Searching for just a few words should be enough to get started. If you need to make more complex queries, use the tips below to guide you.
Article type: Research Article
Authors: Grünblatt, Ednaa; * | Koutsilieri, Elenia | Hoyer, Siegfriedb | Riederer, Petera
Affiliations: [a] Institute of Clinical Neurochemistry and National Parkinson Foundation Centre of Excellence Laboratories, Clinic for Psychiatry and Psychotherapy, Bayerische Julius-Maximilians-University of Würzburg, D-97080 Würzburg, Germany | [b] Department of Pathology, University of Heidelberg, Heidelberg, Germany
Correspondence: [*] Corresponding author: Edna Grünblatt, Clinic for Psychiatry and Psychotherapy, Bayerische Julius-Maximilians-University Würzburg, Füchsleinstr. 15, 97080 Würzburg, Germany. Tel.: +49 931 20177300; Fax: +49 931 20177220; E-mail: [email protected].
Abstract: Streptozotocin is well known inducer of experimental diabetes mellitus when injected peripherally. However, when administered intracerebroventricular, streptozotocin showed a whole spectrum of specific biochemical and behavioural alterations with regard to cognitive functions, feeding, nociception, brain glucose metabolism, neurotransmission and oxidative stress, without producing arterial hyperglycaemia, similarly to Alzheimer's disease. In order to reveal the mechanism of action of neurodegeneration in streptozotocin rat model we investigated the expression of several genes involved in inflammation, oxidative stress, growth- and transcription-factors in the cortex, striatum and cerebellum, using real-time quantitative RT-PCR. Genes such as GDNF, BDNF and integrin-alpha-M were up-regulated, while immediate-early-gene-transcription-factor NGF-IB and metallothionein-1/2 were down-regulated in the cortex of streptozotocin-treated rats. Conversely, NGF-IB, GDNF and BDNF mRNA expression did not alter in the striatum and cerebellum. However, integrin alpha-M and metallothionein-1/2 expressions decreased significantly in the striatum and increased in the cerebellum. These gene changes may provide an insight into the cascade of physiological abnormalities following the inhibition of neuronal insulin signal transduction. Additionally, similarities to neuronal cell death in sporadic Alzheimer's disease may become apparent.
Keywords: Alzheimer's disease, diabetes, insulin, neurodegeneration, quantitative-RT-PCR, rat, streptozotocin
DOI: 10.3233/JAD-2006-9305
Journal: Journal of Alzheimer's Disease, vol. 9, no. 3, pp. 261-271, 2006
IOS Press, Inc.
6751 Tepper Drive
Clifton, VA 20124
USA
Tel: +1 703 830 6300
Fax: +1 703 830 2300
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
IOS Press
Nieuwe Hemweg 6B
1013 BG Amsterdam
The Netherlands
Tel: +31 20 688 3355
Fax: +31 20 687 0091
[email protected]
For editorial issues, permissions, book requests, submissions and proceedings, contact the Amsterdam office [email protected]
Inspirees International (China Office)
Ciyunsi Beili 207(CapitaLand), Bld 1, 7-901
100025, Beijing
China
Free service line: 400 661 8717
Fax: +86 10 8446 7947
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
如果您在出版方面需要帮助或有任何建, 件至: [email protected]