Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 285, Issue 15, Pages 11061-11067Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.R109.072181
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Funding
- Medical Research Council
- European Union Framework VI (EUROSCA)
- National Institute for Health Research Biomedical Research Centre at Addenbrooke's Hospital
- MRC [G0600194] Funding Source: UKRI
- Medical Research Council [G0600194] Funding Source: researchfish
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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.
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