PerspectiveNEURODEGENERATION

Early network dysfunction in Alzheimer's disease

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Science  09 Aug 2019:
Vol. 365, Issue 6453, pp. 540-541
DOI: 10.1126/science.aay5188

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Summary

Aggregation of the β-amyloid peptide (Aβ) in brain regions serving memory and cognition is thought to initiate Alzheimer's disease (AD) (1). Despite myriad studies of the neurobiological effects of the peptide, two central questions remain unsettled: What forms of Aβ are the principal bioactive neurotoxins in humans, and precisely how do these forms undermine neuronal function? Attempts to therapeutically lower or neutralize Aβ in humans have so far failed to definitively slow AD symptoms, and successful approaches may require answers to these two queries. On page 559 of this issue, Zott et al. (2) provide compelling evidence that the first answer is soluble Aβ dimers, and the second answer is through hyperexcitability of glutamatergic neurons when the dimers interfere with the reuptake of extracellular glutamate.

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