scholarly journals A catalytic antioxidant for limiting amyloid-beta peptide aggregation and reactive oxygen species generation

2019 ◽  
Vol 10 (6) ◽  
pp. 1634-1643 ◽  
Author(s):  
Luiza M. F. Gomes ◽  
Atif Mahammed ◽  
Kathleen E. Prosser ◽  
Jason R. Smith ◽  
Michael A. Silverman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Amyloid Beta ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Amyloid Beta Peptide ◽  
Peptide Aggregation ◽  
Oxygen Species ◽  
Beta Peptide ◽  
Catalytic Antioxidant

An Fe corrole is shown to bind to the amyloid-beta peptide and limit reactive oxygen species generation and peptide aggregation of relevance to Alzheimer's disease.

scholarly journals Curcumin-like compounds designed to modify amyloid beta peptide aggregation patterns

RSC Advances ◽  
2017 ◽  
Vol 7 (50) ◽  
pp. 31714-31724 ◽  
Author(s):  
Antonella Battisti ◽  
Antonio Palumbo Piccionello ◽  
Antonella Sgarbossa ◽  
Silvia Vilasi ◽  
Caterina Ricci ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Amyloid Beta Peptide ◽  
Peptide Aggregation ◽  
New Concepts ◽  
Novel Drugs ◽  
Beta Peptide

This study suggests new concepts and potential difficulties in the design of novel drugs against diverse amyloidoses, including Alzheimer’s disease.

P1-039: Inhibitors of amyloid beta peptide aggregation: Toward new drugs against Alzheimer's disease

2015 ◽  
Vol 11 (7S_Part_7) ◽  
pp. P352-P353 ◽  
Author(s):  
Olivia Berthoumieu ◽  
Peter Faller ◽  
Andrew J. Doig ◽  
Philippe Derreumaux
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
New Drugs ◽  
Amyloid Beta Peptide ◽  
Peptide Aggregation ◽  
Beta Peptide

A bifunctional non-natural tetrapeptide modulates amyloid-beta peptide aggregation in the presence of Cu(ii)

Metallomics ◽  
2014 ◽  
Vol 6 (12) ◽  
pp. 2189-2192 ◽  
Author(s):  
Maripaz Márquez ◽  
Luis M. Blancas-Mejía ◽  
Adriana Campos ◽  
Luis Rojas ◽  
Gilberto Castañeda-Hernández ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Therapeutic Potential ◽  
Amyloid Beta Peptide ◽  
Peptide Aggregation ◽  
Beta Peptide ◽  
Aβ Aggregation

A novel bifunctional non-natural tetrapeptide, Met-Asp-d-Trp-Aib, is capable of binding copper, competing with amyloid-beta peptide (Aβ) for Cu(ii), and modulating Aβ aggregation. The study of this tetrapeptide provides further insights into the role of Cu(ii) in the Aβ aggregation pathway, and into the design of compounds with therapeutic potential for Alzheimer's disease.

scholarly journals Modification of Amyloid-beta Peptide Aggregation via Photoactivation of Strained Ru(II) Polypyridyl Complexes

2021 ◽  
Author(s):  
Janaina Bataglioli ◽  
Luiza M. F. Gomes ◽  
Camille Maunoir ◽  
Jason Smith ◽  
Houston D. Cole ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Amyloid Beta ◽  
Neurodegenerative Disorder ◽  
Amyloid Beta Peptide ◽  
Peptide Aggregation ◽  
Irreversible Damage ◽  
Polypyridyl Complexes ◽  
Beta Peptide ◽  
Soluble P ◽  
The Brain

Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by progressive and irreversible damage to the brain. One of the hallmarks of the disease is the presence of both soluble...

scholarly journals Oxidative stress and its effect on cells functional activity of Alzheimer's disease

2015 ◽  
Vol 61 (1) ◽  
pp. 57-69 ◽  
Author(s):  
E.E. Dubinina ◽  
L.V. Schedrina ◽  
N.G. Neznanov ◽  
N.M. Zalutskaya ◽  
D.V. Zakharchenko
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Alzheimer's Disease ◽  
Functional Activity ◽  
Cell Cycle Control ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Regulatory System ◽  
Oxygen Species

The paper summarizes literature data on the importance of oxidative stress as one of the pathogenetic mechanisms in Alzheimer's disease. The paper describes the main specific and nonspecific ways of reactive oxygen species generation in the course of the disease development. The effect of reactive oxygen species generated by the functional activity of cells, i.e. apoptosis and mitotic cycle, is shown. The role of the regulatory system of nodal cells is performed by phosphorylation/dephosphorylation process which is associated with intense phosphorylation of tau protein and mitosis-specific proteins. In Alzheimer's disease, the regulating function of peptidyl-prolyl isomerases in particular of Pin1 associated with maintaining a balanced state of phosphorylation/dephosphorylation processes is disturbed. Taking into consideration the multifactorial impairment of the cell cycle control, this process should be considered from the standpoint of the general state of metabolic processes, and oxidative stress has one of the key positions in aging.

scholarly journals New Insights in the Amyloid-Beta Interaction with Mitochondria

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Carlos Spuch ◽  
Saida Ortolano ◽  
Carmen Navarro
Keyword(s):  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Alzheimer's Disease ◽  
Mitochondrial Dysfunction ◽  
Amyloid Beta ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Mitochondrial Proteins ◽  
Oxygen Species ◽  
Species Production

Biochemical and morphological alterations of mitochondria may play an important role in the pathogenesis of Alzheimer’s disease (AD). Particularly, mitochondrial dysfunction is a hallmark of amyloid-beta-induced neuronal toxicity in Alzheimer’s disease. The recent emphasis on the intracellular biology of amyloid-beta and its precursor protein (APP) has led researchers to consider the possibility that mitochondria-associated and mitochondrial amyloid-beta may directly cause neurotoxicity. Both proteins are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron transport chain, increase reactive oxygen species production, cause mitochondrial damage, and prevent neurons from functioning normally. In this paper, we will outline current knowledge of the intracellular localization of amyloid-beta. Moreover, we summarize evidence from AD postmortem brain as well as animal AD models showing that amyloid-beta triggers mitochondrial dysfunction through a number of pathways such as impairment of oxidative phosphorylation, elevation of reactive oxygen species production, alteration of mitochondrial dynamics, and interaction with mitochondrial proteins. Thus, this paper supports the Alzheimer cascade mitochondrial hypothesis such as the most important early events in this disease, and probably one of the future strategies on the therapy of this neurodegenerative disease.

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