Age-related loss of phospholipid asymmetry in APP(NLh)/APP(NLh) x PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice: relevance to Alzheimer disease.

Age-related loss of phospholipid asymmetry in APP(NLh)/APP(NLh) x PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice: relevance to Alzheimer disease.

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http://www.wikidata.org/entity/Q33712475
The 2013 SFRBM discovery award: selected discoveries from the butterfield laboratory of oxidative stress and its sequela in brain in cognitive disorders exemplified by Alzheimer disease and chemotherapy induced cognitive impairmentAbeta, oxidative stress in Alzheimer disease: evidence based on proteomics studiesRoles of 3-nitrotyrosine- and 4-hydroxynonenal-modified brain proteins in the progression and pathogenesis of Alzheimer's disease.Redox proteomics in selected neurodegenerative disorders: from its infancy to future applications.Using neurolipidomics to identify phospholipid mediators of synaptic (dys)function in Alzheimer's Disease.Pathology supported genetic testing and treatment of cardiovascular disease in middle age for prevention of Alzheimer's disease.BACE1 in the retina: a sensitive biomarker for monitoring early pathological changes in Alzheimer's disease.Comprehensive behavioral characterization of an APP/PS-1 double knock-in mouse model of Alzheimer's diseaseSubcutaneous liraglutide ameliorates methylglyoxal-induced Alzheimer-like tau pathology and cognitive impairment by modulating tau hyperphosphorylation and glycogen synthase kinase-3βOxidative stress and β-amyloid protein in Alzheimer's disease.4-Hydroxy-2-nonenal, a reactive product of lipid peroxidation, and neurodegenerative diseases: a toxic combination illuminated by redox proteomics studiesPrimary phagocytosis of neurons by inflamed microglia: potential roles in neurodegenerationDistinct mechanisms determine organ left-right asymmetry patterning in an uncoupled way.Proteomic identification of specifically carbonylated brain proteins in APP(NLh)/APP(NLh) × PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice model of Alzheimer disease as a function of ageNeuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia.Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease.
P2860

Age-related loss of phospholipid asymmetry in APP(NLh)/APP(NLh) x PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice: relevance to Alzheimer disease.

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http://www.wikidata.org/entity/Q33712475
description
2010 nî lūn-bûn
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2010 թուականի Յունուարին հրատարակուած գիտական յօդուած
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2010 թվականի հունվարին հրատարակված գիտական հոդված
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2010年の論文
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2010年論文
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2010年論文
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2010年論文
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2010年論文
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2010年論文
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2010年论文
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name
Age-related loss of phospholip ...... elevance to Alzheimer disease.
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Age-related loss of phospholip ...... elevance to Alzheimer disease.
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type
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Age-related loss of phospholip ...... elevance to Alzheimer disease.
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Age-related loss of phospholip ...... elevance to Alzheimer disease.
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Age-related loss of phospholip ...... elevance to Alzheimer disease.
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Age-related loss of phospholip ...... elevance to Alzheimer disease.
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Age-related loss of phospholip ...... elevance to Alzheimer disease.
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P2093
P2860
P304
P31
P356
P433
P478
P50
P577
P5875
P698
P921
P932