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Increased Glucose Transport into Neurons Rescues Aβ Toxicity in Drosophila
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2016
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Current Biology 26Neurochemical BiomarkersSynaptic SignalingGlucose UptakeCellular PhysiologySocial SciencesGlucose TransportAlzheimer's DiseaseDegenerative PathologyMetabolic SignalingNeurochemistryMolecular NeuroscienceMolecular PhysiologyNeuropharmacologyNeuroprotectionNeurodegenerationNervous SystemCell BiologyNeurodegenerative DiseasesCellular NeurosciencePhysiologyNeuroscienceMolecular NeurobiologyMedicine
(Current Biology 26, 2291–2300; September 12, 2016) In this article, the neurons shown in Figure 1D were labeled with mtdTomato-3×HA, not GFP as originally stated in the Figure 1D legend and text online and in print. This error, which does not affect the interpretation of our results, has now been corrected in the article online. The authors apologize for the error. Increased Glucose Transport into Neurons Rescues Aβ Toxicity in DrosophilaNiccoli et al.Current BiologyAugust 11, 2016In BriefNiccoli et al. show that overexpression of the glucose transporter Glut1 in neurons rescues Aβ toxicity in a Drosophila Alzheimer’s disease model. This was associated with a reduction in Grp78 levels and induction of the unfolded protein response. This rescue can be mimicked by using metformin, a drug known to induce glucose uptake. Full-Text PDF Open Access