Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum?

By W. Klein, G. Krafft, C. Finch. 2001

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Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007, background): “This new impact on synapses complements previous studies showing that ADDLs selectively compromise synaptic plasticity (Lambert et al., 1998; Klein et al., 2001; Wang et al., 2002) and nerve cell viability (Lambert et al., 1998).”
Progesterone receptors: form and function in brain. (2008, neutral): “Thus, factors that have the net effect of reducing the pool of soluble A β are thought to represent potentially powerful strategies for preventing the development of AD [294;295].”
The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Aβ protofibril formation (2001, background): “Indeed, our findings open new avenues for possible therapeutic intervention using drugs targeted at preventing protofibril formatio”
What is the role of protein aggregation in neurodegeneration? (2005, background): “Several groups have identified soluble oligomeric Aβ aggregates and have called them Aβ diffusible ligands (ADDL), paranuclei, protofibrils or other term”
Paradigm shifts in Alzheimer's disease and other neurodegenerative disorders: The emerging role of oligomeric assemblies (2002, positive): “Mounting evidence, however, suggests that soluble, oligomeric A (cid:1) assemblies cause substantial neuronal dysfunction before the appearance of amyloid deposits (Klein et al., 2001).”