Evidence is accumulating that in chronic neurodegenerative diseases such as Alzheimer disease (AD), Parkinson disease (PD), Huntington disease (HD), and amyotrophic lateral sclerosis (ALS) are due to a combination of events triggered by expression and accumulation of misfolded proteins that impair neuronal function. More recent developments have shown that, in certain diseases, a mutant RNA triggers the formation of nuclear inclusions and pathogenesis. In this meeting, emphasis will placed on understanding cellular pathways that are implicated in some of the more common and intriguing neurodegenerative disorders, with the aim of providing a foundation for their treatment.

Upon completion of this meeting, participants should be able to

• analyze the basic mechanisms by which cells (neurons) fold proteins, and recognize and process misfolded proteins.
• examine the extent to which protein misfolding underlies pathogenesis for several key neruodegenerative disorders (e.g. Alzheimer disease, ALS, and the polyglutamine disease).
• consider the role of various cellular pathways leading to neurodegeneration and how the presence of misfolded proteins may alter the function of these pathways.
• discuss potential strategies for the development of new treatments for neurodegeneration.