Minireviews
Chemical Inducers of Autophagy That Enhance the Clearance of Mutant Proteins in Neurodegenerative Diseases*

https://doi.org/10.1074/jbc.R109.072181Get rights and content
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Many of the neurodegenerative diseases that afflict people are caused by intracytoplasmic aggregate-prone proteins. These include Parkinson disease, tauopathies, and polyglutamine expansion diseases such as Huntington disease. In Mendelian forms of these diseases, the mutations generally confer toxic novel functions on the relevant proteins. Thus, one potential strategy for dealing with these mutant proteins is to enhance their degradation. This can be achieved by up-regulating macroautophagy, which we will henceforth call autophagy. In this minireview, we will consider the reasons why autophagy up-regulation may be a powerful strategy for these diseases. In addition, we will consider some of the drugs and associated signaling pathways that can be used to induce autophagy with these therapeutic aims in mind.

Diseases/Amyloid
Metabolism
Signal Transduction/Protein Kinases/Calmodulin
Subcellular Organelles/Lysosomes
Tissue/Organ Systems/Brain
Toxins/Drugs/Xenobiotics/Drug Action
Autophagy
Drug Screen

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*

This work was supported in part by the Medical Research Council, European Union Framework VI (EUROSCA), and the National Institute for Health Research Biomedical Research Centre at Addenbrooke's Hospital. This is the sixth of six articles in the “Chemical Biology Meets Biological Chemistry Minireview Series.” This minireview will be reprinted in the 2010 Minireview Compendium, which will be available in January, 2011.

1

Both authors contributed equally to this work.