Model of insulin's influence on amyloid β

By Kerry Grens LITERATUREARTICLE EXTRASRelated ArticleAlzheimer's: Type 3 Diabetes?Channel CandidatesA Channel at LargeThe Inner Workings of Hearing MachineryCracking Open a New Channel FamilyFacelessness, facedThe singing earBaby brain bankOpening Potassium Channels to ScrutinyDownstream of insulin signaling are links to amyloid β (Aβ), the principle peptide that forms the plaqu

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LITERATURE

Related Article

Alzheimer's: Type 3 Diabetes?

Channel Candidates

A Channel at Large

The Inner Workings of Hearing Machinery

Cracking Open a New Channel Family

Facelessness, faced

The singing ear

Baby brain bank

Opening Potassium Channels to Scrutiny

Downstream of insulin signaling are links to amyloid β (Aβ), the principle peptide that forms the plaques in brains of patients with Alzheimer's disease. It begins with insulin receptor activation turning on the phosphoinositide kinase, PI3K, which generates the lipid messenger, PIP3. PIP3 activates the signaling protein AKT (serine/threonine kinase).

AKT can affect Aβ in two ways. One is that AKT mediates the upregulation of insulin degrading enzyme, IDE, which not only breaks down insulin, but is also thought to degrade Aβ. Conversely, AKT restricts GSK3β, a kinase thought to be involved in stimulating Aβ production. The activation of either pathway can therefore reduce Aβ levels, either by degrading the peptide or ...

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Meet the Author

  • kerry grens

    Kerry Grens

    Kerry served as The Scientist’s news director until 2021. Before joining The Scientist in 2013, she was a stringer for Reuters Health, the senior health and science reporter at WHYY in Philadelphia, and the health and science reporter at New Hampshire Public Radio. Kerry got her start in journalism as a AAAS Mass Media fellow at KUNC in Colorado. She has a master’s in biological sciences from Stanford University and a biology degree from Loyola University Chicago.

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