共 67 条
[1]
Hardy J(2002)The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics Science 297 353-6
[2]
Selkoe DJ(1989)Alzheimer’s disease: mismatch between amyloid plaques and neuritic plaques Neurosci. Lett. 103 24-28
[3]
Braak H(2009)gamma-Secretase: successive tripeptide and tetrapeptide release from the transmembrane domain of beta-carboxyl terminal fragment J. Neurosci. 29 13042-52
[4]
Braak E(2013)C-terminal turn stability determines assembly differences between Abeta40 and Abeta42 J. Mol. Biol. 425 292-308
[5]
Ohm T(2014)gamma-Secretase processing and effects of gamma-secretase inhibitors and modulators on long Abeta peptides in cells J. Biol. Chem. 289 3276-87
[6]
Bohl J(2006)Distinct early folding and aggregation properties of Alzheimer amyloid-beta peptides Abeta40 and Abeta42: stable trimer or tetramer formation by Abeta42 J. Biol. Chem. 281 24414-22
[7]
Takami M(1999)Neurotoxicity and oxidative damage of beta amyloid 1–42 versus beta amyloid 1–40 in the mouse cerebral cortex Ann. N. Y. Acad. Sci. 893 314-20
[8]
Roychaudhuri R(2014)Alzheimer presenilin-1 mutations dramatically reduce trimming of long amyloid beta-peptides (Abeta) by gamma-secretase to increase 42-to-40-residue Abeta J. Biol. Chem. 289 31043-52
[9]
Ran Y(2010)Neurotoxicity of Alzheimer’s disease Abeta peptides is induced by small changes in the Abeta42 to Abeta40 ratio EMBO J. 29 3408-20
[10]
Chen YR(2008)The ratio of monomeric to aggregated forms of Abeta40 and Abeta42 is an important determinant of amyloid-beta aggregation, fibrillogenesis, and toxicity J. Biol. Chem. 283 28176-89