Soluble Aβ oligomer production and toxicity

Authors

  • Megan E. Larson,

    1. Departments of Neuroscience, University of Minnesota, Minneapolis, Minnesota, USA
    2. N. Bud Grossman Center for Memory Research and Care, University of Minnesota, Minneapolis, Minnesota, USA
    3. Institute for Translational Neuroscience, University of Minnesota, Minneapolis, Minnesota, USA
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  • Sylvain E. Lesné

    1. Departments of Neuroscience, University of Minnesota, Minneapolis, Minnesota, USA
    2. N. Bud Grossman Center for Memory Research and Care, University of Minnesota, Minneapolis, Minnesota, USA
    3. Institute for Translational Neuroscience, University of Minnesota, Minneapolis, Minnesota, USA
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Address correspondence and reprint requests to Sylvain E. Lesné, PhD, Assistant Professor, Institute for Translational Neuroscience Scholar, University of Minnesota, Department of Neuroscience, Wallin Medical Biosciences Building, 5-180, 2101 Sixth Street SE, CDC 2641, Minneapolis, MN 55414, USA. E-mail: lesne002@umn.edu

Abstract

J. Neurochem. (2012) 120 (Suppl. 1), 125–139.

Abstract

For nearly 100 years following the first description of this neurological disorder by Dr Alois Alzheimer, amyloid plaques and neurofibrillary tangles have been hypothesized to cause neuronal loss. With evidence that the extent of insoluble, deposited amyloid poorly correlated with cognitive impairment, research efforts focused on soluble forms of Aβ, also referred as Aβ oligomers. Following a decade of studies, soluble oligomeric forms of Aβ are now believed to induce the deleterious cascade(s) involved in the pathophysiology of Alzheimer’s disease. In this review, we will discuss our current understanding about endogenous oligomeric Aβ production, their relative toxicity in vivo and in vitro, and explore the potential future directions needed for the field.

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