Ananth K. Vellimana

Andrew W. Johnson

Byung Hee Han

Christie

David M. Holtzman

Eric Milner

Fan Liao

Fryer

Gregory Joseph Zipfel

Hans H. Dietrich

Itender Singh

Itoh

Jacob Basak

James W. Nelson

John R. Cirrito

Kawarabayashi

Mann

Meng-liang Zhou

Min Yoo

Niwa

Okazaki

Price

Revesz

Selkoe

Stefanska

Significance
          One of the hallmarks of Alzheimer’s disease (AD) is cerebral amyloid angiopathy (CAA), which is a strong and independent risk factor for cerebral hemorrhage, ischemic stroke, and dementia. However, the mechanisms by which CAA contributes to these conditions are poorly understood. Results from the present study provide strong evidence that vascular oxidative stress plays a causal role in CAA-induced cerebrovascular dysfunction, CAA-induced cerebral hemorrhage, and CAA formation, itself. They also suggest that NADPH oxidase is the source of this oxidative stress and that strategies to inhibit NADPH oxidase may have therapeutic potential in patients with AD and CAA.</jats:p

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Proceedings of the National Academy of Sciences

Contribution of reactive oxygen species to cerebral amyloid angiopathy, vasomotor dysfunction, and microhemorrhage in aged Tg2576 mice

Contribution of reactive oxygen species to cerebral amyloid angiopathy, vasomotor dysfunction, and microhemorrhage in aged Tg2576 mice

Abstract

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