Characterization of copper binding to the peptide amyloid-β(1–16) associated with Alzheimer's disease

Biopolymers ◽  
2006 ◽  
Vol 83 (1) ◽  
pp. 20-31 ◽  
Author(s):  
Qing-Feng Ma ◽  
Jia Hu ◽  
Wei-Hui Wu ◽  
Hua-Dong Liu ◽  
Jin-Tang Du ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Copper Binding

Alzheimer's disease amyloid β-clipping enzyme (APP secretase): Identification, purification, and characterization of the enzyme

1991 ◽  
Vol 177 (1) ◽  
pp. 377-387 ◽  
Author(s):  
Kazuhiko Tagawa ◽  
Tatsuhide Kunishita ◽  
Kei Maruyama ◽  
Kazuaki Yoshikawa ◽  
Eiki Kominami ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Purification And Characterization

scholarly journals Copper Binding to the Amyloid-β (Aβ) Peptide Associated with Alzheimer's Disease

2004 ◽  
Vol 279 (18) ◽  
pp. 18169-18177 ◽  
Author(s):  
Christopher D. Syme ◽  
Rebecca C. Nadal ◽  
Stephen E. J. Rigby ◽  
John H. Viles
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Aβ Peptide ◽  
Copper Binding

Mass Spectrometric Characterization of Amyloid-β Species in the 7PA2 Cell Model of Alzheimer's Disease

2012 ◽  
Vol 33 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Erik Portelius ◽  
Maria Olsson ◽  
Gunnar Brinkmalm ◽  
Ulla Rüetschi ◽  
Niklas Mattsson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Model ◽  
Amyloid Β ◽  
Mass Spectrometric ◽  
Model Of Alzheimer’S Disease ◽  
7Pa2 Cell

Affinity of Cu+for the Copper-Binding Domain of the Amyloid-β Peptide of Alzheimer’s Disease

2011 ◽  
Vol 50 (5) ◽  
pp. 1614-1618 ◽  
Author(s):  
Heather A. Feaga ◽  
Richard C. Maduka ◽  
Monique N. Foster ◽  
Veronika A. Szalai
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Binding Domain ◽  
Amyloid Β Peptide ◽  
Copper Binding

Computational models explain how copper binding to amyloid-β peptide oligomers enhances oxidative pathways

2019 ◽  
Vol 21 (17) ◽  
pp. 8774-8784 ◽  
Author(s):  
Giovanni La Penna ◽  
Mai Suan Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Computational Models ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Copper Binding ◽  
Aβ Peptides ◽  
Intrinsically Disordered ◽  
Disordered Peptides

Amyloid-β (Aβ) peptides are intrinsically disordered peptides and their aggregation is the major hallmark of Alzheimer's disease (AD) development.

scholarly journals Characterization of stable complexes involving apolipoprotein E and the amyloid β peptide in Alzheimer's disease brain

Neuron ◽  
1995 ◽  
Vol 15 (1) ◽  
pp. 219-228 ◽  
Author(s):  
Jan Näslund ◽  
Johan Thyberg ◽  
Lars O. Tjernberg ◽  
Christer Wernstedt ◽  
Anders R. Karlström ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Amyloid Β ◽  
Amyloid Β Peptide

scholarly journals Characterization of Alzheimer’s tau biomarker discordance using plasma, CSF, and PET

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Yu Guo ◽  
◽  
Yu-Yuan Huang ◽  
Xue-Ning Shen ◽  
Shi-Dong Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Amyloid Β ◽  
Regions Of Interest ◽  
Emission Tomography ◽  
Braak Stage ◽  
Positron Emission ◽  
Tau Pet

Abstract Background We aimed to investigate the tau biomarker discrepancies of Alzheimer’s disease (AD) using plasma tau phosphorylated at threonine 181 (p-tau181), cerebrospinal fluid (CSF) p-tau181, and AV1451 positron emission tomography (PET). Methods In the Alzheimer’s Disease Neuroimaging Initiative, 724 non-demented participants were categorized into plasma/CSF and plasma/PET groups. Demographic and clinical variables, amyloid-β (Aβ) burden, flortaucipir-PET binding in Braak regions of interest (ROIs), longitudinal changes in clinical outcomes, and conversion risk were compared. Results Across different tau biomarker groups, the proportion of participants with a discordant profile varied (plasma+/CSF− 15.6%, plasma−/CSF+ 15.3%, plasma+/PET− 22.4%, and plasma−/PET+ 6.1%). Within the plasma/CSF categories, we found an increase from concordant-negative to discordant to concordant-positive in the frequency of Aβ pathology or cognitive impairment, rates of cognitive decline, and risk of cognitive conversion. However, the two discordant categories (plasma+/CSF− and plasma−/CSF+) showed comparable performances, resulting in similarly reduced cognitive capacities. Regarding plasma/PET categories, as expected, PET-positive individuals had increased Aβ burden, elevated flortaucipir retention in Braak ROIs, and accelerated cognitive deterioration than concordant-negative persons. Noteworthy, discordant participants with normal PET exhibited reduced flortaucipir uptake in Braak stage ROIs and slower rates of cognitive decline, relative to those PET-positive. Therefore, individuals with PET abnormality appeared to have advanced tau pathological changes and poorer cognitive function, regardless of the plasma status. Furthermore, these results were found only in individuals with Aβ pathology. Conclusions Our results indicate that plasma and CSF p-tau181 abnormalities associated with amyloidosis occur simultaneously in the progression of AD pathogenesis and related cognitive decline, before tau-PET turns positive.

scholarly journals Characterization of the Alzheimer's Disease-associated CLAC Protein and Identification of an Amyloid β-Peptide-binding Site

2004 ◽  
Vol 280 (2) ◽  
pp. 1007-1015 ◽  
Author(s):  
Linda Söderberg ◽  
Hiroyoshi Kakuyama ◽  
Anna Möller ◽  
Akira Ito ◽  
Bengt Winblad ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Binding Site ◽  
Peptide Binding ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Peptide Binding Site
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