Amyloid b protein

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Bitan, G., Kirkitadze, M.D., Lomakin, A., Vollers, S.S., Benedek, G.B., and Teplow, D.B. (2003) Amyloid B-protein (otP) assembly ap40 and ap42 oligomerize through distinct pathways. Proc. Natl. Acad. Sci. USA 100, 330-335. 

Hung AY, Haass C, Nitsch RM, et al. Activation of protein kinase C inhibits cellular production of the amyloid b-protein. J Biol Chem 1993 268 22,959-22,962. 

Arvanitakis Z, Lucas JA, YounMn LH, Younldn SG, GrafF-Radford NR. Serum creatinine levels correlate with plasma amyloid B protein. Alzheimer Dis Assoc Disord 2002 16 187-190. 

Lomakin A, Teplow DB, Kirschner DA et al (1997) Kinetic theory of fibrillogenesis of amyloid b-protein. Proc Natl Acad Sci USA 94 7942-7947... 

Figure 18.2 Production of senile plaque (S/A4 amyloid protein. Amyloid fS4 protein (/S/A4) is part of a 695, 751 or 770 amino-acid amyloid precursor protein APP. This is a transmembrane protein which is normally cleared within the fi/A4 amino acid sequence to give short 40 amino-acid soluble derivatives. It seems that under some circumstances as in Alzheimer s disease, APP is cleared either side of the fi/A4 sequence to release the 42/43 amino acid P/A4 which aggregates into the amyloid fibrils of a senile plaque (a). (See also Fig. 18.5.) Some factors, e.g. gene mutation, must stimulate this abnormal clearage leading to the deposition of P/A4 amyloid protein as plaques and tangles and the death of neurons (b)...

Davis, J.B., McMurray, H.F. and Schubert, D. (1992). The amyloid beta-protein of Alzheimer s disease is chemotactic for mononuclear phagocytes. Biochem. Biophys. Res. Commun. 189, 1096-1100. 

Berezovska, O., Lleo, A., Fieri, L. D., Frosch, M. P., Stern, E. A., Bacskai, B. J. and Flyman, B. T. (2005). Familial Alzheimer s disease presenilin 1 mutations cause alterations in the conformation of presenilin and interactions with amyloid precursor protein. J. Neurosci. 25, 3009-17. 

Kinoshita, A., Whelan, C. M., Smith, C. J., Mikhailenko, I., Rebeck, G. W., Strickland, D. K. and Hyman, B. T. (2001). Demonstration by fluorescence resonance energy transfer of two sites of interaction between the low-density lipoprotein receptor-related protein and the amyloid precursor protein Role of the intracellular adapter protein Fe65. J. Neurosci. 21, 8354-61. 

Vassar, R., Bennett, B. D., Babu-Khan, S. et al. P-secretase cleavage of Alzheimer s amyloid precusor protein by the transmembrane aspartic protease BACE. Science 286 735-741, 1999. 

Arispe, N., Rojas, E., and Pollard, H. B. (1993). Alzheimer disease amyloid beta protein forms calcium channels in bilayer membranes Blockade by tromethamine and aluminum. Proc. Natl. Acad. Sci. USA 90, 567-571. 

Hartley, D. M., Walsh, D. M., Ye, C. P., Diehl, T., Vasquez, S., Vassilev, P. M., Teplow, D. B., and Selkoe, D. J. (1999). Protofibrillar intermediates of amyloid beta-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical... 

Lashuel, H. A., Petre, B. M., Wall, J., Simon, M., Nowak, R. J., Walz, T., and Lansbury, P. T., Jr. (2002). Alpha-synuclein, especially the Parkinson s disease-associated mutants, forms pore-like annular and tubular protofibrils./. Mol. Biol. 322,1089-1102. LeVine, H. (1993). Thioflavine T interaction with synthetic Alzheimer s disease beta-amyloid peptides Detection of amyloid aggregation in solution. Protein Sci. 2, 404—410. Lin, H., Bhatia, R., and Lai, R. (2001). Amyloid beta protein forms ion channels Implications for Alzheimer s disease pathophysiology. FASEB J. 15, 2433-2444. Lorenzo, A., and Yankner, B. A. (1994). Beta-amyloid neurotoxicity requires fibril formation and is inhibited by Congo red. Proc. Natl. Acad. Sci. USA 91, 12243-12247. Luhrs, T., Ritter, C., Adrian, M., Riek-Loher, D., Bohrmann, B., Dobeli, H., Schubert, D., and Riek, R. (2005). 3D structure of Alzheimer s amyl o id-( be la) (1—12) fibrils. Proc. Natl. Acad. Sci. USA 102, 17342-17347. 

Kang, J., Lemaire, H. G., Unterbeck, A., Salbaum, J. M., Masters, C. L., Grzeschik, K. H., Multhaup, G., Beyreuther, K., and Muller-Hill, B. (1987). The precursor of Alzheimer s disease amyloid A4 protein resembles a cell-surface receptor. Nature 325, 733-736. 

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., et al. (1999). Beta-secretase cleavage of Alzheimer s amyloid precursor protein by the transmembrane aspartic protease BAGE. Science 286, 735—741. 

Murrell, J., Farlow, M., Ghetti, B., Benson, M.D. (1991) A mutation in the amyloid precursor protein associated with hereditary Alzheimer s disease. Science, 254,97-99. 

Baek, S.H., Ohgi, K.A., Rose, D.W., Koo, E.H., Glass, C.K., Rosenfeld, M.G. (2002) Exchange of N-CoR corepressor and Tip60 coactivator complexes links gene expression by NF-kappa-B and beta-amyloid precursor protein. Cell, 110, 55-67. 

Lamb, B.T., Bardel, K.A., Kulnane, L.S., et al. (1999) Amyloid production and deposition in mutant amyloid precursor protein and presenUin-1 yeast artificial chromosome transgenic mice. Nat. Neurosci., 2, 695-697. 

De Strooper, B., Saftig, P., Craessaerts, K., Vanderstichele, H., et al. (1998) Deficiency of prese-nUin-l inhibits the normal cleavage of amyloid precursor protein. Nature, 391,387-390. 

Konishi, Y., Beach, T., Sue, L.I., et al. (2003) The temporal localization of frame-shift ubiq-uitin-B and amyloid precursor protein, and complement proteins in the brain of non-demented control patients with increasing Alzheimer s disease pathology. Neurosci. Lett., 348, 46-50. 

Puglielli, L., Ellis, B.C., Saunders, A.J., Kovacs, D.M. (2003) Ceramide stabdizes P-site amyloid precursor protein-cleaving enzyme-1 and promotes amyloid P-peptide biogenesis. /. Biol. Chem., 278, 19777-19783. 

Cole, S.L., Grudzien, A., Manhart, I.O., Kelly, B.L., Oakley, H., Vassar, R. (2005) Statins cause intracellular accumulation of amyloid precursor protein, P-secretase-cleaved fragments, and amyloid P-peptide via an isoprenoid-dependent mechanism. J. Biol. Chem., 280, 18755-18770. 

Flood, F., Murphy, S., Cowburn, R., Lannfelt, L., Walker, B., Johnston, J.A. (2005) Proteasome-mediated effects of amyloid precursor protein processing at the y-secretase site. Biochem. J., 5, 545-550. 

Roher AE, Lowenson JD, Clarke S, Wolkow C, Wang R, Cotter RJ, Reardon IM, Ziircher-Neely HA, Heinrikson RL, Ball MJ, Greenberg B. (1993) Structural alterations in the peptide backbone of beta-amyloid core protein may account for its deposition and stability in Alzheimer s disease. J Biol Chem268 3072-3083. 

Farris, W., Mansourian, S., Chang, Y., Linsley, L., Eckman, E. A., Frosch, M. P., Eckman, C. B., Tanzi, R. E., Selkoe, D. J., and Guennette, S. (2005). Insulin-degrading enzyme regulates the levels of insulin, amyloid beta-protein, and the beta-amyloid precursor protein intracellular domain in vivo. Proc. Natl. Acad. Sci. USA 100, 4162—4167. 

Figure 8.7 Top Sequence of Api 3 and sites of secretase cleavage. y-Secretase has low specificity, cleaving the amyloid precursor protein (APP) anywhere between residues 39 to 43 of Ap. The transmembrane portion of APP is indicated. Bottom processing of amyloid precursor protein (APP) (A) Normal cleavage within AP region by a-secretase (B) pathogenic cleavage of APP by P- and y-secretase, liberating Ap, which can become incorporated into growing plaques. (Note AP = P-Amyloid Peptide)...

Petryniak, M. A., Wurtman, R. J., and Slack, B. E. (1996). Elevated intracellular calcium concentration increases secretory processing of the amyloid precursor protein by a tyrosine phosphorylation-dependent mechanism. Biochem J 320 ( Pt 3), 957-963. 

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