title: Cerebral amyloid angiopathy in streptozotocin rat model of sporadic Alzheimer's disease: a long-term follow up study.
abstract: Cerebral amyloid angiopathy is manifested as accumulation of amyloid β (Aβ) peptide in the wall of meningeal and cerebral arteries, arterioles and capillaries and is frequently found postmortem in sporadic Alzheimer's disease (sAD) patients. It is difficult to assess when and how cerebral amyloid angiopathy develops and progresses in humans in vivo, which is why animal AD models are used. Streptozotocin-intracerebroventricularly (STZ-icv) treated rats have been recently proposed as the model of sAD which develops insulin resistant brain state preceding Aβ pathology development. Vascular Aβ deposits in the brain of STZ-icv-treated rats (3 months old at the time of icv treatment) were visualized by Thioflavine-S staining, Congo red staining and Aβ immunohistochemistry. Thioflavine-S and Congo red staining revealed diffuse congophilic deposits in the wall of meningeal and cortical blood vessels both 6 and 9 months after the STZ-icv treatment. Preliminary Aβ1-42 and Aβ1-16 immunohistochemistry experiments showed positive staining in blood vessels 3 and 9 months after the STZ-icv treatment, respectively. Results suggest that cerebral amyloid angiopathy observed 6 and 9 months after the STZ-icv treatment seems to be a continuation and progression of the amyloid pathology observed already 3 months following the STZ-icv treatment in this non-transgenic sAD animal model.
authors.affiliation: Department of Pharmacology, School of Medicine, University of Zagreb, Zagreb, Croatia. melitas@mef.hr
authors.forename: Melita
authors.initials: M
authors.lastname: Salkovic-Petrisic
authors.forename: Jelena
authors.initials: J
authors.lastname: Osmanovic-Barilar
authors.forename: Martina K
authors.initials: MK
authors.lastname: Brückner
authors.forename: Siegfried
authors.initials: S
authors.lastname: Hoyer
authors.forename: Thomas
authors.initials: T
authors.lastname: Arendt
authors.forename: Peter
authors.initials: P
authors.lastname: Riederer
mesh_terms: D000544:Alzheimer Disease / Q000139:chemically induced* / Q000150:complications*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D052160:Benzothiazoles; D016657:Cerebral Amyloid Angiopathy / Q000209:etiology* / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D008137:Longitudinal Studies; D008297:Male; D010446:Peptide Fragments / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013194:Staining and Labeling / Q000379:methods; D013311:Streptozocin / Q000633:toxicity*; D013844:Thiazoles
chemical_list: D016229:Amyloid beta-Peptides; D000903:Antibiotics, Antineoplastic; D052160:Benzothiazoles; D010446:Peptide Fragments; D013844:Thiazoles; C075222:amyloid beta-protein (1-42); C009462:thioflavin T; D013311:Streptozocin