Natural oligomers of the amyloid-β protein specifically disrupt cognitive function
By J. Cleary, D. Walsh, J. Hofmeister, G. Shankar, M. Kuskowski, D. Selkoe, K. Ashe. Nature Neuroscience, 2005
1,747 citations recorded by the source corpus.
Subfields: Computational Theory and Mathematics, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/47013b5e93cf4450d6feb0673de391e560ffee53
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Computational Theory and Mathematics
In Molecular Biology
In Physiology
- D. Selkoe
- G. Shankar
- D. Walsh
- Bradley T. Hyman
- Matthew Townsend
- V. Lee
- T. Spires-Jones
- Bernardo L. Sabatini
Citations in the corpus
- Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, background): “Application of A or soluble oligomers (e.g., ADDLs), either in vitro or in vivo, adversely affects LTP and synaptic transmission (Lambert et al., 1998; Walsh et al., 2002; Wang et al., 2002; Cleary et al., 2005).”
- Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques (2009, background): “Interaction of oligomeric A with synapses may contribute to electrophysiological and behavioral deficits observed when it is injected into the brain (25, 26).”
- Progesterone receptors: form and function in brain. (2008, neutral): “In turn, elevated soluble Ab leads to the formation of an array of soluble oligomeric, minimally soluble aggregated, and eventually insoluble fibrillar Ab species, all of which are linked in a variety of ways to neurodegenerative cascades [53,217,216,245,179,190,251,164].”
- Effects of secreted oligomers of amyloid β‐protein on hippocampal synaptic plasticity: a potent role for trimers (2006, background): “Importantly, the same Aβ oligomers microinjected intraventricularly into healthy behaving rats impair their ability to recall a complex learned behaviour (Cleary et al. 2005).”
- Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway (2007, background): “Furthermore, physiologically relevant levels of cellderived A oligomers, but not monomers, acutely interrupt hippocampal synaptic plasticity in vivo and in slices and transiently impair learned behavior in rats (Walsh et al., 2002; Cleary et al., 2005; Townsend et al., 2006a).”
- Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease (2017, background): “Extensive studies also support the notion that soluble A oligomers represent the most toxic species that affect multiple early molecular mechanisms leading to synaptic dysfunction in AD [15].”