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Ann N Y Acad Sci. 2000;920:256-8.

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

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Department of Pathochemistry & General Neurochemistry, University of Heidelberg, Im Neuenheimer Feld 220/221, D-69120 Heidelberg, Germany.


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.

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