Inhibition of the neuronal insulin receptor. An in vivo model for sporadic Alzheimer disease?

Abstract:

:It has been hypothesized that a central even in the early pathogenesis of sporadic Alzheimer disease (SAD) is the dysfunction of the neuronal insulin receptor signal transduction. To prove this, this receptor was inhibited by a triplicate icv application of STZ. Insulin binding sites were upregulated as in SAD. With respect to glucose transport proteins, detailed investigations are necessary.

journal_name

Ann N Y Acad Sci

authors

Hoyer S,Lee SK,Löffler T,Schliebs R

doi

10.1111/j.1749-6632.2000.tb06932.x

subject

Has Abstract

pub_date

2000-01-01 00:00:00

pages

256-8

eissn

0077-8923

issn

1749-6632

journal_volume

920

pub_type

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