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Elevated glucose and oligomeric [beta]-amyloid disrupt synapses via a common pathway of aberrant pro...

Elevated glucose and oligomeric [beta]-amyloid disrupt synapses via a common pathway of aberrant pro...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_journals_1754531650

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

About this item

Full title

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

Publisher

London: Nature Publishing Group

Journal title

Nature communications, 2016-01, Vol.7, p.10242

Language

English

Formats

Publication information

Publisher

London: Nature Publishing Group

More information

Scope and Contents

Contents

Metabolic syndrome (MetS) and Type 2 diabetes mellitus (T2DM) increase risk for Alzheimer's disease (AD). The molecular mechanism for this association remains poorly defined. Here we report in human and rodent tissues that elevated glucose, as found in MetS/T2DM, and oligomeric β-amyloid (Aβ) peptide, thought to be a key mediator of AD, coordinatel...

Alternative Titles

Full title

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

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_proquest_journals_1754531650

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_journals_1754531650

Other Identifiers

E-ISSN

2041-1723

DOI

10.1038/ncomms10242

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