engleski

Amyloid-β pathology in the brain of a streptozotocin rat model of sporadic Alzheimer’s disease

Introduction: Streptozotocin-intracerebroventricularly (STZ-icv) treated rats represent experimental non-transgenic model of sporadic Alzheimer´s disease (sAD) which develop cerebral amyloid pathology in the form of β-amyloid aggregation in the blood vessel wall, found three months after icv administration of 3 mg/kg STZ dose. We have investigated the STZ-icv dose-dependency of β-amyloid pathology development 1 week and 3 months after the STZ-icv treatment. Methods: Adult male Wistar rats were administered STZ (0.1, 1 and 3 mg/kg dose) or vehicle (controls) icv injections and sacrificed 1 week and 3 months afterwards. Paraffin-embedded brain sections of pre-mortally fixative perfused animals were analysed by Congo Red and Bielschowsky Silver staining and Aβ1-42 immunohistochemistry. Results: Congo Red staining revealed β-amyloid aggregation in the meningeal capillaries only with the highest STZ-icv dose 3 months following the treatment with no specific signal being found with lower doses and at 1 week time-point. This finding has been supported by some positive Bielschowsky Silver staining signal in the blood vessel wall. No plaque-like formations of positive Aβ1-42 aggregation with any of the dose could have been detected by immunohistochemistry at both time-points. Conclusions: Development of cerebral β-amyloid pathology in the STZ-icv rat model of sAD is a dose-dependent, non-acute effect which takes at least 3 months to be manifested in the form of angiopathy. Acknowledgement: Supported by the Unity Through Knowledge Fund (UKF 64-10) and MZOS.

amyloid-beta; streptozotocin; angiopathy

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