Research article summary (published 30 Dec 2006):

Central insulin resistance as a trigger for sporadic Alzheimer-like pathology: an experimental approach.

Full Abstract

A growing body of evidence implicates impairments in brain insulin signaling in early sporadic Alzheimer disease (sAD) pathology. However, the most widely accepted hypothesis for AD aetiology stipulates that pathological aggregations of the amyloid beta (Abeta) peptide are the cause of all forms of Alzheimer's disease. Streptozotocin-intracerebroventricularly (STZ-icv) treated rats are proposed as a probable experimental model of sAD. The current work reviews evidence obtained from this model indicating that central STZ administration induces brain pathology and behavioural alterations resembling those in sAD patients. Recently, alterations of the brain insulin system resembling those in sAD have been found in the STZ-icv rat model and are associated with tau protein hyperphosphorylation and Abeta-like aggregations in meningeal vessels. In line with these findings the hypothesis has been proposed that insulin resistance in the brain might be the primary event which precedes the Abeta pathology in sAD.

Author information

Author/s: Salkovic-Petrisic, M (M); Hoyer, S (S);

Affiliation: Department of Pharmacology and Croatian Institute for Brain Research, Medical School, University of Zagreb, Zagreb, Croatia. melitas(-atsign-)mef.hr

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review

Journal: Journal of neural transmission. Supplementum (J Neural Transm Suppl), published in Austria. (Language: eng)

Reference: 2007-; vol (issue 72) : pp 217-33

Dates: Created 2007/11/06; Completed 2007/12/10;

PMID: 17982898, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Alzheimer Disease - chemically induced; pathology; physiopathology Amyloid beta-Protein - metabolism Amyloid beta-Protein Precursor - metabolism Animals Blood Glucose - metabolism Brain - drug effects; pathology; physiopathology Disease Models, Animal Glucose Transporter Type 4 - drug effects; physiology Humans Injections, Intraventricular Insulin - physiology

Insulin - physiology Insulin Resistance - physiology Learning - drug effects; physiology Memory - drug effects; physiology Neurotoxins - pharmacology Rats Receptor, Insulin - drug effects; physiology Receptors, Cell Surface - metabolism Signal Transduction - drug effects; physiology Streptozocin - pharmacology tau Proteins - metabolism

Associated Chemicals: Amyloid beta-Protein (0) ; Amyloid beta-Protein Precursor (0) ; Blood Glucose (0) ; Glucose Transporter Type 4 (0) ; Neurotoxins (0) ; Receptors, Cell Surface (0) ; protease nexins (0) ; tau Proteins (0) ; Insulin (11061-68-0) ; Streptozocin (18883-66-4) ; Receptor, Insulin (EC 2.7.1.112)

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