Specifically, in a transgenic AD mouse model (APP23), targeted Abca1 disruption (APP23/Abca1−/−) increased amyloid deposition, increased the level of cerebral amyloid angiopathy, exacerbated cerebral amyloid angiopathy-related microhemorrhage, and caused a sharp decrease of soluble, but not of insoluble brain apoE levels [167]. The gene discussed is ABCA1; the disease is amyloidosis.