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. 2015 Nov 20;6:278. doi: 10.3389/fphar.2015.00278

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Copyright © 2015 Gardner and Levin.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ApoA-I reduces inflammation in the CNS by preventing contact between the T cells and macrophages. HDL produced in the periphery has access to the CNS whereas LDL has no ability to enter the CNS from the circulation. The membrane associated ATP-binding cassette subfamily A member 1 (ABCA1) and ABCA G1 act as the primary sterol transporters for ApoA-I/HDL. HDL associated ApoA-I is then recognized by the lipoprotein receptors (LDL, SR-BI) in the CNS. Brain cholesterol homeostasis is supported by the reverse cholesterol transport and efflux of 24 (24S-OH) and 27 (27-OH) hydroxysterols through the blood–brain barrier (BBB).