Soluble Aβ oligomer production and toxicity
Top Cited Papers
Open Access
- 28 November 2011
- journal article
- review article
- Published by Wiley in Journal of Neurochemistry
- Vol. 120 (s1) , 125-139
- https://doi.org/10.1111/j.1471-4159.2011.07478.x
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.Keywords
This publication has 90 references indexed in Scilit:
- Aβ Oligomer-Induced Synapse Degeneration in Alzheimer’s DiseaseCellular and Molecular Neurobiology, 2011
- The prion protein as a receptor for amyloid-βNature, 2010
- Prion protein in Alzheimer's pathogenesis: a hot and controversial issueEMBO Molecular Medicine, 2010
- Prion protein and Aβ‐related synaptic toxicity impairmentEMBO Molecular Medicine, 2010
- Deleterious Effects of Amyloid β Oligomers Acting as an Extracellular Scaffold for mGluR5Neuron, 2010
- Cognitive effects of cell-derived and synthetically derived Aβ oligomersNeurobiology of Aging, 2010
- Biochemical and immunohistochemical analysis of an Alzheimer's disease mouse model reveals the presence of multiple cerebral Aβ assembly forms throughout lifeNeurobiology of Disease, 2009
- Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate UptakeNeuron, 2009
- Plaque-bearing mice with reduced levels of oligomeric amyloid-β assemblies have intact memory functionNeuroscience, 2007
- RAGE and amyloid-β peptide neurotoxicity in Alzheimer's diseaseNature, 1996