| Literature DB >> 11193160 |
S Hoyer1, S K Lee, T Löffler, R Schliebs.
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.Entities:
Mesh：
Substances：
Year: 2000 PMID： 11193160 DOI： 10.1111/j.1749-6632.2000.tb06932.x
Source DB: PubMed Journal: Ann N Y Acad Sci ISSN： 0077-8923 Impact factor: 5.691