prikaz prve stranice dokumenta Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway
  Download
PDF 463.02 KB
Scientific paper - Original scientific paper
Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway
Journal of Neurochemistry, 96 (2006), 4; 1005-1015. https://doi.org/10.1111/j.1471-4159.2005.03637.x
Šalković-Petrišić, Melita; Tribl, Florian; Schmidt, Manuela; Hoyer, Siegfried; Riederer, Peter

Institutional repository: Dr Med - University of Zagreb School of Medicine Digital Repository

Cite this document

Šalković Petrišić, M., Tribl, F., Schmidt, M., Hoyer, S. & Riederer, P. (2006). Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway. Journal of Neurochemistry, 96. (4), 1005-1015. doi: 10.1111/j.1471-4159.2005.03637.x

Šalković Petrišić, Melita, et al. "Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway." Journal of Neurochemistry, vol. 96, no. 4, 2006, pp. 1005-1015. https://doi.org/10.1111/j.1471-4159.2005.03637.x

Šalković Petrišić, Melita, Florian Tribl, Manuela Schmidt, Siegfried Hoyer and Peter Riederer. "Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway." Journal of Neurochemistry 96, no. 4 (2006): 1005-1015. https://doi.org/10.1111/j.1471-4159.2005.03637.x

Šalković Petrišić, M., et al. (2006) 'Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway', Journal of Neurochemistry, 96(4), pp. 1005-1015. doi: 10.1111/j.1471-4159.2005.03637.x

Šalković Petrišić M, Tribl F, Schmidt M, Hoyer S, Riederer P. Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway. Journal of Neurochemistry [Internet]. 2006 February [cited 2024 November 22];96(4):1005-1015. doi: 10.1111/j.1471-4159.2005.03637.x

M. Šalković Petrišić, F. Tribl, M. Schmidt, S. Hoyer and P. Riederer, "Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway", Journal of Neurochemistry, vol. 96, no. 4, pp. 1005-1015, February 2006. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:105:268970. [Accessed: 22 November 2024]

Metadata
Title (english)Alzheimer-like changes in protein kinase B and glycogen synthase kinase-3 in rat frontal cortex and hippocampus after damage to the insulin signalling pathway
AuthorMelita Šalković-Petrišić
AuthorFlorian Tribl
AuthorManuela Schmidt
AuthorSiegfried Hoyer
AuthorPeter Riederer
Author's institutionUniversity of Zagreb
School of Medicine
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
The insulin-resistant brain state is related to late-onset sporadic Alzheimer's disease, and alterations in the insulin receptor (IR) and its downstream phosphatidylinositol-3 kinase signalling pathway have been found in human brain. These findings have not been confirmed in an experimental model related to sporadic Alzheimer's disease, for example rats showing a neuronal IR deficit subsequent to intracerebroventricular (i.c.v.) treatment with streptozotocin (STZ). In this study, western blot analysis performed 1 month after i.c.v. injection of STZ showed an increase of 63% in the level of phosphorylated glycogen synthase kinase-3α/β (pGSK-3α/β) protein in the rat hippocampus, whereas the levels of the unphosphorylated form (GSK-3α/β) and protein kinase B (Akt/PKB) remained unchanged. Three months after STZ treatment, pGSK-3α/β and Akt/PKB levels tended to decrease (by 8 and 9% respectively). The changes were region specific, as a different pattern was found in frontal cortex. Structural alterations were also found, characterized by β-amyloid peptide-like aggregates in brain capillaries of rats treated with STZ. Similar neurochemical changes and cognitive deficits were recorded in rats treated with i.c.v. 5-thio-d-glucose, a blocker of glucose transporter (GLUT)2, a transporter that is probably involved in brain glucose sensing. The IR signalling cascade alteration and its consequences in rats treated with STZ are similar to those found in humans with sporadic Alzheimer's disease, and our results suggest a role for GLUT2 in Alzheimer's pathophysiology.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review
Publication versionAccepted version
Journal titleJournal of Neurochemistry
Numberingvol. 96, no. 4, pp. 1005-1015
p-ISSN0022-3042
DOIhttps://doi.org/10.1111/j.1471-4159.2005.03637.x
URN:NBNurn:nbn:hr:105:268970
Publication2006-02
Document URLhttps://doi.org/10.1111/j.1471-4159.2005.03637.x
Type of resourceText
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2024-03-28 08:37:39