Kinetics of the Interactions between Copper and Amyloid‐β with FAD Mutations and Phosphorylation at the N terminus

Girvan, Paul; Miyake, Toru; Teng, Xiangyu; Branch, Thomas; Ying, Liming

doi:10.1002/cbic.201600255

Cited by 14 publications

(18 citation statements)

References 48 publications

(78 reference statements)

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“…The kinetic model, by which the Aβ peptides form the amyloid fibrils, is believed to follow a nucleation-growth model, with a lag phase of several days [ 89 , 150 , 284 , 285 , 286 , 287 , 288 , 289 , 290 , 291 , 292 , 293 ]. Oligomerization is very sensitive to amino-acid variations [ 123 , 294 , 295 ].…”

Section: Understanding the Outputs Of Artificial And Pathological mentioning

confidence: 99%

Insights into the Molecular Mechanisms of Alzheimer’s and Parkinson’s Diseases with Molecular Simulations: Understanding the Roles of Artificial and Pathological Missense Mutations in Intrinsically Disordered Proteins Related to Pathology

Coskuner‐Weber

Uversky

2018

IJMS

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Amyloid-β and α-synuclein are intrinsically disordered proteins (IDPs), which are at the center of Alzheimer’s and Parkinson’s disease pathologies, respectively. These IDPs are extremely flexible and do not adopt stable structures. Furthermore, both amyloid-β and α-synuclein can form toxic oligomers, amyloid fibrils and other type of aggregates in Alzheimer’s and Parkinson’s diseases. Experimentalists face challenges in investigating the structures and thermodynamic properties of these IDPs in their monomeric and oligomeric forms due to the rapid conformational changes, fast aggregation processes and strong solvent effects. Classical molecular dynamics simulations complement experiments and provide structural information at the atomic level with dynamics without facing the same experimental limitations. Artificial missense mutations are employed experimentally and computationally for providing insights into the structure-function relationships of amyloid-β and α-synuclein in relation to the pathologies of Alzheimer’s and Parkinson’s diseases. Furthermore, there are several natural genetic variations that play a role in the pathogenesis of familial cases of Alzheimer’s and Parkinson’s diseases, which are related to specific genetic defects inherited in dominant or recessive patterns. The present review summarizes the current understanding of monomeric and oligomeric forms of amyloid-β and α-synuclein, as well as the impacts of artificial and pathological missense mutations on the structural ensembles of these IDPs using molecular dynamics simulations. We also emphasize the recent investigations on residual secondary structure formation in dynamic conformational ensembles of amyloid-β and α-synuclein, such as β-structure linked to the oligomerization and fibrillation mechanisms related to the pathologies of Alzheimer’s and Parkinson’s diseases. This information represents an important foundation for the successful and efficient drug design studies.

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Section: Understanding the Outputs Of Artificial And Pathological mentioning

confidence: 99%

Insights into the Molecular Mechanisms of Alzheimer’s and Parkinson’s Diseases with Molecular Simulations: Understanding the Roles of Artificial and Pathological Missense Mutations in Intrinsically Disordered Proteins Related to Pathology

Coskuner‐Weber

Uversky

2018

IJMS

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“…Such data have been obtained previously for Cu II Ab 1Àx complexes. [15][16][17] Here, we studied the reaction mechanism for Cu II binding to the model peptide Ab 4-16 and found that the reaction follows a hierarchical fashion, going through two intermediate states and then reaching the final tight complex.…”

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confidence: 99%

Hierarchical binding of copperII to N-truncated Aβ4–16 peptide

et al. 2020

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“…It is most likely instigated by the genetic factors, such as familial AD that is an early onset AD. In this case, the individual has a heritable mutation that causes an onset of the clinical symptoms earlier in life, usually under the age of 65 [ 24 ]. The clinical course and neuropathology of familial AD and sporadic AD are highly similar [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Development of Regional Disparities in Alzheimer’s Disease Mortality in the Slovak Republic from 1996 to 2015

Gavurová

Kováč

Jarcusková

2018

International Journal of Alzheimer's Disease

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Alzheimer's disease—subsequently as AD in the text—represents a chronic neurodegenerative disease discussed very often in the recent period. It involves the G30 diagnosis expressing exactly AD and also the F00 diagnosis epitomising dementia in AD. The Slovak Republic has a very various population in terms of the disparities of the population localisation. The analysis is executed on the basement of the standardised mortality rate. It is calculated for the individual districts of the Slovak Republic to get a detailed spatial view and for each year of the explored period from 1996 to 2015 to get a time development. It has a considerably rising tendency. Therefore, the regional disparities of the standardised mortality rate of AD are analysed from an angle of view of its similarity, by its measurement in a form of a Euclidean distance approach. The results of the analysis offer the heat maps as the distance matrices in a graphic form and the maps of the individual districts too. These outputs reveal a very heterogeneous structure of the standardised mortality rate. Another graphic outcome demonstrates a distribution of its values among the districts throughout the whole Slovak Republic for the whole observed period. The results offer a comparison among the districts of the Slovak Republic too. The highest values and also the lowest values are reached in the different districts for the both sexes. Even, one district reaches the opposite result for the individual sexes. The age structure of the deceased population on the G30 diagnosis is also executed and the extreme values from an angle of a view of the districts are picked up. There are evident high differentiations between the individual districts of the Slovak Republic. The conclusion section involves the several key points and the potential suggestions for further research.

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Kinetics of the Interactions between Copper and Amyloid‐β with FAD Mutations and Phosphorylation at the N terminus

Cited by 14 publications

References 48 publications

Insights into the Molecular Mechanisms of Alzheimer’s and Parkinson’s Diseases with Molecular Simulations: Understanding the Roles of Artificial and Pathological Missense Mutations in Intrinsically Disordered Proteins Related to Pathology

Insights into the Molecular Mechanisms of Alzheimer’s and Parkinson’s Diseases with Molecular Simulations: Understanding the Roles of Artificial and Pathological Missense Mutations in Intrinsically Disordered Proteins Related to Pathology

Hierarchical binding of copperII to N-truncated Aβ4–16 peptide

Development of Regional Disparities in Alzheimer’s Disease Mortality in the Slovak Republic from 1996 to 2015

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