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Here, we characterize\u00a0the susceptibility of the WSB\/EiJ genetic context to human AD\u2010relevant cerebrovascular phenotypes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      CAA and parenchymal plaque analysis and in vivo neurovascular imaging were performed on WSB.\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      brains. Transcriptomics was performed on WSB.\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      and B6.\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      brains. B6 and WSB cerebrovascular reactivity was assayed\n                      <jats:italic>ex vivo<\/jats:italic>\n                      . Additional CAA and parenchymal plaque analysis was performed on WSB.\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      mice with\n                      <jats:italic>\n                        APOE\n                        <jats:sup>2<\/jats:sup>\n                      <\/jats:italic>\n                      ,\n                      <jats:italic>\n                        APOE\n                        <jats:sup>3<\/jats:sup>\n                      <\/jats:italic>\n                      , or\n                      <jats:italic>\n                        APOE\n                        <jats:sup>4<\/jats:sup>\n                      <\/jats:italic>\n                      alleles.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      WSB.\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      brains\u00a0exhibited plaque deposition, CAA, transcriptomic overlap with human AD, myelin deficits, cerebrovascular\/metabolic uncoupling, and altered cerebrovascular morphology. Aged WSB vasculature retained vasoreactivity but exhibited increased stiffness. Compared to WSB.\n                      <jats:italic>\n                        APOE\n                        <jats:sup>2\/2<\/jats:sup>\n                        APP\/PS1\n                      <\/jats:italic>\n                      , WSB.\n                      <jats:italic>\n                        APOE\n                        <jats:sup>4\/4<\/jats:sup>\n                        APP\/PS1\n                      <\/jats:italic>\n                      mice had increased CAA and plaque\u2010associated microglial area.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>These data illustrate the utility of the WSB genetic context to model CAA and uncover vascular contributions to AD.<\/jats:p>\n                  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