Neuronal function of Alzheimer's protein

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Science  11 Jan 2019:
Vol. 363, Issue 6423, pp. 123-124
DOI: 10.1126/science.aaw0636

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For a long time, the huge importance of the cleavage product of the amyloid precursor protein (APP), amyloid-β (Aβ), in the etiology of Alzheimer's disease (AD) (1) has occluded the view of the physiological function of APP. But over the years, it has become clear that APP and its proteolytic products have important physiological functions (2) during brain development or in the adult brain in processes of activity-dependent synaptic plasticity (3) and possibly even protection against neurodegeneration (4, 5). On page 143 of this issue, Rice et al. (6) discovered that a sushi-containing neurotransmitter receptor in the brain, GABABR1a (γ-aminobutyric acid type B receptor subunit 1a), has a new interaction partner, APP. This provides important insights about the physiological function of APP and might open new avenues to treat AD—not only through targeting Aβ but also by strengthening alternate routes of cleaving APP and utilizing nonamylogenic pathways.