參考文獻 |
[1] Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed,
R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola,
K. L., Wals, P., Finch, C. E., Krafft, G. A., and Klein, W. L.,
“Diffusible, nonfibrillar ligands derived from Aß1-42 are potent
central nervous system neurotoxins."Proceedings of the National
Academy of Sciences of the United States of America, 1998, 95,
6448-6453.
[2] Xing, Y., and Higuchi, K.,“Amyloid fibril proteins."Mechanisms
of Ageing and Development, 2002, 123,1625-1636.
[3] Sommer, B.,“Alzheimer’s disease and the amyloid cascade
hypothesis:ten years on."Neurosciences, 2002, 1, 87-92.
[4] Davies, P.,“A very incomplete comprehensive theory of
Alzheimer’s disease."Annals of the New York Academy of
Sciences, 2000, 924, 8-16.
[5] Seiffert, D., Bradley, J. D., Rominger, C. M., Rominger, D. H., Yang,
F., Meredith, J., Wang, Q., Roach, A. H., Thompson, L. A., Spitz, S.
M., Higaki, J. N., Prakash, S. R., Combs, A. P.,Copeland, R. A.,
Arneric, S. P., Hartig, P. R., Robertson, D. W., Cordell, B., Stern, A.
M., Olson, R. E., and Zaczek, R.,“Presenilin-1 and 2 are molecular
targets for gamma secretase inhibitors."Journal of Biological
Chemistry, 2000, 275, 34086-34091.
[6] Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D.
E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., and
PericakVance, M. A.,“Gene dose of apolipoprotein E type 4 allae
and the risk of Alzheimer’ s disease in late onset families."Science,
1993, 261, 921-923.
[7] Holtzman, D. M., Bales, K. R., Tenkova, T., Fagan, A. M.,
Parsadanian, M., Sartorius, L. J., Mackey, B., Olney, J., McKeel, D.,
Woznizk, D., and Paul, S. M.,“Apolipoprotein E
isoform-dependent amyloid deposition and neuritic degeneration in a
mouse model of Alzheimer’s disease."Proceedings of the National
Academy of Sciences, 2000, 97, 2892-2897.
[8] Hardy, J., Selkoe2, D. J.,“The Amyloid Hypothesis of Alzheimer’s
Disease:Progress and Problems on the Road to Therapeutics."
Science, 2002, 297, 353-356.
[9] Shoghi-Jadid, K., Barrio, J. R., Kepe, V., Wu, H. M., Small, G. W.,
Phelps, M. E., and Huang, S. C.,“Imaging β-amyloid fibrils in
Alzheimer’s disease:a critical analysis through simulation of
amyloid fibril polymerization."Nuclear Medicine and Biology,
2005, 32, 337-351.
[10]Buxbaum, J. D., Liu, K. N., Luo, Y., Slack, J. L., Stocking, K. L.,
Peschon, J. J., Johnson, R. S., Castner, B. J., Cerretti, D. P., and
Black, R. A.,“Evidence that tumor necrosis factor alpha converting
enzyme is involved in regulated alphasecretase cleavage of the
Alzheimer amyloid protein precursor."Journal of Biological
Chemistry, 1998, 273, 27765-27767.
[11]Lammich, S., Kojro, E., Postina, R., Gilbert, S., Pfeiffer, R.,
Jasionowski, M., Haass, C., and Fahrenholz, F.,“Constitutive and
regulated alpha-secretase cleavage of Alzheimer’s amyloid precursor
protein by a disintegrin metalloprotease."Proceedings of the
National Academy of Sciences, 1999, USA 96, 3922-3927.
[12]Vassar, R., Bennett, B. D., Babu-Khan, S., Kahn, S., Mendiaz, E. A.,
Denis, P., Teplow, D. B., Ross, S., Amarante, P., Loeloff, R., Luo,
Y., Fisher, S., Fuller, J., Edenson, S., Lile, J., Jarosinski, M. A.,
Biere, A. L., Curran, E., Burgess, T., Louis, J. C., Collins, F.,
Treanor, J., Rogers, G., and Citron, M.,“Beta-secretase cleavage of
Alzheimer’s amyloid precursor protein by the transmembrane
aspartic protease BACE."Science, 1999, 286, 735-741.
[13]Sinha, S., Anderson, J. P., Barbour, R., Basi, G. S., Caccavello, R.,
Davis, D., Doan, M., Dovey, H. F., Frigon, N., Hong, J.,
Jacobson-Croak, K., Jewett, N., Keim, P., Knops, J., Lieberburg, I.,
Power, M., Tan, H., Tatsuno, G., Tung, J., Schenk, D., Seubert, P.,
Suomensaari, S. M., Wang, S., Walker, D., and John, V.,
“Purification and cloning of amyloid precursor protein
beta-secretase from human brain."Nature, 1999, 402, 537-540.
[14]Yan, R., Bienkowski, M. J., Shuck, M. E., Miao, H., Tory, M. C.,
Pauley, A. M., Brashier, J. R., Stratman, N. C., Mathews, W. R.,
Buhl, A. E., Carter, D. B., Tomasselli, A. G., Parodi, L. A.,
Heinrikson, R. L., and Gurney, M. E.,“Membrane-anchored
aspartyl protease with Alzheimer’s disease beta-secretase activity."
Nature, 1999, 402, 533-537.
[15]De Strooper, B., Saftig, P., Craessaerts, K., Vanderstichele, H.,
Guhde, G., Annaert, W., Von Figura, K., and Van Leuven, F.,
“Deficiency of presenilin-1 inhibits the normal cleavage of amyloid
precursor protein."Nature, 1998, 391, 387-390.
[16]Allsop, D., Swanson, L., Moore, S., Davies, Y., York, A., El-Agnaf,
O. M. A., Soutar, I.,“Fluorescence Anisotropy: A Method for Early
Detection of Alzheimer β-Peptide (Aβ) Aggregation."Biochemical
and Biophysical Research Communications, 2001, 285, 58-63.
[17]Terzi E., Holzemann, G., Seelig, J.,“Reversible Random
Coil-β-Sheet Transition of the Alzheimer β-Amyloid
Fragment(25-35)."Biochemistry, 1994, 33, 1345-1350.
[18]Nilsson, M. R.,“Techniques to study amyloid fibril formation in
vitro."Methods, 2004, 34, 151-160.
[19]Hideki, H., Kimura, N., Yamaguchi, H., Hasegawa, K., Yokoseki,
T., Shibata, M., Yamamoto, N., Michikawa, M., Yoshikawa, Y.,
Terao, K., Matsuzaki, K., Lemere, C. A., Selkoe, D. J., Naiki, H.,
and Yanagisawa, K.,“A Seed for Alzheimer Amyloid in the
Brain."The Journal of Neuroscience, 2004, 24, 4894-4902.
[20]Petkova, A. T., Ishii, Y., Balbach, J. J., Antzutkin, O. N., Leapman,
R. D., Delaglio, F., and Tycko, R.,“A structural model for
Alzheimer’s β-amyloid fibrils based on experimental constraints
from solid state NMR. "Proceedings of the National Academy of
Sciences, 2002, 99, 16742-16747.
[21]Luhrs, T., Ritter, C., Adrian, M., Riek-Loher, D., Bohrmann, B.,
Dobeli, H., Schubert, D., and Riek, R.,“3D structure of
Alzheimer’s amyloid-β(1– 42) fibrils"Proceedings of the National
Academy of Sciences, 2005, 102, 17342-17347.
[22]Kamihira, M., Naito, A., Tuzi, S., Nosaka, A. Y., and Saito, H.,
“Conformational transitions and fibrillation mechanism of human
calcitonin as studied by high-resolution solid-state 13C NMR."
Protein Science, 2000, 9, 867-877.
[23]Sabat´e, R., Gallardo, M., and Estelrich, J.,“Temperature
dependence of the nucleation constant rate in β amyloid
fibrillogenesis."International Journal of Biological
Macromolecules, 2005, 35, 9-13.
[24]Naiki, H., and Gejyo, F.,“Kinetic Analysis of Amyloid Fibril
Formation."Methods in Enzymology, 1999, 309, 305-318.
[25]Burdick, D., Soreghan, B., Kwon, M., Kosmoski, J., Knauer, M.,
Henschen, A., Yates, J., Cotman, C., and Glabe, C.,“Assembly and
Aggregation Properties of Synthetic Alzheimer’s A4/β Amyloid
Peptide Analogs."Journal of Biological Chemistry, 1992, 267,
546-554.
[26]Jarrett, J. T., Berger, E. P., and Lansbury, P. T., Jr.,“The Carboxy
Terminus of the Amyloid Protein Is Critical for the Seeding of
Amyloid Formation: Implications for the Pathogenesis of
Alzheimer's Disease."Biochemistry, 1993, 32, 4693-4697.
[27]Stine, W. B., Jr., Dahlgren, K. N., Krafft, G. A., and LaDu, M. J.,
“In Vitro Characterization of Conditions for Amyloid-β Peptide
Oligomerization and Fibrillogenesis."Journal of Biological
Chemistry, 2003, 278, 11612-11622.
[28]Tashima, Y., Oe, R., Lee, S., Sugihara, G., Chambers, E. J.,
Takahashi, M., and Yamada, T.,“The Effect of Cholesterol and
Monosialoganglioside (GM1) on the Release and Aggregation of
Amyloid -Peptide from Liposomes Prepared from Brain
Membrane-like Lipids."Journal of Biological Chemistry, 2004, 279,
17587–17595.
[29]Terzi, E., Holzemann, G., and Seelig, J.,“Self-association
of β-Amyloid Peptide (1–40) in Solution and Binding to Lipid
Membranes."Journal of Molecular Biology, 1995, 252, 633-642.
[30]Gursky, O., Aleshkov, S.,“Temperature-dependent β-sheet
formation in β-amyloid Aβ1-40 peptide in water: uncoupling
β-structure folding from aggregation."Biochimica et Biophysica
Acta, 2000, 1476, 93-102.
[31]Choo-Smith, L. P., Garzon-Rodriguez, W., Glabe, C. G., and
Surewicz, W. K.,“Acceleration of Amyloid Fibril Formation by
Specific Binding of Aβ-(1–40) Peptide to Gangliosidecontaining
Membrane Vesicles."Journal of Biological Chemistry, 1997, 272,
22987-22990.
[32]Wood, S. J., Maleeff, B., Hart, T., and Wetzel, R.,“Physical,
Morphological and Functional Differences between pH 5.8 and 7.4
Aggregates of the Alzheimer’s Amyloid Peptide Aβ."Journal of
Molecular Biology, 1996, 256, 870-877.
[33]Nichols, M. R., Moss, M. A., Reed, D. K., Lin, W. L.,
Mukhopadhyay, R., Hoh, J. H., and Rosenberry, T. L.,“Growth of
β-Amyloid(1-40) Protofibrils by Monomer Elongation and Lateral
Association. Characterization of Distinct Products by Light
Scattering and Atomic Force Microscopy."Biochemistry, 2002, 41,
6115-6127.
[34]Barrow, C. J., Yasuda, A., Kenny, P. T., and Zagorski, M. G.,
“Solution Conformations and Aggregational Properties of
Synthetic Amyloid β-Peptides of Alzheimer’s Disease Analysis of
Circular Dichroism Spectra."Journal of Molecular Biology, 1992,
225, 1075-1093.
[35]LeVine III, H.,“4,4’-Dianilino-1,1’-binaphthyl-5,5’-disulfonate:
report on non- β-sheet conformers of Alzheimer’s peptide
β(1–40)." Archives of Biochemistry and Biophysics, 2002, 404,
106-115.
[36]Nichols, M. R., Moss, M. A., Reed, D. K., Cratic-McDaniel, S., Hoh,
J. H., and Rosenberry, T. L.,“Amyloid- β Protofibrils Differ from
Amyloid-β Aggregates Induced in Dilute Hexafluoroisopropanol in
Stability and Morphology."Journal of Biological Chemistry, 2005,
280, 2471-2480.
[37]Rodger, A., and Nordén, B.,“Circular dichroism and linear
dichroism."Oxford, 1997.
[38]Lightner, D. A., Gurst, J. E.,“Organic conformational analysis and
stereochemistry from circular dichroism spectroscopy."John Wiley
& Sons, Inc., 2000.
[39]Velluz, L., Legrand, M., Grosjean, M.,“Optical circular
dichroism." Academic Press, Inc., 1965.
[40]Choo-Smith, L. P., and Surewicz, W. K.,“The interaction between
Alzheimer amyloid β(1-40) peptide and ganglioside GM1-containing
membranes."FEBS Letters, 1997, 402, 95-98.
[41]Ladbury, J. E.,“Application of Isothermal Titration Calorimetry in
the Biological Sciences: Things Are Heating Up!"BioTechniques,
2004, 37, 885-887.
[42]LeVINE, H.,“Thioflavine T interaction with synthetic
Alzheimer’s disease β-amyloid peptides:Detection of amyloid
aggregation in solution."Protein Science, 1993, 2, 404-410.
[43]LeVine, H.,“Stopped-flow kinetics reveal multiple phases of
thioflavin T binding to Alzheimer β(1-40) amyloid fibrils."
Archives of Biochemistry and Biophysics, 1997, 342, 306-316.
[44]Wakabayashi, M., Okada, T., Kozutsumib, Y.and Matsuzaki,
K.,“GM1 ganglioside-mediated accumulation of amyloid β-protein
on cell membranes."Biochemical and Biophysical Research
Communications, 2005, 328, 1019-1023.
[45]Yip, C. M., Elton, E. A., Darabie, A. A., Morrison, M. R. and
McLaurin, J.,“Cholesterol, a Modulator of Membrane-associated
Aβ-Fibrillogenesis and Neurotoxicity."Journal of Molecular
Biology, 2001, 311, 723-734. |