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A. Stubbe und M. Vogt 《Molecular & general genetics : MGG》1940,78(1):255-260
Ohne ZusammenfassungMit 2 Textfiguren 相似文献
124.
H. Stubbe 《Molecular & general genetics : MGG》1935,70(1):533-537
Ohne ZusammenfassungVortrag auf der Tagung d. Dtsch. Ges. f. Vererbungswissenschaft, Jena 1935.Mit 1 Kurve, 2 Tabellen 相似文献
125.
One of the major pathological features of Alzheimer's disease (AD) is the presence of extracellular amyloid plaques that are composed predominantly of the amyloid-beta peptide (Abeta). Diffuse plaques associated with AD are composed predominantly of Abeta42, whereas senile plaques contain both Abeta40 and Abeta42. Recently, it has been suggested that diffuse plaque formation is initiated as a plasma membrane-bound Abeta species and that Abeta42 is the critical component. In order to investigate this hypothesis, we have examined Abeta42-membrane interactions using in situ atomic force microscopy and fluorescence spectroscopy. Our studies demonstrate the association of Abeta42 with planar bilayers composed of total brain lipids, which results initially in peptide aggregation and then fibre formation. Modulation of the cholesterol content is correlated with the extent of Abeta42-assembly on the bilayer surface. Although Abeta42 was not visualized directly on cholesterol-depleted bilayers, fluorescence anisotropy and fluorimetry demonstrate Abeta42-induced membrane changes. Our results demonstrate that the composition of the lipid bilayer governs the outcome of Abeta interactions. 相似文献
126.
Cyclohexanehexol inhibitors of Abeta aggregation prevent and reverse Alzheimer phenotype in a mouse model 总被引:2,自引:0,他引:2
McLaurin J Kierstead ME Brown ME Hawkes CA Lambermon MH Phinney AL Darabie AA Cousins JE French JE Lan MF Chen F Wong SS Mount HT Fraser PE Westaway D St George-Hyslop P 《Nature medicine》2006,12(7):801-808
When given orally to a transgenic mouse model of Alzheimer disease, cyclohexanehexol stereoisomers inhibit aggregation of amyloid beta peptide (Abeta) into high-molecular-weight oligomers in the brain and ameliorate several Alzheimer disease-like phenotypes in these mice, including impaired cognition, altered synaptic physiology, cerebral Abeta pathology and accelerated mortality. These therapeutic effects, which occur regardless of whether the compounds are given before or well after the onset of the Alzheimer disease-like phenotype, support the idea that the accumulation of Abeta oligomers has a central role in the pathogenesis of Alzheimer disease. 相似文献
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Fallahi-Sichani M Flynn JL Linderman JJ Kirschner DE 《Journal of immunology (Baltimore, Md. : 1950)》2012,188(7):3169-3178
Increased rates of tuberculosis (TB) reactivation have been reported in humans treated with TNF-α (TNF)-neutralizing drugs, and higher rates are observed with anti-TNF Abs (e.g., infliximab) as compared with TNF receptor fusion protein (etanercept). Mechanisms driving differential reactivation rates and differences in drug action are not known. We use a computational model of a TB granuloma formation that includes TNF/TNF receptor dynamics to elucidate these mechanisms. Our analyses yield three important insights. First, drug binding to membrane-bound TNF critically impairs granuloma function. Second, a higher risk of reactivation induced from Ab-type treatments is primarily due to differences in TNF/drug binding kinetics and permeability. Apoptotic and cytolytic activities of Abs and pharmacokinetic fluctuations in blood concentration of drug are not essential to inducing TB reactivation. Third, we predict specific host factors that, if augmented, would improve granuloma function during anti-TNF therapy. Our findings have implications for the development of safer anti-TNF drugs to treat inflammatory diseases. 相似文献
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Zimanyi CM Ando N Brignole EJ Asturias FJ Stubbe J Drennan CL 《Structure (London, England : 1993)》2012,20(8):1374-1383
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130.