The levels of soluble amyloid beta in different high density lipoprotein subfractions distinguish Alzheimer's and normal aging cerebrospinal fluid: implication for brain cholesterol pathology?

Several previous studies reported the association of the soluble form of amyloid β (sAβ) protein, a major constituent of amyloid deposits in Alzheimer's disease (AD), with normal blood, cerebrospinal fluid (CSF) and central nervous system high density lipoproteins (HDLs). The present report aim...

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Bibliographic Details
Published in:Neuroscience letters 2001-11, Vol.314 (3), p.115-118
Main Authors: Koudinov, Alexei R, Berezov, Temirbolat T, Koudinova, Natalia V
Format: Article
Language:English
Subjects:
Alzheimer Disease - cerebrospinal fluid
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Amyloid beta-Peptides - cerebrospinal fluid
Apolipoproteins - cerebrospinal fluid
Binding Sites - physiology
Blood-Brain Barrier - physiology
Brain - metabolism
Brain - pathology
Brain - physiopathology
Cholesterol - metabolism
Diagnostic
Electrophoresis, Polyacrylamide Gel
Humans
Immunoblotting
Lipoprotein receptor
Lipoproteins, HDL - cerebrospinal fluid
Neuritic plaque
Phospholipids
Plaque, Amyloid - metabolism
Receptors, Lipoprotein - metabolism
Reverse cholesterol transport
Synaptic plasticity
Up-Regulation - physiology
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Summary:Several previous studies reported the association of the soluble form of amyloid β (sAβ) protein, a major constituent of amyloid deposits in Alzheimer's disease (AD), with normal blood, cerebrospinal fluid (CSF) and central nervous system high density lipoproteins (HDLs). The present report aimed to elucidate the pattern of sAβ and apolipoprotein (apo) distribution in AD CSF-HDL subfractions. We studied AD CSF-HDL subfractions by SDS/PAGE and immunoblot analysis after CSF fractionation via density flotation ultracentrifugation. AD CSF was characterized by (i) increased sAβ and apo content of the HDL 1, and (ii) sAβ association with apoE and apoJ in HDL 2, HDL 3 and very high density lipoproteins. The finding supports our proposed hypothesis that upregulation of brain cholesterol dynamics is a fundamental event in the pathophysiology of AD and that sAβ binding to apo and lipid may have important structure-functional consequences.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(01)02263-7