α-synuclein levels affect autophagosome numbers in vivo and modulate Huntington disease pathology

• Published in: Autophagy 2012-03, Vol.8 (3), p.431-432
• Main Authors: Corrochano, Silvia, Renna, Maurizio, Tomas-Zapico, Cristina, Brown, Steve D.M., Lucas, Jose J., Rubinsztein, David C., Acevedo-Arozena, Abraham
• Format: Article
• Language: English
• Subjects: alpha-Synuclein - metabolism; Animals; Autophagy; Binding; Biology; Bioscience; Calcium; Cancer; Cell; Cycle; Disease Models, Animal; Drosophila melanogaster - metabolism; Humans; Huntington disease; Huntington Disease - metabolism; Huntington Disease - pathology; Landes; Mice; Microtubule-Associated Proteins - metabolism; mouse models; Mutant Proteins - metabolism; Organogenesis; Parkinson disease; Phagosomes - metabolism; Proteins; α-synuclein
• ISSN: 1554-8627; 1554-8635
• DOI: 10.4161/auto.19259

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 α-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.