Autophagy and Neurodegeneration

Tuesday, November 20th, 2018 - 9 am CST / 3pm GMT / 4pm CET 


Intra­cellular pro­tein ag­gre­gation is a feature of many late-onset neuro­degenerative dis­eases, including Parkinson’s dis­ease, tauopathies, and poly­glutamine expansion dis­eases (like Huntington’s dis­ease (HD)). Many of these mutant pro­teins, like that causing HD, cause dis­ease via toxic gain-of-func­tion mecha­nisms. There­fore, the factors regu­lating their clearance are crucial for under­standing dis­ease patho­genesis and for de­velop­ing rational thera­peutic strategies. 

The two major in­tra­cellular pro­tein degradation pathways are the ubiquitin-pro­teasome system and (macro­)auto­phagy. We showed that the auto­phagy inducer, rapamycin, re­duced the levels of mutant huntingtin and attenuated its toxicity in cells, and in Drosophila and mouse HD models. We have ex­tended the range of in­tra­cellular pro­teinopathy substrates that are cleared by auto­phagy to other related neuro­degenerative dis­eases including Parkinson’s dis­ease. Autophagy induction is generally considered neuroprotective in various neurodegenerative models, and certain genetic variants in neurodegenerative diseases are associated with compromised autophagy.

Learning Objectives:

  • Understand the basic biology of autophagy and its role in neurodegeneration
  • Understand how genetic variants in Parkinson’s disease, Alzheimer’s disease and polyglutamine diseases impact autophagosome biogenesis.

David Rubinsztein, Ph.D.
University of Cambridge, Alzheimer’s Research Cambridge Drug Discovery Institute, and UK Dementia Research Institute
View Biography
Ray Chan, Ph.D.
View Biography

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