TY - JOUR T1 - Spontaneous Hemorrhagic Stroke in a Mouse Model of Cerebral Amyloid Angiopathy JF - The Journal of Neuroscience JO - J. Neurosci. SP - 1619 LP - 1627 DO - 10.1523/JNEUROSCI.21-05-01619.2001 VL - 21 IS - 5 AU - David T. Winkler AU - Luca Bondolfi AU - Martin C. Herzig AU - Lukas Jann AU - Michael E. Calhoun AU - Karl-Heinz Wiederhold AU - Markus Tolnay AU - Matthias Staufenbiel AU - Mathias Jucker Y1 - 2001/03/01 UR - http://www.jneurosci.org/content/21/5/1619.abstract N2 - A high risk factor for spontaneous and often fatal lobar hemorrhage is cerebral amyloid angiopathy (CAA). We now report that CAA in an amyloid precursor protein transgenic mouse model (APP23 mice) leads to a loss of vascular smooth muscle cells, aneurysmal vasodilatation, and in rare cases, vessel obliteration and severe vasculitis. This weakening of the vessel wall is followed by rupture and bleedings that range from multiple, recurrent microhemorrhages to large hematomas. Our results demonstrate that, in APP transgenic mice, the extracellular deposition of neuron-derived β-amyloid in the vessel wall is the cause of vessel wall disruption, which eventually leads to parenchymal hemorrhage. This first mouse model of CAA-associated hemorrhagic stroke will now allow development of diagnostic and therapeutic strategies. ER -