Abstract:
:An inflammatory response involving activated microglia in neuritic beta-amyloid plaques is found in Alzheimer's disease (AD) brain. Because HDL lipoproteins have been shown to carry the beta-amyloid peptide (Abeta) in plasma and CSF, we have investigated the influence of plasma high-density lipoprotein (HDL) and lipidated ApoE and ApoJ particles on the interaction of cultured rat microglia with Abeta1-42. Microglia degraded Abeta via a pathway sensitive to cytochalasin D and the scavenger receptor inhibitor, fucoidan. HDL increased the degradation of Abeta and the ratio of multimeric/monomeric Abeta in a dose-dependent manner. In contrast, lipidated ApoJ and ApoE decreased the degradation of Abeta, and the effects were ApoE isoform-dependent. Immuno-electron microscopy revealed internalized Abeta in endosomes and lysosomes as well as cell-associated Abeta in deep invaginations, which may be related to caveolae and surface-connected compartments. These data suggest that lipoprotein-dependent Abeta trafficking to microglia could be relevant to plaque pathogenesis in AD.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Cole GM,Beech W,Frautschy SA,Sigel J,Glasgow C,Ard MDkeywords:
subject
Has Abstractpub_date
1999-08-15 00:00:00pages
504-20issue
4eissn
0360-4012issn
1097-4547pii
10.1002/(SICI)1097-4547(19990815)57:4<504::AID-JNRjournal_volume
57pub_type
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