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Analysis of oxidative stress in mouse model of cerebral amyloid angiopathy (CAA)
Author(s) -
FernandezKim Sun Ok,
Zhang Le,
Liu Ying,
Dasuri Kalavathi,
Ebenezer Philip J.,
BruceKeller Annadora,
Van Nostrand William E.,
Keller Jeffrey N.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.926.5
Subject(s) - oxidative stress , cerebral amyloid angiopathy , genetically modified mouse , amyloid (mycology) , antioxidant , transgene , stroke (engine) , medicine , reactive oxygen species , endocrinology , dementia , chemistry , pathology , biochemistry , gene , mechanical engineering , disease , engineering
Cerebral amyloid angiopathy (CAA) is an important cause of cerebral hemorrhage stroke and dementia in the elderly. CAA is mediated in part by the effects of amyloid β‐protein (Aβ), with the Tg‐SWDI transgenic mouse model closely recapitulating key aspects of CAA in humans. In this report we measured the levels of key oxidative stress indices within the frontal cortex of Tg‐SWDI mice (6‐8 months) and age‐matched non‐transgenic mice of the same background (C57Bl/6). Specifically we report on the level of oxidative stress by measuring the amount of protein carbonyls, protein nitroxylation, antioxidant enzyme levels, and the levels of the transcription factor Nrf2. Taken together these data indicate a role for oxidative stress in the development of CAA, and suggest that strategies which ameliorate increases in oxidative stress may be beneficial in the treatment and management of CAA. This work was supported by a grant from the Alzheimer's Association and NIA (P01AG005119) to Dr. Jeffrey Keller