scholarly journals Effects of the English (H6R) and Tottori (D7N) Familial Alzheimer Disease Mutations on Amyloid β-Protein Assembly and Toxicity

2010 ◽  
Vol 285 (30) ◽  
pp. 23186-23197 ◽  
Author(s):  
Kenjiro Ono ◽  
Margaret M. Condron ◽  
David B. Teplow
Keyword(s):  
Alzheimer Disease ◽  
Amyloid Β ◽  
Protein Assembly ◽  
Amyloid Β Protein ◽  
Disease Mutations ◽  
Β Protein ◽  
Familial Alzheimer Disease

scholarly journals The Tottori (D7N) and English (H6R) Familial Alzheimer Disease Mutations Accelerate Aβ Fibril Formation without Increasing Protofibril Formation

2006 ◽  
Vol 282 (7) ◽  
pp. 4916-4923 ◽  
Author(s):  
Yukiko Hori ◽  
Tadafumi Hashimoto ◽  
Yosuke Wakutani ◽  
Katsuya Urakami ◽  
Kenji Nakashima ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Amyloid Fibril ◽  
Amyloid Β ◽  
Fibril Formation ◽  
Amyloid Β Protein ◽  
Protein Precursor ◽  
Amyloid Fibril Formation ◽  
Β Protein ◽  
Familial Alzheimer Disease ◽  
Aβ Production

A subset of Alzheimer disease cases is caused by autosomal dominant mutations in genes encoding the amyloid β-protein precursor or presenilins. Whereas some amyloid β-protein precursor mutations alter its metabolism through effects on Aβ production, the pathogenic effects of those that alter amino acid residues within the Aβ sequence are not fully understood. Here we examined the biophysical effects of two recently described intra-Aβ mutations linked to early-onset familial Alzheimer disease, the D7N Tottori-Japanese and H6R English mutations. Although these mutations do not affect Aβ production, synthetic Aβ(1-42) peptides carrying D7N or H6R substitutions show enhanced fibril formation. In vitro analysis using Aβ(1-40)-based mutant peptides reveal that D7N or H6R mutations do not accelerate the nucleation phase but selectively promote the elongation phase of amyloid fibril formation. Notably, the levels of protofibrils generated from D7N or H6R Aβ were markedly inhibited despite enhanced fibril formation. These N-terminal Aβ mutations may accelerate amyloid fibril formation by a unique mechanism causing structural changes of Aβ peptides, specifically promoting the elongation process of amyloid fibrils without increasing metastable intermediates.

scholarly journals Amyloid β-Protein Assembly and Alzheimer Disease

2008 ◽  
Vol 284 (8) ◽  
pp. 4749-4753 ◽  
Author(s):  
Robin Roychaudhuri ◽  
Mingfeng Yang ◽  
Minako M. Hoshi ◽  
David B. Teplow
Keyword(s):  
Alzheimer Disease ◽  
Amyloid Β ◽  
Protein Assembly ◽  
Amyloid Β Protein ◽  
Β Protein

scholarly journals Isolation and Characterization of Patient-derived, Toxic, High Mass Amyloid β-Protein (Aβ) Assembly from Alzheimer Disease Brains

2009 ◽  
Vol 284 (47) ◽  
pp. 32895-32905 ◽  
Author(s):  
Akihiko Noguchi ◽  
Satoko Matsumura ◽  
Mari Dezawa ◽  
Mari Tada ◽  
Masako Yanazawa ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Amyloid Β ◽  
High Mass ◽  
Amyloid Β Protein ◽  
Isolation And Characterization ◽  
Β Protein

scholarly journals Amyloid β-Protein Assembly: The Effect of Molecular Tweezers CLR01 and CLR03

2015 ◽  
Vol 119 (14) ◽  
pp. 4831-4841 ◽  
Author(s):  
Xueyun Zheng ◽  
Deyu Liu ◽  
Frank-Gerrit Klärner ◽  
Thomas Schrader ◽  
Gal Bitan ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Protein Assembly ◽  
Amyloid Β Protein ◽  
Molecular Tweezers ◽  
Β Protein

scholarly journals Increased T cell reactivity to amyloid β protein in older humans and patients with Alzheimer disease

2003 ◽  
Vol 112 (3) ◽  
pp. 415-422 ◽  
Author(s):  
Alon Monsonego ◽  
Victor Zota ◽  
Arnon Karni ◽  
Jeffery I. Krieger ◽  
Amit Bar-Or ◽  
...  
Keyword(s):  
T Cell ◽  
Alzheimer Disease ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Cell Reactivity ◽  
Β Protein ◽  
T Cell Reactivity

scholarly journals Effects of Familial Alzheimer’s Disease Mutations on the Folding Nucleation of the Amyloid β-Protein

2008 ◽  
Vol 381 (1) ◽  
pp. 221-228 ◽  
Author(s):  
Mary Griffin Krone ◽  
Andrij Baumketner ◽  
Summer L. Bernstein ◽  
Thomas Wyttenbach ◽  
Noel D. Lazo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Familial Alzheimer’S Disease ◽  
Disease Mutations ◽  
Β Protein ◽  
Familial Alzheimer's Disease
Sign in / Sign up

Export Citation Format

Share Document