Autophagy and Neuroprotection

October 19 - 27, 2013

Coordinator: A.M. Cuervo

Albert Einstein College of Medicine, New York, USA

Faculties:

Anne Simonsen, Oslo University, Oslo, Norway

David Rubinsztein, Cambridge University, Cambridge, UK

Ivan Dikic, Frankfurt University Medical School, Frankfurt, Germany

Rajat Singh, Albert Einstein College of Medicine, New York, USA

Steven Finkbeiner, The Gladstone Institute, San Francisco, USA

Ralph Nixon, New York University, New York, USA

Roberta Gottlieb, San Diego State University, San Diego, USA

Autophagy has revealed in recent years as an essential mechanism for maintenance of cellular homeostasis and as part of the cellular response to stress. Far away are now the days in which the occurrence of autophagy in neurons was questioned based on the pre-conception that autophagy was only activated during nutrient deprivation and the brain was protected from such stress. Growing evidence supports now that not only autophagy occurs normally in neurons, but that proper functioning of this catabolic pathway is required for normal functioning of neuronal cells. Autophagy, as in many other organs, plays diverse roles in CNS that include among others, quality control, through the elimination of abnormal or pathogenic cellular components, adaptation to metabolic changes, through the mobilization of intracellular energy stores, defense against stressors that cause cellular damage, through the elimination of damaged structures, and first front of response against neurotropic pathogens.

This advanced Course will provide an in-depth overview of the molecular mechanisms, steps and variations of the autophagic process with emphasis on the peculiarities relevant to neurons. The important role of autophagy as part of the neuronal mechanisms for quality control will be discussed using as reference the elimination of pathogenic proteins through this pathway. Several lecturers will conceptualize our current understanding on how these pathogenic proteins are identified and delivered for degradation and how the different proteolytic systems may act coordinately in the fight against proteotoxicity. Attention will also be placed on the recent findings that support the contribution of alterations of autophagy to the pathogenic basis of important neurodegenerative disorders such as Parkinson's Disease, Alzheimer's disease, Huntington's diseases and tauopathies. Novel state-of-the-art procedures to track the autophagic system in neurons will be discussed along with some of the successful recent stories of use of autophagy modulators to protect neurons against stressors such as proteotoxicity. The Course will also cover the importance of autophagy as a catabolic process that contributes to modulate the cellular energetic balance through processes such as mitophagy or lipophagy. Structured discussion sessions and opportunities for informal afternoon and evening gatherings will make the Course a venue particularly suitable for intense interaction with the Faculties.

The generous support of Roche (Switzerland) is acknowledged.