Li S, Hong S, Shepardson NE et al.Harvard Medical School, Boston, MA, USA. Neuron 2009;62:788–801.
Editor’s note: This article provides impressive, basic science laboratory evidence for a mechanism of brain damage by the soluble oligomers of amyloid, the species of amyloid that are currently credited with being the damaging moieties according to the latest resurrection of the “amyloid cascade hypothesis”. In these experiments, such amyloid fractions interfered with uptake of the critical neurotransmitter glutamate. The data are solid, and this article is likely to be widely cited. However, it is not clear whether the effects that are noted are primarily due to free radical damage from oxidized forms of amyloid (which themselves have the potential to act as oxidizing agents). One wishes that evidence were cited on whether or not the effect would have been modified by pretreating the responsible amyloid preparations with a strong reducing agent (such as BH4, which would remove all oxidized moieties.)