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The origin of sporadic alzheimer disease – Is it brain insulin resistant state? (CROSBI ID 561885)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | domaća recenzija

Šalković-Petrišić, Melita ; Osmanović, Jelena ; Grünblatt, Edna ; Hoyer, Siegfried ; Riederer, Peter The origin of sporadic alzheimer disease – Is it brain insulin resistant state?. 2009

Podaci o odgovornosti

Šalković-Petrišić, Melita ; Osmanović, Jelena ; Grünblatt, Edna ; Hoyer, Siegfried ; Riederer, Peter

engleski

The origin of sporadic alzheimer disease – Is it brain insulin resistant state?

Background. Sporadic Alzheimer disease (sAD) is associated with brain insulin receptor (IR) signalling abnormalities whose ethiopathogenesis is unclear in the course of sAD. Rats that have been intracerebroventricularly treated with streptozotocin (STZ-icv), a drug selectively toxic for insulin producing/secreting cells and IR, have been recognized recently as the non-transgenic, experimental sAD model, suitable for brain IR signalling cascade exploration. Aim. We investigated the time course of brain IR signalling dysfunction in relation to amyloid pathology development in STZ-icv rat model of sAD. Methods. RT-PCR and immunoblotting were used for hippocampal IR signalling cascade gene and protein expression measurements, respectively and data were analyzed by Cruscal-Wallis ANOVA median/Mann- Whitney U test. Amyloid β (Aβ) aggregation was detected by Congo red staining and immunohistochemistry. Results. Our results demonstrated alterations in brain IR signalling cascade starting from the decreased insulin gene expression, followed by a decreased expression of IR mRNA and protein, found as early as 1 month following the induction of sAD-like condition and persisting up to 9 months afterwards. Downstream dysfunction of IR signalling pathway manifested as decreased ratio of phosphorylated/non-phosphorylated glycogen synthase kinase-3 was found not earlier than 3 months after STZ-icv treatment and was followed by tau protein hyperphosphorylation, cerebral amyloid angiopathy, intraneuronal Aβ aggregation and plaque-like formation (not earlier than 6 months after the STZ-icv treatment). No change in amyloid precursor protein gene expression was found while the expression of insulin degrading enzyme gene/protein was decreased. Conclusion. Based on this experimental approach, sAD could be considered as an insulin resistant brain state which precedes and eventually triggers Aβ pathology.

Sporadic Alzheimer disease; insulin receptor; streptozotocin; amyloid beta

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Podaci o prilogu

2009.

nije evidentirano

objavljeno

Podaci o matičnoj publikaciji

Podaci o skupu

The Third Croatian Neuroscience Meeting

pozvano predavanje

01.01.2009-01.01.2009

Zadar, Hrvatska

Povezanost rada

Temeljne medicinske znanosti