Inhibition of the Neuronal Insulin Receptor An <i>in Vivo</i> Model for Sporadic Alzheimer Disease?

Abstract excerpt

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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