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 …