasgo muy común en muchas enfermedades neurodegenerativas como la Enfermedad de Parkinson (EP), enfermedad de Alzheimer (EA) o Adrenoleucodistrofia asociada a X (X-ALD). Sin embargo, las vías moleculares que regulan este proceso se desconocen. Recientemente hemos demostrado en C. elegans que la actividad de Rac1 en la fagocitosis de las células apoptóticas, íntimamente relacionada con la autofagia, está regulada por el proteasoma [1]. A parte, tenemos también datos preliminares en C. elegans que sugieren una influencia metabólica en la integridad axonal [41]. El transporte axonal es necesario para asegurar la homeóstasis neuronal, cuyo mantenimiento está parcialmente regulado por mecanismos de degradación celulares, como la autofagia [2]. El objetivo principal del proyecto es el de entender la influencia del metabolismo en el papel que tienen los mecanismos de limpieza celular para el desarrollo de las enfermedades neurodegenerativas. Metodologia: Utilitzaremos al nematodo C. elegans como modelo de enfermedad neurodegenerativa por las ventajas de este organismo respecto otros modelos animales. Destacamos la alta homología entre sus genes y los genes humanos, la alta tasa de reproducción, un ciclo vital de entre 10 y 12 días a 20ºC y mantenimiento muy económico de las estirpes. La metodología utilizada en el nematodo incluye básicamente a) generación de líneas transgénicas b) técnicas estándar de clonaje y microinyección c) estudios de comportamiento neuronal d) microscopía confocal y d) librerías genéticas de RNAi. Finalmente, esperamos corroborar estos resultados en cultivos celulares procedentes de pacientes con EP (Spanish)
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Axonal degeneration or axonopathy is a very common feature in many neurodegenerative diseases such as Parkinson’s Disease (PD), Alzheimer’s disease (AD) or X-associated Adrenoleucodystrophy (X-ALD). However, the molecular pathways that regulate this process are unknown. We have recently shown in C. elegans that the activity of Rac1 in phagocytosis of apoptotic cells, intimately related to autophagia, is regulated by proteasome [1]. Besides, we also have preliminary data in C. elegans that suggest a metabolic influence on axonal integrity [41]. Axonal transport is necessary to ensure neuronal homeostasis, the maintenance of which is partially regulated by cellular degradation mechanisms, such as autophagia [2]. The main objective of the project is to understand the influence of metabolism on the role of cellular cleansing mechanisms for the development of neurodegenerative diseases. Methodology: We will use the nematode C. elegans as a model of neurodegenerative disease because of the advantages of this organism over other animal models. We highlight the high homology between its genes and human genes, the high reproduction rate, a life cycle between 10 and 12 days at 20 °C and very economical maintenance of the strains. The methodology used in the nematode includes basically a) generation of transgenic lines b) standard cloning and microinjection techniques c) neuronal behavioral studies d) confocal microscopy and d) genetic libraries of RNAi. Finally, we hope to corroborate these results in cell cultures from patients with PE (English)
12 October 2021
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Cerdanyola del Vallès
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Identifiers
PI15_01255
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