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Enzymatically active LCAT was present in human CSF as well as PLTP activity and mass; no CETP mass was detected. On the contrary, increasing cellular cholesterol concentrations by adding β-VLDL to Cos1 cells causes a decrease of the secretion of the soluble form of APP (s APP).

In CSF from AD patients, LCAT activity was 50% lower than in CSF from normal controls. These observations suggest that CSF lipoproteins may fulfill an important role in maintaining the neuronal cholesterol levels, thereby regulating indirectly the production of amyloidogenic peptides.

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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.

Apo A-IV concentrations varied widely in human CSF, but were not associated with any clinical condition. CSF lipoproteins are needed for delivery of cholesterol during nerve growth, but it is not known whether they are also actively involved in taking up excess cholesterol from nerve cells.

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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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