1. For the involvement of amyloid peptides in Alzheimer's disease, see the following and references cited therein: (a) Gold, M.; Felsenstein, K. M.; Molinoff, P. Treatment approaches for Alzheimer's disease. In Contemporary Clinical Neuroscience: Molecular Mechanisms of Neurodegenerative Diseases; Chesselet, M.-F., Ed.; Humana: Totowa, NJ, 2000; p 131. (b) Wang, H.-Y.; Lee, D. H. S.; D'Andrea, M. R.; Peterson, P. A.; Shank, R. P.; Reitz, A. B. J. Biol. Chem. 2000, 275, 5625. (c) Findeis, M. A. Curr. Opin. CPNS Invest. Drugs 1999, 1, 333. (d) Soto, C. CNS Drugs 1999, 12, 347. (e) Bandiera, T.; Lansen, J.; Post, C.; Varasi, M. Curr. Med. Chem. 1997, 4, 159. (f) Twyman, L. J.; Allsop, D. Tetrahedron Lett. 1999, 40, 9383. (g) Selkoe, D. J. J. Biol. Chem. 1996, 271, 18295.
2. Amyloid β protein-induced neuronal cell death: neurotoxic properties of aggregated amyloid β protein
3. Diffusible, nonfibrillar ligands derived from A 1-42 are potent central nervous system neurotoxins
4. Inhibition of Amyloid β Protein Aggregation and Neurotoxicity by Rifampicin