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Intravascular infusions of soluble β-amyloid compromise the blood- brain barrier, activate CNS glial cells and induce peripheral hemorrhage

Lookup NU author(s): Professor Raj KalariaORCiD


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Vascular wall levels of soluble β-amyloid1-40 (Aβ1-40) are elevated in Alzheimer's disease (AD). Moreover, plasma Aβ levels are increased in familial AD, as well as in some cases of sporadic AD. To determine the histopathologic and behavioral consequences of elevated vascular Aβ levels, Aβ1-40 (50 μg in distilled water) or vehicle was intravenously infused twice daily into 3-month old male Sprague-Dawley rats for 2 weeks. Intravenous Aβ infusions impaired blood-brain barrier integrity, as indicated by substantial perivascular and parenchyma IgG immunostaining within the brain. Also evident in Aβ-infused animals was an increase in GFAP immunostaining around cerebral blood vessels, and an enhancement of OX-42 microglial immunostaining in brain white matter. Gross pulmonary hemorrhage was noted in most Aβ-infused animals. All the observed changes occurred in the absence of Congo red birefringence. No significant cognitive deficits were present in Aβ-infused animals during water maze acquisition and retention testing, which was conducted during the second week of treatment. These results indicate that circulating Aβ can: (1) induce vessel dysfunction/damage in both the brain and the periphery without complex Aβ fibril formation/deposition, and (2) induce an activation of brain astrocytes and microglia. Taken together, our results suggest that if circulating Aβ is elevated in AD, it is likely to have a pathophysiologic role.

Publication metadata

Author(s): Su GC, Arendash GW, Kalaria RN, Bjugstad KB, Mullan M

Publication type: Article

Publication status: Published

Journal: Brain Research

Year: 1999

Volume: 818

Issue: 1

Pages: 105-117

Print publication date: 22/01/1999

ISSN (print): 0006-8993

ISSN (electronic): 1872-6240

Publisher: Elsevier BV


DOI: 10.1016/S0006-8993(98)01143-3

PubMed id: 9914443


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