APOE and Cognitive impairment: This may explain why deleting the ATP-binding cassette transporter 1 (ABCA1) - which regulates apoE lipidation in the CNS17 – increases the deposition of Aβ plaques70,71, while overexpressing or upregulating ABCA1 relieves cognitive impairment caused by Aβ and reverses memory deficits in transgenic animals72.