Extracellular Zn(2+) Is Essential for Amyloid β(1–42)-Induced Cognitive Decline in the Normal Brain and Its Rescue

Brain Aβ(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 Aβ(1–42) with ex...

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Pubblicato in:J Neurosci
Autori principali: Takeda, Atsushi, Tamano, Haruna, Tempaku, Munekazu, Sasaki, Miku, Uematsu, Chihiro, Sato, Shoko, Kanazawa, Hiroaki, Datki, Zsolt L., Adlard, Paul A., Bush, Ashley I.
Natura: Artigo
Lingua:Inglês
Pubblicazione: Society for Neuroscience 2017
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Research Articles
Accesso online:https://ncbi.nlm.nih.gov/pmc/articles/PMC6705735/
https://ncbi.nlm.nih.gov/pubmed/28652412
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1523/JNEUROSCI.0954-17.2017
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