天美传媒

Abstract

For a century, the cardinal features of Alzheimer锟絪 disease (AD), amyloid plaques and neurofibrillary tangles, were thought to underlie this chronic neurological disorder. However, based on the evidence accumulated over the past ten to fifteen years, the toxicity of these lesions has been questioned. Instead the emerging soluble aggregation-intermediate forms of amyloid-beta (A尾) and tau proteins, which compose plaques and tangles, are now believed to underlie the synaptic and neuronal losses observed in AD. Studies focusing on oligomeric A尾 assemblies have paved the way for other amyloid proteins including tau, alpha-synuclein and the prion protein PrP in the field of neurodegenerative disorders. This paradigm shift also contributed to complicating even more the putative sequence of biological events responsible for these diseases. The modern view of the amyloid hypothesis suggests the involvement of a multitude of endogenous bioactive A尾 molecules that includes A尾 dimers, trimers, A尾*56, annular protofibrils and amyloid plaques, as opposed to a single culprit (i.e. plaques). This increased complexity of the problem coupled with a lack of adequate experimental descriptions of the A尾 oligomers used renders interpretation and comparison of the observed phenomena between different research groups arduous and impedes on our progress to better understand the role of A尾 oligomers in AD. Here, I will try to answer key questions related to A尾 oligomers using our recent data on endogenous A尾 oligomers and argue why we should care about A尾 oligomers and how asking simple questions might generate impactful answers.

Biography

Sylvain Lesne attended college at the Universite de Caen, Basse-Normandie where he graduated with a master锟絪 degree in Biochemistry (major in Neuroscience) and a Ph.D. in Molecular and Cellular Biology (major in Neuroscience). He joined Karen H. Ashe锟絪 laboratory at the University of Minnesota in November 2002 as a postdoctoral research associate and moved on to becoming a research associate 2 years later. In December 2009, he joined the N. Bud Grossman Center for Memory Research and Care as an Institute for Translational Neuroscience Scholar and tenure-track Assistant Professor (Department of Neuroscience).