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It is not known in what form HDL precursors are synthesized in the brain and whether remodeling occurs within the CSF.HDL remodeling in the circulation is largely mediated by the enzyme lecithin:cholesterol acyltransferase (LCAT) and the lipid transfer proteins cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP), but in the brain these pathways remain largely obscure.In humans, such pre β particles have not yet been identified, and one of the aims of this study is to identify such precursor particles and the factors that may remodel them.These small particles are likely candidates for participating in the process of “reverse cholesterol transport” as has been suggested for the interstitial fluid lipoproteins. (19) have demonstrated a unique profile of HDL generation and cholesterol efflux from rat astrocytes, whereby cholesterol-rich (apo E-HDL) and cholesterol-poor (apo A-I-HDL) are generated.Other reports show that a reduction in brain tissue membrane lipids (gangliosides, phospholipids, and cholesterol) is correlated with reduced synaptic function in patients with early onset form (EOAD) Alzheimer's disease, independent of the β amyloid depositions (17).Apo E and apo A-I are the major CSF apolipoproteins, which are present in high density lipoproteins (HDL), while apo B-containing very low or low density lipoproteins (VLDL or LDL) were never identified in CSF. (4) and later reports by Borghini et al (10) suggest that apo E-enriched HDL is the predominant lipoprotein in CSF. Several observations suggest a close relationship between the lipoprotein metabolism in the brain and the development of Alzheimer's disease (AD) (1, 2).

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Finally, cholesterol efflux from rat astrocytes by human CSF lipoproteins was correlated with the CSF (apo)lipoprotein content.

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