Experimental Model and Subject Details

Three-to-five months old male C57BL/6J mice (Jackson laboratories) and seven-to-nine months old male and female transgenic (Tg) APPswe/PSEN1dE9 (APP/PS1) mice and their wild-type (WT) littermates were used for the experiments described in this study. The APP/PS1 mouse model expresses the human mutant amyloid precursor protein (APP) gene containing the Swedish mutation K594N/M595L and the human presenilin 1 gene lacking exon 9, both under the control of the PrP promotor (Jankowsky et al., 2001). In this model, parenchymal Aβ plaques start to deposit around five months of age and around the same time CAA appears in the form of vascular Aβ deposits on pial arteries and arterioles, increasingly with age (Garcia-Alloza et al., 2006). Since sex does not influence CAA progression in this model (Garcia-Alloza et al., 2006), both sexes were used in this study. APP/PS1 mice were purchased from The Jackson Laboratory and bred in our animal facility to produce offspring. Mice were housed with up to four individuals in one cage and alone after surgical procedures on a 12-hour light/dark cycle and food and water was provided ad libitum. All animal procedures were performed with the approval of the Massachusetts General Hospital Animal Care and Use Committee and in compliance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.