64th Annual Meeting of the American Academy of Neurology
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Pharm Med 2012; 26 (5): 309-316 1178-2595/12/0005-0309/$49.95/0 Adis ª 2012 Springer International Publishing AG. All rights reserved.
64th Annual Meeting of the American Academy of Neurology 21-28 April 2012; New Orleans, LA, USA Sue Pochon Adis, Auckland, New Zealand
The 2012 annual meeting of the American Academy of Neurology (AAN) was held in New Orleans, LA, USA during the last week of April and offered a diverse programme of educational and scientific highlights in the field of neurology. The annual meeting also provided an ideal forum for the Academy to announce a change in their name and branding, and to reposition the organization as a world leader in raising money to cure brain diseases. Henceforth, the AAN will be known as the American Brain Foundation (www. curebraindisease.org). The following meeting report reviews some of the most interesting science from the plenary and scientific sessions at this year’s annual meeting. 1. Presidential Plenary Session The chosen theme for the presidential plenary session was RNA. The Chair of the Science Committee, Dr Lisa DeAngelis, opened the session by introducing the Academy President Dr Bruce Sigsbee. Dr Sigsbee announced the winner of the 2012 Presidential Award – Dr John Corboy – for his work on launching the Clinical Practice Journal. Dr Sisgbee then introduced the Presidential Lecture, entitled Epigenetics: A New Science of Brain and Behaviour, which was given by Dr Mark F. Mehler from Albert Einstein College of Medicine, Bronx, NY, USA. Dr Mehler began his lecture by telling the audience that we are in a scientific revolution to transform the practice of medicine. Epigenetics will help us to decipher the evolution of human brain form and function and the complexity of cellular identities and connectivity, he said. In essence, we now know that humans have a second, more sophisticated genome. The discovery came from the realization that not all RNA encodes for proteins. There are at least a million, and likely several million, non-coding RNAs (ncRNAs) in humans and we see an
explosive growth of these ncRNAs during evolution with regards to brain complexity. Epigenetics is the modification of gene expression and function not requiring primary changes in nucleotide sequence (see figure 1). We are now beginning to develop paradigms for understanding epigenetic mechanisms in neurological disease states. For example, repressor element-1 silencing transcription factor (REST) and corepressor for element-1 silencing transcription factor (CoREST) are known to be master transcriptional/ epigenetic regulators, and REST has been shown to be deregulated in several diseases. It was an insight with the potential to transform our understanding of the biology of disease when we learned that a single pathogenetic mutation in a single base pair could interrupt a series of ncRNA networks. Key features of ncRNAs include: bioenergetics: they have a lower demand for energy; sensitivity: to intracellular and environmental stimuli; versatile: seamless links between DNA, RNA
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