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Analysis of Heterogeneous βA4 Peptides in Human Cerebrospinal Fluid and Blood by a Newly Developed Sensitive Western Blot Assay*
It is found that CSF βA4 1-42 level is lower in AD patients compared with non-demented controls, although there was a significant overlap between the groups.
Imaging β-amyloid burden in aging and dementia
Pittsburgh Compound B PET findings match histopathologic reports of β-amyloid (Aβ) distribution in aging and dementia, and suggest that Aβ may influence the development of dementia with Lewy bodies, and therefore strategies to reduce A β may benefit this condition.
Aggregation and secondary structure of synthetic amyloid beta A4 peptides of Alzheimer's disease.
A heparin-binding domain in the amyloid protein precursor of Alzheimer's disease is involved in the regulation of neurite outgrowth
- D. Small, V. Nurcombe, C. Masters
- Biology, ChemistryThe Journal of neuroscience : the official…
- 1 April 1994
Results indicate that the binding of APP to HSPG in the ECM may stimulate the effects of APP on neurite outgrowth.
Transgenic Drosophila expressing human amyloid precursor protein show gamma-secretase activity and a blistered-wing phenotype.
- A. Foßgreen, B. Brückner, C. Czech, C. Masters, K. Beyreuther, R. Paro
- BiologyProceedings of the National Academy of Sciences…
- 10 November 1998
Interestingly, transgenic flies expressing full-length forms of APP have a blistered-wing phenotype, which suggests that human APP expression interferes with cell adhesion/signaling pathways in Drosophila, independently of betaA4 generation.
Copper and zinc binding modulates the aggregation and neurotoxic properties of the prion peptide PrP106-126.
It is shown that PrP106-126 aggregation, as assessed by turbidometry, is abolished in Chelex-100-treated buffer, and Mutagenesis of either His-111, Met-109, or Met-112 abolished PrP 106-126 neurotoxicity and its ability to form fibrils.
What the evolution of the amyloid protein precursor supergene family tells us about its function
Determinants of diagnostic investigation sensitivities across the clinical spectrum of sporadic Creutzfeldt-Jakob disease.
Age at disease onset and disease duration were independent determinants of typical changes on EEG, while illness duration significantly influenced positive CSF 14-3-3 protein detection; changes on brain MRI were not influenced by either of these clinical parameters, but overall, imaging data were less complete and consequently conclusions are more tentative.
Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease