نتایج جستجو برای: beta amyloid

تعداد نتایج: 215549  

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1988
D Patterson K Gardiner F T Kao R Tanzi P Watkins J F Gusella

The gene encoding the beta-amyloid precursor protein has been assigned to human chromosome 21, as has a gene responsible for at least some cases of familial Alzheimer disease. Linkage studies strongly suggest that the beta-amyloid precursor protein and the product corresponding to familial Alzheimer disease are from two genes, or at least that several million base pairs of DNA separate the mark...

Journal: :Bioorganic & medicinal chemistry 2009
Hiroyuki Watanabe Masahiro Ono Ryoichi Ikeoka Mamoru Haratake Hideo Saji Morio Nakayama

This paper describes the synthesis and biological evaluation of a new series of 2,5-diphenyl-1,3,4-oxadiazole (1,3,4-DPOD) derivatives for detecting beta-amyloid plaques in Alzheimer's brains. The affinity for beta-amyloid plaques was assessed by an in vitro binding assay using pre-formed synthetic Abeta42 aggregates. The new series of 1,3,4-DPOD derivatives showed affinity for Abeta42 aggregat...

Journal: :Journal of molecular biology 2006
Riccardo Pellarin Amedeo Caflisch

Amyloid fibrils are insoluble mainly beta-sheet aggregates of proteins or peptides. The multi-step process of amyloid aggregation is one of the major research topics in structural biology and biophysics because of its relevance in protein misfolding diseases like Alzheimer's, Parkinson's, Creutzfeld-Jacob's, and type II diabetes. Yet, the detailed mechanism of oligomer formation and the influen...

2012
Luxiang Cao Benjamin R. Schrank Steve Rodriguez Eric G. Benz Thomas W. Moulia Gregory T. Rickenbacher Alexis C. Gomez Yona Levites Sarah R. Edwards Todd E. Golde Bradley T. Hyman Gilad Barnea Mark W. Albers

The amyloid beta peptide aggregates into amyloid plaques at presymptomatic stages of Alzheimer's disease, but the temporal relationship between plaque formation and neuronal dysfunction is poorly understood. Here we demonstrate that the connectivity of the peripheral olfactory neural circuit is perturbed in mice overexpressing human APPsw (Swedish mutation) before the onset of plaques. Expressi...

Journal: :International Journal of Alzheimer's Disease 2011

Journal: :Yeungnam University Journal of Medicine 2018

Journal: :Structure 2003
Pawel Sikorski Edward D T Atkins Louise C Serpell

Amyloid fibril deposition is central to the pathology of Alzheimer's disease. X-ray diffraction from amyloid fibrils formed from full-length Abeta(1-40) and from a shorter fragment, Abeta(11-25), have revealed cross-beta diffraction fingerprints. Magnetic alignment of Abeta(11-25) amyloid fibrils gave a distinctive X-ray diffraction texture, allowing interpretation of the diffraction data and a...

Journal: :Current Issues in Molecular Biology 2023

A multifactorial syndrome, Alzheimer’s disease is the main cause of dementia, but there no existing therapy to prevent it or stop its progression. One earliest events disruption calcium homeostasis that just a prelude disease’s devastating impact. Calcium does not work alone must interact with downstream cellular components which small regulatory protein calmodulin central, if primary. This rev...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2002
Dan Frenkel Beka Solomon

Early diagnosis of Alzheimer's disease is prevented by lack of means to visualize and target beta amyloid plaques in the brains of affected people. There are many methods of detecting amyloid plaques by staining postmortem brain tissue, but none are available for monitoring in living patients. We propose anti-beta amyloid antibodies as a highly specific probe to monitor amyloid plaque formation...

2015
Christian Humpel

Alzheimer's disease is a severe neurodegenerative disorder of the brain, pathologically characterized by extracellular beta-amyloid plaques, intraneuronal Tau inclusions, inflammation, reactive glial cells, vascular pathology and neuronal cell death. The degradation and clearance of beta-amyloid plaques is an interesting therapeutic approach, and the proteases neprilysin (NEP), insulysin and ma...

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