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Extracellular Zn2+Is Essential for Amyloid β1–42-Induced Cognitive Decline in the Normal Brain and Its Rescue
Journal of Neuroscience
Brain A␤ 1-42 accumulation is considered an upstream event in pathogenesis of Alzheimer's disease. However, accumulating evidence indicates that other neurochemical changes potentiate the toxicity of this constitutively generated peptide. Here we report that the interaction of A␤ 1-42 with extracellular Zn 2ϩ is essential for in vivo rapid uptake of A␤ 1-42 and Zn 2ϩ into dentate granule cells in the normal rat hippocampus. The uptake of both A␤ 1-42 and Zn 2ϩ was blocked by CaEDTA, andoi:10.1523/jneurosci.0954-17.2017 pmid:28652412 fatcat:lygjp4l3m5gepe67uek6mellnm