Results 11 to 20 of about 120,218 (348)
Early Divergence in Misfolding Pathways of Amyloid-Beta Peptides. [PDF]
AbstractThe amyloid cascade hypothesis proposes that amyloid‐beta (Aβ) aggregation is the initial triggering event in Alzheimer's disease. Here, we utilize NMR spectroscopy and monitor the structural dynamics of two variants of Aβ, Aβ40 and Aβ42, as a function of temperature.
Mamone S +3 more
europepmc +6 more sources
Adsorption of Amyloid Beta Peptide by Metal–Organic Frameworks [PDF]
Metal-organic frameworks (MOFs) are capable of adsorbing a wide range of molecules. In addition to the more commonly investigated small molecules, researchers have demonstrated that MOFs adsorb much larger molecules, such as proteins and peptides. We have investigated whether MOFs are capable of adsorbing amyloid beta peptide.
Zachary L. Mensinger +2 more
openalex +4 more sources
Characterizing Heparin Tetrasaccharides Binding to Amyloid-Beta Peptide [PDF]
The aggregation of β-amyloid peptide (Aβ) is one potential cause for Alzheimer’s disease (AD). Heparin can either promote or inhibit Aβ aggregation. The sulfation pattern and chain size determine its binding affinity and its role. Using 2D-NMR analysis and molecular modelling, the binding motif of heparin oligoaccharides to Aβ was determined to be HexA-
Xiang Zhou +5 more
openaire +3 more sources
Familial Alzheimer’s Disease (FAD) caused by Presenilin-1 (PS1) mutations is characterized by early onset, cognitive impairment, and dementia. Impaired gamma secretase function favors production of longer beta-amyloid species in PS1 FAD.
Felix Dinkel +7 more
doaj +1 more source
Astrocytic Redox Remodeling by Amyloid Beta Peptide [PDF]
Astrocytes are critical for neuronal redox homeostasis providing them with cysteine needed for glutathione synthesis. In this study, we demonstrate that the astrocytic redox response signature provoked by amyloid beta (Aβ) is distinct from that of a general oxidant (tertiary-butylhydroperoxide [t-BuOOH]).
Garg, Sanjay K. +3 more
openaire +3 more sources
Alzheimer's disease is a progressive neurodegenerative disorder. In this disease neurodegeneration occurs due to deposition of aggregated amyloid-beta plaques and neurofibrillary tangles (hyperphosphorylated tau proteins).
Rupali Kumari +2 more
doaj +1 more source
Insight into the structure of amyloid fibrils from the analysis of globular proteins. [PDF]
The conversion from soluble states into cross-beta fibrillar aggregates is a property shared by many different proteins and peptides and was hence conjectured to be a generic feature of polypeptide chains.
Antonio Trovato +3 more
doaj +1 more source
Fibrillisation of hydrophobically modified amyloid peptide fragments in an organic solvent [PDF]
The self-assembly of a hydrophobically modified fragment of the amyloid beta(A beta) peptide has been studied in methanol. The peptide FFKLVFF is based on A beta(16-20) extended at the N terminus by two phenylalanine residues.
Castelletto, Valeria +2 more
core +1 more source
Alzheimer’s Disease affects approximately 33 million people worldwide and is characterized by progressive loss of memory at the cognitive level. The formation of toxic amyloid oligomers, extracellular amyloid plaques and amyloid angiopathy in brain
Raluca Ştefănescu +5 more
doaj +1 more source
Oxidation destabilizes toxic amyloid beta peptide aggregation [PDF]
AbstractThe aggregation of insoluble amyloid beta (Aβ) peptides in the brain is known to trigger the onset of neurodegenerative diseases, such as Alzheimer’s disease. In spite of the massive number of investigations, the underlying mechanisms to destabilize the Aβ aggregates are still poorly understood. Some studies indicate the importance of oxidation
J. Razzokov, M. Yusupov, A. Bogaerts
openaire +3 more sources

