Journal of Alzheimers Disease & Parkinsonism
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For a century, the cardinal features of Alzheimer?s 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?)
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? 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? molecules that includes A? dimers, trimers, A?*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?
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? oligomers in AD.
Here, I will try to answer key questions related to A? oligomers using our recent data on endogenous A? oligomers and argue
why we should care about A? oligomers and how asking simple questions might generate impactful answers.
Sylvain Lesne attended college at the Universite de Caen, Basse-Normandie where he graduated with a master?s degree in Biochemistry (major
in Neuroscience) and a Ph.D. in Molecular and Cellular Biology (major in Neuroscience). He joined Karen H. Ashe?s 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).
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