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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.HDL density range, while apo A-IV was not associated with lipoproteins but appeared in a lipid-free form, co-localizing with LCAT immunoreactivity. This cholesterol could then be removed from the CSF via arachnoid granulations or by redistribution to other cells in the brain compartment (9).Others report an apo E-enriched very low density HDL fraction that represents a minor subclass (12).As intact lipoprotein particles cannot cross the blood–brain barrier, the synthesis, remodeling, and redistribution of lipids in the brain must take place in this compartment.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.
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Bi-dimensional analysis demonstrated pre-β and α apo A-I-containing particles; apo E and apo A-II were detected only in α-migrating particles. Such active lipid redistribution might prove to be functionally important because several recent studies have shown that the neuronal membrane cholesterol content influences processing of the amyloid precursor protein (APP) (13–15).
Apo A-IV distributed both to pre-β and γ-migrating particles; the LCAT signal was co-localized in this γ-migrating fraction. Decreasing the neuronal cell cholesterol content, by combining a treatment with lovastatin (HMG-Co A reductase inhibitor) and α-methyl-β-cyclodextrin, reduces amyloid β production.
In this study, we carried out a detailed analysis of lipids and lipoproteins in CSF collected from patients affected by AD, by other forms of dementia, or from non-demented controls in order to look for major differences in the lipid and lipoprotein composition among the different diagnostic groups.
Lipoproteins were isolated by density gradient ultracentrifugation and combined with sensitive and specific apolipoprotein assays enabling the direct lipoprotein analysis on small sample amounts.