Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8303543 | Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids | 2006 | 10 Pages |
Abstract
Inflammation is a risk factor for Alzheimer's disease. Serum amyloid A (SAA) is an acute phase protein that dissociates apolipoprotein AI (apoAI) from plasma HDL. In cerebrospinal fluid (CSF), the SAA concentration is much higher in subjects with Alzheimer's disease than in controls. CSF-HDL is rich in apoE, which plays an important role as a ligand for lipoprotein receptors in the central nervous system (CNS). To clarify whether SAA dissociates apoE from CSF-HDL, we added recombinant SAA to CSF and determined the apoE distribution in the CSF using native two-dimensional gel electrophoresis. We found that SAA dissociated apoE from CSF-HDL in a dose-dependent manner. This effect was more evident in apoE4 carriers than in apoE3 or apoE2 carriers. After a 24-h incubation at 37 °C, SAA continuously dissociated apoE from CSF-HDL. Amyloid β (Aβ) fragments (1-42) were bound to large CSF-HDL but not to apoE dissociated by SAA. In conclusion, SAA dissociates apoE from CSF-HDL. We postulate that inflammation in the CNS may impair Aβ clearance due to the loss of apoE from CSF-HDL.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Biochemistry
Authors
Takashi Miida, Toshiyuki Yamada, Utako Seino, Masayuki Ito, Yuriko Fueki, Akihiro Takahashi, Keiichiro Kosuge, Satoshi Soda, Osamu Hanyu, Konen Obayashi, Osamu Miyazaki, Masahiko Okada,