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Elevated glucose and oligomeric β-amyloid disrupt synapses via a common pathway of aberrant protein S-nitrosylation

Academic Article
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Overview

authors

  • Akhtar, M. W.
  • Sanz-Blasco, S.
  • Dolatabadi, N.
  • Parker, J.
  • Chon, K.
  • Lee, M. S.
  • Soussou, W.
  • McKercher, S. R.
  • Ambasudhan, Rajesh
  • Nakamura, T.
  • Lipton, Stuart

publication date

  • January 2016

journal

  • Nature Communications  Journal

subject areas

  • Adult
  • Aged
  • Aged, 80 and over
  • Alzheimer Disease
  • Amyloid beta-Peptides
  • Animals
  • Brain
  • Case-Control Studies
  • Cerebral Cortex
  • Dendritic Spines
  • Diabetes Mellitus, Type 2
  • Disease Models, Animal
  • Dynamins
  • Excitatory Amino Acid Antagonists
  • Female
  • GTP Phosphohydrolases
  • Glucose
  • Hippocampus
  • Humans
  • Hyperglycemia
  • Immunoblotting
  • Induced Pluripotent Stem Cells
  • Insulin
  • Insulysin
  • Long-Term Potentiation
  • Male
  • Memantine
  • Metabolic Syndrome
  • Mice
  • Mice, Transgenic
  • Microtubule-Associated Proteins
  • Mitochondrial Proteins
  • Neurons
  • Nitric Oxide
  • Nitroso Compounds
  • Oxygen Consumption
  • Rats
  • Reactive Nitrogen Species
  • Synapses
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Identity

PubMed Central ID

  • PMC4729876

International Standard Serial Number (ISSN)

  • 2041-1723

Digital Object Identifier (DOI)

  • 10.1038/ncomms10242

PubMed ID

  • 26743041
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Additional Document Info

volume

  • 7

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