Conférence le 7 avril : Mitochondrial, lysosomal and peroxisomal dysfunctions in neurodegenerative diseases: biological and pharmacological aspects

Gerard Lizard Pasteur TunisLundi 7 avril 2014, dans l'amphithéâtre du bâtiment recherche, Gérard Lizard, de l'Université de Bourgogne / chef de l'Equipe Bio-peroxIL (Biochimie du peroxysome, inflammation et métabolisme lipidique ; EA 7270) / INSERM, Dijon, France, proposera une conférence intitulée : "Mitochondrial, lysosomal and peroxisomal dysfunctions in neurodegenerative diseases: biological and pharmacological aspects".

Résumé de la conférence :
Neurodegeneration results from a combination of various genetic, lifestyle, and environmental factors. In neurodegenative diseases, especially age-related degenerative diseases, the part taken by organelle (mitochondria, peroxisome, and lysosome) dysfunctions seems important. It is now well admitted that morphologic, topographic, and biochemical mitochondrial changes (bioenergetic failure) are involved in neurodegeneration, and could be a consequence of reactive oxygen species overproduction resulting from a rupture of RedOx homeostasia. This oxidative stress leading to mitochondrial dysfunctions could contribute to activate cell death and promote neurodegeneration. Beside mitochondria, peroxisome is also an important organelle. These two organelles are tightly connected for fatty acid metabolism. Peroxisome is present in all cell types, excepted in erythrocytes, and contributes to lipid and RedOx homeostasia, as well as to non-cytokinic equilibrium. The activity of catalase, a specific peroxisomal enzyme, is known to decline with age (hypocatalasemia) suggesting a decrease of peroxisomal metabolism. This could further contribute to favor a decrease of DHA (C22:6 n-3), endogeneouly produced by peroxisomal beta-oxidation, and subsequently metabolized to neuroprotectine D1 (NPD1) which is one of the main DHA derivatives in brain cells, and which is produced as an early response to neurodegeneration. As mitophagy and pexophagy could also contribute to enhanced mitochondrial and peroxisomal dysfunctions, these events which require lysomal activities, may also play critical roles in neurodegenerative diseases. Therefore, the part taken by lysosome in demyelinating or non-demyelinating neurodegenerative disease is also widely suspected. As several studies support that organelle dysfunctions can contribute to different types of neurological diseases, they constitute major new pharmacological targets in order to prevent or treat neurological diseases which will further increase in future years and decades.

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