Inhibition of the Neuronal Insulin Receptor An in Vivo Model for Sporadic Alzheimer Disease?

: It has been hypothesized that a central event 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 upregul...

Full description

Saved in:
Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2000-12, Vol.920 (1), p.256-258
Main Authors: HOYER, SIEGFRIED, LEE, SAE KYUNG, LÖFFLER, THOMAS, SCHLIEBS, REINHARD
Format: Article
Language:English
Subjects:
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Animals
ATP-Binding Cassette Transporters
Autoradiography
Brain - drug effects
Brain - physiology
Brain - physiopathology
Cerebral Ventricles - drug effects
Cerebral Ventricles - physiology
Cerebral Ventricles - physiopathology
Disease Models, Animal
Glyburide - metabolism
Injections, Intraventricular
Insulin - metabolism
Iodine Radioisotopes
Neurons - drug effects
Neurons - physiology
Potassium Channels - drug effects
Potassium Channels - metabolism
Potassium Channels, Inwardly Rectifying
Rats
Receptor, Insulin - antagonists & inhibitors
Receptors, Drug - drug effects
Receptors, Drug - metabolism
Streptozocin - administration & dosage
Streptozocin - pharmacology
Sulfonylurea Receptors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:: It has been hypothesized that a central event 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.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.2000.tb06932.x