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Early network dysfunction in Alzheimer's disease


Aggregation of β-amyloid peptide (Aβ) in brain regions that serve memory and cognition are thought to initiate Alzheimer's disease (AD) (1) Despite extensive studies on the neurobiological effects of the peptide, two central questions remain unresolved: What forms of Aβ are the major bioactive neurotoxins in humans, and exactly how do these forms undermine neuronal function? Attempts at therapeutically lowering or neutralizing Av in humans have so far failed to substantially slow the symptoms of AD, and successful approaches may require answers to these two questions. On page 559 of this issue, Lot et al. (2) to provide compelling evidence that the first response is soluble in Ae dimers, and the second response is through hypersensitivity to glutamatergic neurons when the dimers are mixed to receive extracellular glutamate again.

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