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

Autophagy
Silvia CorrochanoAbraham Acevedo-Arozena

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 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.

Citations

May 8, 2013·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Anne Messer, Shubhada N Joshi
Sep 1, 2012·Nature Reviews. Drug Discovery·David C RubinszteinBeth Levine
Aug 18, 2012·Journal of Biophysics·María Elena Chánez-Cárdenas, Edgar Vázquez-Contreras
Aug 5, 2015·Journal of Neuroscience Methods·Elizabeth A Lewis, Gaynor A Smith
May 29, 2016·Molecular and Cellular Neurosciences·Juan PeruchoMaría José Casarejos
Jan 25, 2019·Translational Neurodegeneration·Shen-Zhao LuJia-Wei Zhou
Aug 21, 2019·Ageing Research Reviews·Paramita ChaudhuriKarunakar Kar
Dec 30, 2020·Journal of Neurochemistry·Marijn KuijpersTolga Soykan
Apr 21, 2021·Biomolecules & Therapeutics·McNeil ValenciaSung Hoon Lee

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