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- W2017281720 abstract "Cerebrovascular amyloid angiopathy (CAA) is characterized by accumulation of the shorter b -amyloid isoform(s) (predominantly A b 40) in the walls of leptomeningeal and cortical arterioles and is likely a contributory factor to vascular dysfunction leading to stroke and dementia in the elderly. We utilized transgenic mouse models that display prominent CAA to investigate the ability of ponezumab, an anti-A b 40 monoclonal antibody, to attenuate cerebral vessel A b accrual and to restore vascular reactivity. Following chronic administration of ponezumab to PS1APP transgenic mice, we measured amyloid and A b 40 by immunohistochemistry and intravital 2 photon imaging in both leptomeningeal and cortical vessels. We also measured A b levels in brain tissue extracts that were enriched for cerebral vascular elements using a sensitive ELISA. Following acute administration of ponezumab to APP transgenic mice, we measured a brain interstitial fluid (ISF) pool of A b 40 via microdialysis as well as pial arteriole reactivity using cranial window imaging in living animals. Chronic administration of ponezumab to PS1APP transgenic mice, led to a significant attenuation in amyloid accrual in both leptomeningeal and cortical vessels, and a significant reduction in A b levels in brain vasculature. Acute administration of ponezumab effectively mobilized a brain ISF pool of A b 40 in plaque bearing mice that was accompanied by a beneficial effect on cerebrovascular function even in vessels with a significant CAA burden. These results demonstrate that ponezumab administration to transgenic mice can decrease CAA burden, as well as restore, even after a single peripheral administration, vasomotor responses in vessels with a high CAA burden." @default.
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- W2017281720 date "2014-07-01" @default.
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- W2017281720 title "P4-234: IMPROVED VASCULAR REACTIVITY AND REDUCED CEREBRAL AMYLOID ANGIOPATHY FOLLOWING PASSIVE IMMUNOTHERAPY IN TRANSGENIC MICE" @default.
- W2017281720 doi "https://doi.org/10.1016/j.jalz.2014.07.006" @default.
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