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Inhibition of the Neuronal Insulin Receptor An in Vivo Model for Sporadic Alzheimer Disease?
Author(s) -
HOYER SIEGFRIED,
LEE SAE KYUNG,
LÖFFLER THOMAS,
SCHLIEBS REINHARD
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06932.x
Subject(s) - insulin receptor , downregulation and upregulation , pathogenesis , receptor , insulin , in vivo , disease , alzheimer's disease , signal transduction , neuroscience , endocrinology , medicine , biology , insulin resistance , microbiology and biotechnology , biochemistry , gene , genetics
A bstract : 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.