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
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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

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Šalković Petrišić, M., Tribl, F., Schmidt, M., Hoyer, S. i 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, br. 4, 2006, str. 1005-1015. https://doi.org/10.1111/j.1471-4159.2005.03637.x

Šalković Petrišić, Melita, Florian Tribl, Manuela Schmidt, Siegfried Hoyer i 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, br. 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), str. 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]. 02.2006. [pristupljeno 01.05.2024.];96(4):1005-1015. doi: 10.1111/j.1471-4159.2005.03637.x

M. Šalković Petrišić, F. Tribl, M. Schmidt, S. Hoyer i 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, br. 4, str. 1005-1015, Veljača 2006. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:105:268970. [Citirano: 01.05.2024.]

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Podaci o radu
Naslov (engleski)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
AutorMelita Šalković-Petrišić
AutorFlorian Tribl
AutorManuela Schmidt
AutorSiegfried Hoyer
AutorPeter Riederer
Autorova ustanovaSveučilište u Zagrebu
Medicinski fakultet
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Sažetak (engleski)
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.
Ključne riječi (engleski)
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran
Verzija publikacijeZavršna verzija rukopisa prihvaćena za objavljivanje (postprint)
Naslov časopisaJournal of Neurochemistry
Brojčani podacivol. 96, br. 4, str. 1005-1015
p-ISSN0022-3042
DOIhttps://doi.org/10.1111/j.1471-4159.2005.03637.x
URN:NBNurn:nbn:hr:105:268970
Datum objave publikacije2006-02
URL dokumentahttps://doi.org/10.1111/j.1471-4159.2005.03637.x
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
Uvjeti korištenjaIkona licence Zaštićeno autorskim pravom.
Datum i vrijeme pohrane2024-03-28 08:37:39