ABCA1 is required for normal brain ApoE levels and for lipidation of astrocyte-secreted ApoE [197], and the absence of ABCA1 decreases soluble ApoE levels but does not diminish Aβ deposition in AD murine models [198], whereas others have reported increased Aβ deposition in APP23 and PDAPP mice in the absence of ABCA1, suggesting that despite substantially lower ApoE levels, poorly lipidated ApoE produced in the absence of ABCA1 is strongly amyloidogenic [199, 200]. The gene discussed is APOE; the disease is Alzheimer disease.