Sökning: "Amyloid Fibrils"
Visar resultat 16 - 20 av 106 avhandlingar innehållade orden Amyloid Fibrils.
16. Studies on Pathogenesis of Experimental AA Amyloidosis : Effects of Amyloid Enhancing Factor and Amyloid-Like Fibrils in Rapid Amyloid Induction
Sammanfattning : Amyloidosis is a group of diseases, caused by an extracellular deposition of a characteristic proteinaceous material, amyloid, in various organs. Fibril formation occurs in all of amyloid related diseases, making it a crucial mechanism to understand. LÄS MER
17. Amyloid Fibril Formation - Dye Detection and Effects of Lipids
Sammanfattning : Amyloid fibrils are long fibrillar homopolymers of self-assembled proteins. They can be formed by essentially any polypeptide, but are of particular interest because of their occurrence in several incurable and debilitating human diseases, e.g. Alzheimer’s disease (AD). LÄS MER
18. Roles of intermolecular interactions in amyloid fibril formation mechanisms
Sammanfattning : Amyloid fibrils, a major pathological feature of several neurodegenerative disorders, are highly stable, insoluble aggregates of misfolded proteins. The formation of such aggregates involves a complex equilibrium between protein monomers, different on- and off-pathway transient oligomeric species, and amyloid fibrils. LÄS MER
19. Cellular Uptake of Amyloid Forming Proteins Related to Neurodegenerative Disease
Sammanfattning : Aggregation and deposition of disease-associated protein is a pathological hallmark of several human disorders, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). These diseases are characterized by the formation of amyloid-β (Aβ) and α-synuclein (α-syn) amyloid fibrils, in extracellular and intracellular locations, respectively. LÄS MER
20. The Molecular Chaperone DNAJB6 - A Suppressor of Disease Related Amyloid Fibril Formation
Sammanfattning : Several neurodegenerative diseases are caused by peptides or proteins forming amyloid fibrils such as the Aβ peptide involved in Alzheimer’s disease and the huntingtin exon-1 with a prolonged polyglutamine (polyQ) stretch involved in Huntington’s disease. The ability to form amyloid fibrils is an intrinsic feature in all proteins. LÄS MER