Serum amyloid A in Alzheimer's disease brain is predominantly localized to myelin sheaths and axonal membrane

References

• Fazekas F, Schmidt R, Scheltens P. Pathophysiologic mechanisms in the development of age-related white matter changes of the brain. Dement Geriatr Cogn Disord 1998; 9 (Suppl. 1): 2–5
   PubMedGoogle Scholar
• Yankner B A. Mechanisms of neuronal degeneration in Alzheimer's Disease. Neuron 1996; 16: 921–932
   PubMed Web of Science ®Google Scholar
• Sipe J. Amyloidosis. Crit Rev Clin Lab Sci 1994; 31: 325–354
   PubMed Web of Science ®Google Scholar
• Kumon Y, Sipe J D, Brinckerhoff C E, Schreiber B M. Regulation of extrahepatic apolipoprotein serum amyloid A (apoS AA) gene expression by interleukin-1α alone: Synthesis and secretion of apoSAA by cultured aortic smooth muscle cells. Scand J Immunol 1997; 46: 284–292
   PubMed Web of Science ®Google Scholar
• Hardardottir I, Sipe J D, Moser A H, Fielding C J, Feingold K R, Grunfeld C. LPS and cytokines regulate extrahepatic mRNA levels of apolipoproteins during the acute phase response in Syrian hamsters. Biochim Biophys Acta 1997; 1344: 210–220
   PubMedGoogle Scholar
• Afagh A, Cummings B J, Cribbs D H, Cotman C W, Tenner A J. Localization and cell association of Clq in Alzheimer's Disease. Exp Neurol 1996; 138: 22–32
   PubMed Web of Science ®Google Scholar
• McGeer P L, McGeer E G. The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases. Brain Res Rev 1995; 21: 195–218
   PubMed Web of Science ®Google Scholar
• Rogers J. Inflammation as a pathogenic mechanism in Alzheimer's disease. Arzneim-Forsch/Drug Res 1995; 45: 39–44
   Google Scholar
• Liang J-s, Sloane J A, Wells J, Abraham C R, Fine R E, Sipe J D. Evidence for local production of the acute phase response apolipoprotein serum amyloid A in Alzheimer's disease brain. Neurosci Lett 1997; 225: 73–76
   PubMed Web of Science ®Google Scholar
• Godenir N L, Jeenah M S, Coetzee G A, van der Westhuysen D R, de Beer F C. Standardization of the quantitation of serum amyloid A protein (SAA) in human serum. J Immunol Methods 1985; 83: 217–225
   PubMed Web of Science ®Google Scholar
• Wood P L. Role of CNS macrophages in neurodegeneration. Neuroinflammation: Mechanisms and Management, P L Wood. Humana Press. 1998; 1–59
   Google Scholar
• Griffin W ST, Sheng J G, Roberts G W, Mrak R E. Interleukin-1 expression in different plaque types in Alzheimer's disease: significance in plaque evolution. J Neuropathol Exp Neurol 1995; 54: 276–281
   PubMed Web of Science ®Google Scholar
• Wood J A, Wood P L, Ryan R, Graff-Radford N R, Pilapil C, Robitaille Y, Quirion R. Cytokine indices in Alzheimer's temporal cortex: no changes in mature IL-1b˜ or IL-1RA but increases in the associated acute phase proteins IL-6, a2-macroglobulin and C-reactive protein. Brain Res 1993; 625: 245–252
   Google Scholar
• Morrison J H, Lewis D A, Campbell M J, Huntley G W, Benson D L, Bouras C. Amonoclonal antibody to non-phos-phorylated neurofilament protein marks the vulnerable cortical neurons in Alzheimer's disease. Brain Res 1987; 416: 331–336
   PubMedGoogle Scholar
• Liang J-s, Schreiber B M, Salmona M, Phillip G, Gonnerman W A, de Beer F C, Sipe J D. The amino terminal region of acute phase, but not constitutive, serum amyloid A (apoSAA) specifically binds and transports cholesterol into aortic smooth muscle cells and Hep G2 cells. J Lipid Res 1996; 37: 2109–2116
   PubMed Web of Science ®Google Scholar
• Schreiber B M, Veverbrants M, Fine R E, Blusztajn J K, Salmona M, Patel A, Sipe J D. 1999, Apolipoprotein serum amyloid A (SAA) down regulates smooth muscle cell lipid biosynthesis. Biochem J, in press
   Google Scholar
• Blusztajn J K, Lopez Gonzalez-Coviella I, Logue M, Growdon J H, Wurtman R J. Levels of phospholipid catabolic intermediates, glycerophosphocholine and gly-cerophosphoethanolamine, are elevated in brains of Alzheimer's disease but not of Down's syndrome patients. Brain Res 1990; 536: 240–244
   PubMedGoogle Scholar
• Nitsch R M, Blusztajn J K, Pittas A J, Slack B E, Growdon J H, Wurtman R J. Evidence for a membrane defect in Alzheimer's disease brain. Proc Natl Acad Sci USA 1992; 89: 1671–1675
   PubMed Web of Science ®Google Scholar
• Gottfries C G, Karlsson I, Svennerholm L. Membrane components separate early-onset Alzheimer's disease from senile dementia of the Alzheimer type. Int Psychogeriatr 1996; 8: 365–372
   PubMedGoogle Scholar
• Svennerholm L, Gottfries C G. Membrane lipids, selectively diminished in Alzheimer brains, suggest synapse loss as a primary event in early-onset form (type I) and demyelination in late-onset form (type II). J Neurochem 1994; 62: 1039–1047
   PubMed Web of Science ®Google Scholar
• Liang J-s, Stone P J, Sipe J D. Serum Amyloid A (ApoSAAp) catabolism: Dual Cellular mechanisms and attenuation by lipids and lipoprotein. FASEB J 1995; 9: A1043
   PubMedGoogle Scholar
• Ristori G, Laurenti F, Stacchini P, Gasperini C, Buttinelli C, Pozzilli C, Salvetti M. Serum amyloid A protein is elevated in relapsing-remitting multiple sclerosis. J Neuroimmunol 1998; 88: 9–12
   PubMed Web of Science ®Google Scholar