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2. α-Synuclein levels affect autophagosome numbers in vivo and modulate Huntington disease pathology

Author

Cristina Tomás-Zapico, Abraham Acevedo-Arozena, José J. Lucas, Steve D.M. Brown, Silvia Corrochano, David C. Rubinsztein, Maurizio Renna, Corrochano, Silvia, Renna, Maurizio, Tomas-Zapico, Cristina, Brown, Steve D. M., Lucas, Jose J., Rubinsztein, David C., and Acevedo-Arozena, Abraham

Subjects
Autophagosome, Pathology, medicine.medical_specialty, Huntingtin, Mutant, α, Biology, Mouse models, Mouse model, chemistry.chemical_compound, Mice, Downregulation and upregulation, Mutant Protein, In vivo, Phagosomes, mental disorders, medicine, Autophagy, Animals, Humans, Molecular Biology, Phagosome, Alpha-synuclein, Animal, Microtubule-Associated Protein, Cell Biology, Huntington disease, In vitro, Cell biology, nervous system diseases, Parkinson disease, Disease Models, Animal, a-synuclein, Drosophila melanogaster, Huntington Disease, chemistry, nervous system, alpha-Synuclein, Mutant Proteins, synuclein, Microtubule-Associated Proteins, Human
Abstract

Huntington and Parkinson diseases (HD and PD) are two major neurodegenerative disorders pathologically characterized by the accumulation of the aggregate-prone proteins mutant huntingtin (in HD) and a-synuclein (in PD). Mutant huntingtin is an autophagy substrate and autophagy modulators affect HD pathology both in vitro and in vivo. In vitro, α-synuclein levels are able to modulate autophagy: α-synuclein overexpression inhibits autophagy, whereas downregulation promotes autophagy. Here, we review our recent studies showing that α-synuclein levels modulate mutant huntingtin toxicity in mouse models. This phenotypic modification is accompanied by the in vivo modulation of autophagosome numbers in mouse brains from both control and HD mice expressing different levels of α-synuclein. © 2012 Landes Bioscience.

Published
2012

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