Avancerad sökning
Visar resultat 6 - 10 av 37 avhandlingar som matchar ovanstående sökkriterier.
6. Self-assembly of amyloid-β peptides in the presence of metal ions and interacting molecules – a detour of amyloid building blocks
Sammanfattning : Misfolding of proteins into amyloid structures is implicated as a pathological feature in several neurodegenerative diseases and the molecular causes are still unclear. One typical characteristic of Alzheimer’s disease is self-assembly and accumulation of soluble amyloid-β (Aβ) peptides into insoluble fibrils and plaques. LÄS MER
7. Processing of the amyloid precursor protein and its paralogues amyloid precursor-like proteins 1 and 2
Sammanfattning : Alzheimer’s disease (AD) is a neurodegenerative disorder which is histopathologically characterised by amyloid plaques and neurofibrillary tangles. Amyloid plaques consist of the amyloid β-peptide (Aβ) that can form aggregates in the brain. Aβ is generated from the amyloid precursor protein (APP) through proteolytic cleavage. LÄS MER
8. Secondary Nucleation in Amyloid Formation
Sammanfattning : Research into Alzheimer's disease is still hampered by a lack of fundamental understanding of the underlying mechanisms. While the aggregation of the amyloid β peptide (Aβ) into amyloid fibrils is highly implicated as a key factor in the disease, the molecular nature of its involvement has proven complex and elusive. LÄS MER
9. Pathogenesis of Alzheimer's disease : focus on amyloid β-peptide, homocysteine and metals
Sammanfattning : Alzheimer's disease (AD) is a complex dementia disorder. It is characterized by the neuronal and synaptic loss, presence of neurofibrillary tangles and senile plaques, composed of amyloid β-peptide (Aβ) in the brain. LÄS MER
10. Alzheimer disease : a super-resolved picture of the amyloid β-peptide producing machinery
Sammanfattning : Alzheimer disease (AD) is the most common neurodegenerative disease, influencing 40 million patients in the world. Pathologically, AD is hallmarked by intracellular tau tangles and extracellular Amyloid-β peptide (Aβ) plaques. Aβ is generated from the amyloid precursor protein (APP) and its C-terminal fragment (APP-CTF). LÄS MER