The paper:
J.L. Cleary et al., "Natural oligomers of the amyloid-β protein specifically disrupt cognitive function," Nat Neurosci, 8:79?84, 2005. (Cited in 124 papers)
The finding:
James Cleary at the Minneapolis VA Medical Center and colleagues revealed that soluble human forms of amyloid-β oligomer (a-β), a protein implicated in Alzheimer disease, disrupted rats' memory of a learned lever-pressing task. "We didn't see any neurotoxicity, yet we saw cognitive deficits show up shortly after we gave them [the a-β]," Cleary says. The effect went away within just a few hours. "If you tested the animal again a day later, it was able to do the task beautifully," says coauthor Dennis Selkoe.
The significance: While previous studies had found cognitive impairments from mixtures of synthetic fibrils, monomers, and oligomers, the effects on cognition of the isolated form of a-β oligomers had never been characterized. "I think it was an important step in ...
