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Protective Roles for Induction of Autophagy in Multiple Proteinopathies

Fiona M. Menzies, Brinda Ravikumar and David C. Rubinsztein

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Many late-onset neurodegenerative diseases, including Parkinson’s disease, tauopathies, Huntington’s disease and forms of spinocerebellar ataxia, are caused by aggregate-prone proteins. Previously we showed that mutant huntingtin is an autophagy substrate and that autophagy induction reduced soluble and aggregated huntingtin and attenuated its toxicity in cell, fly and mouse models of disease. We have recently shown in cell and fly models that autophagy induction may have general protective effects across a range of diseases caused by aggregate-prone intracellular proteins. First, we showed that this strategy reduces the levels of the primary toxin, the aggregate-prone mutant protein. Second, our recent work suggests that autophagy induction may have additional cytoprotective effects by protecting cells against a range of subsequent pro-apoptotic insults.

Authors

Fiona M. Menzies

Brinda Ravikumar

David C. Rubinsztein

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If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.