Amyloid formation

Come JH, Fraser PE, Lansbury PT, Jr. A kinetic model for amyloid formation in the prion diseases importance of seeding. Proc Natl Acad Sci USA 1993 90 5959-5963. 

Kayed R, Bernhagen J, Greenfield N, Sweimeh K, Brunner H, Voelter W, Kapurniotu A. Conformational transitions of islet amyloid polypeptide (IAPP) in amyloid formation in vitro. J Mol Biol 1999 287 781-796. 

Soto C, Castano EM, Frangione B, Inestrosa NC. The alpha-helica to beta-strand transition in the amino-terminal fragment of the amyloid beta-peptide modulates amyloid formation. J Biol Chem 1995 270 3063-3067. 

Evans KC, Berger EP, Cho CG, Weisgraber KH, Lansbury PT Jr. Apolipoprotein E is a kinetic but not a thermodynamic of amyloid formation implications for the pathogenesis and treatment of Alzheimer disease. Proc Natl Acad Sci USA 1995 92 763-767. 

Salomon AR, Marcinowski KJ, Friedland RP, Zagorski MG. Nicotine inhibits amyloid formation by the beta-peptide. Biochemistry 1996 35 13568-13578. 

The lack of zinc can also be a problem in biological systems and is responsible for disease states. For example, nitric oxide-dependent apoptosis can be induced in motor neurons by zinc-deficient SOD, and in some cases of amyotrophic lateral sclerosis, zinc-deficient SOD may participate in this type of oxidative mechanism involving nitric oxide.969 One form of hereditary human hair loss or alopecia was mapped to a specific gene and a mutation found in affected individuals. The gene encodes a single zinc finger transcription factor protein with restricted expression in the brain and skin.970 Zinc has been implicated in Alzheimer s via beta amyloid formation, and a role has been attributed for the cerebral zinc metabolism in the neuropathogenesis of Alzheimer s disease.971... 

It appears that amyloid formation involves unordered or at least partly unfolded precursors. Thus, it is worthwhile to examine the fibrillation... 

Roberti, M. J., Bertoncini, C. W., Klement, R., Jares-Erijman, E. A. and Jovin, T. M. (2007). Fluorescence imaging of amyloid formation in living cells by a functional, tetracysteine-tagged ot-synuclein. Nat. Methods 4, 345-51. 

Sunde, M., and Blake, C. C. F. (1998). From the globular to the fibrous state Protein structure and structural conversion in amyloid formation. Q. Rev. Biophys. 31, 1-39. 

Taylor, K. L., Cheng, N., Williams, R. W., Steven, A. C., and Wickner, R. B. (1999). Prion domain initiation of amyloid formation in vitro from native Ure2p. Science 283, 1339-1343. 

Zhu, L., Zhang, X. J., Wang, L. Y., Zhou, J. M., and Perrett, S. (2003). Relationship between stability of folding intermediates and amyloid formation for the yeast prion Ure2p A quantitative analysis of the effects of pH and buffer system./ Mol. Biol. 328, 235-254. 

Green,J. D., Goldsbury, C., Kistler.J., Cooper, G.J., and Aebi, U. (2004a). Human amylin oligomer growth and fibril elongation define two distinct phases in amyloid formation./. Biol. Chem. 279, 12206-12212. 

Huff, M. E., Balch, W. E., and Kelly, J. W. (2003). Pathological and functional amyloid formation orchestrated by the secretory pathway. Curr. Opin. Struct. Biol. 13, 674-682. Jansen, R., Dzwolak, W., and Winter, R. (2005). Amyloidogenic self-assembly of insulin aggregates probed by high resolution atomic force microscopy. Biophys. J. 88, 1344-1353. 

Additional factors may influence fibril stability in vivo. The glycan molecules and amyloid P component found in amyloid deposits may stabilize amyloid fibrils (Pepys, 2006, and references therein). Also, monomer concentration is important to amyloid formation and stability in vivo several amyloidoses are associated with elevated levels of the fibril precursor protein, and deposits regress when the levels of the precursor protein are sufficiently reduced (Pepys, 2006, and references therein). 

Liu, Y., Gotte, G., Libonati, M., and Eisenberg, D. (2001). A domain-swapped RNase A dimer with implications for amyloid formation. Nat. Struct. Biol. 8, 211-214. 

Olofsson, A., Ippel, H. J., Baranov, V., Horstedt, P., Wijmenga, S., and Lundgren, E. (2001). Capture of a dimeric intermediate during transthyretin amyloid formation. / Biol. Chem. 276, 39592-39599. 

Smith, D. P., Jones, S., Serpell, L. C., Sunde, M., and Radford, S. E. (2003). A systematic investigation into the effect of protein destabilisation on beta 2-microglobulin amyloid formation./. Mol. Biol. 330, 943-954. 

CordeU, B. (1994) [3-Amyloid formation as a potential therapeutic target for Alzheimer s disease. Annu. Rev. Pharmacol. Toxicol., 34, 69-89. 

Dietary intervention with crude MegaNatural-AZ grape seed extract significantly reduced (by 30-50%) Alzheimer s disease-type cognitive deterioration in mice by prevention of amyloid formation in the brain [8]. However, it is essential to determine which components of the extract exhibited bioactivity in the transgenic... 

Other mechanisms, such as the inhibition of -amyloid formation. There are several other alkaloids which are nicotinic agonists at the cholinergic receptor such as lobeline (89) from Lobelia inflata. Lobelia inflata a could be exploited to influence cholinergic function in AD. Sophoramine (90) and cytisine (91), found in members of the Leguminosae, have nicotinic actions but they do not appear to have been developed for any pharmaceutical purposes, probably because of their toxicity. 

Kammerer RA, Kostrewa D, Zurdo J, Detken A, Garcia-Echeverria C, Green JD, Mueller SA, Meier BH, Winkler FK, Dobson CM, Steinmetz MO. Exploring amyloid formation by a de novo design. Proc Natl Acad Sci USA 2004 101 4435-4440. 

Zhang S, Rich A. Direct conversion of an oligopeptide fi om a 8-sheet to an a-helix a model for amyloid formation. Proc Natl Acad Sci USA 1997 94 23-28. 

Coppen A, Ghose K, Montgomery S, et al Continuation therapy with amitriptyline in depression. Br J Psychiatry 133 28-33, 1978 Coppen A, Swade C, Wood K Lithium restores abnormal platelet 5-HT transport in patients with affective disorders. Br J Psychiatry 136 235-238, 1980 Coppen A, Swade C, Jones SA, et al Depression and tetrahydrobiopterin the folate connection. J Affect Disord 16 103-107, 1989 Cordell B 3-Amyloid formation as a potential therapeutic target for Alzheimer s disease. Annu Rev Pharmacol Toxicol 34 69-89, 1994 Corkin S Acetylcholine, aging, and Alzheimer s disease imphcations of treatment. Trends Neurosci 4 287-290, 1981... 

While we tend to think of proteins as having fixed structures, conformational changes are basic to life. Many proteins are very flexible and in part disordered.6553 At the same time proteins can be misfolded leading to amyloid formation (Box 29-E) and to other diseases.65513-6... 

FIGURE 12-38. Another current therapeutic approach to preventing the neuronal destruction in Alzheimer s disease is also based on the molecular neurobiology of beta amyloid formation but emphasizes the involvement of APO-E binding protein in this process. If the synthesis of good APO-E could be ensured or the synthesis of bad APO-E prevented, possibly amyloid would not accumulate in the neuron. Changing the deposition of beta amyloid would hopefully prevent the progressive course of Alzheimer s disease. 

Bush AI, Pettingell WH, Multhaup G, Paradis M, Vonsattel JP, Gusella JF, Beyreuther K, Masters CL, Tanzi RE. 1994. Rapid induction of Alzheimer A beta amyloid formation by zinc. Science 265 1464-1467. 

Jarrett, J.T., Berger, E.P. and Lansbury, Jr. P.T. (1993) The carboxy terminus of the beta amyloid protein is critical for the seeding of amyloid formation implications for the pathogenesis of Alzheimer s disease. Biochemistry 32,4693 1697. 

Nilsson MR, Driscoll M, Raleigh DP (2002), Low levels of asparagine deamidation can have a dramatic effect on aggregation of amyloidogenic peptides implications for the study of amyloid formation. Protein Sci. 11 342-349. 

---