Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology. - Test2 - elhamkhani - TriplyDB

Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology.

Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology.

http://www.wikidata.org/entity/Q35016226

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In vivo imaging reveals sigmoidal growth kinetic of β-amyloid plaques.Cystatin C modulates cerebral beta-amyloidosis ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models Targeting innate immunity for neurodegenerative disorders of the central nervous system Growing up in a Bubble: Using Germ-Free Animals to Assess the Influence of the Gut Microbiota on Brain and Behavior Epigenetic Alterations in Alzheimer's Disease Connectivity of Pathology: The Olfactory System as a Model for Network-Driven Mechanisms of Alzheimer's Disease Pathogenesis Elusive roles for reactive astrocytes in neurodegenerative diseases Breaking the Code of Amyloid-β Oligomers Endogenous murine Aβ increases amyloid deposition in APP23 but not in APPPS1 transgenic mice.Cerebral β-Amyloidosis in Mice Investigated by Ultramicroscopy Small-animal PET imaging of amyloid-beta plaques with [11C]PiB and its multi-modal validation in an APP/PS1 mouse model of Alzheimer's disease Cellular and molecular characterization of multipolar Map5-expressing cells: a subset of newly generated, stage-specific parenchymal cells in the mammalian central nervous system APP intracellular domain impairs adult neurogenesis in transgenic mice by inducing neuroinflammation Functional impairment of microglia coincides with Beta-amyloid deposition in mice with Alzheimer-like pathology Early-onset and robust amyloid pathology in a new homozygous mouse model of Alzheimer's disease Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities The collagen chaperone HSP47 is a new interactor of APP that affects the levels of extracellular beta-amyloid peptides Systematic Aβ Analysis in Drosophila Reveals High Toxicity for the 1-42, 3-42 and 11-42 Peptides, and Emphasizes N- and C-Terminal Residues Comment on "ApoE-Directed Therapeutics Rapidly Clear -Amyloid and Reverse Deficits in AD Mouse Models"The Psen1-L166P-knock-in mutation leads to amyloid deposition in human wild-type amyloid precursor protein YAC transgenic mice.APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD).Alzheimer disease models and human neuropathology: similarities and differences Reducing HDAC6 ameliorates cognitive deficits in a mouse model for Alzheimer's disease A coimmunization vaccine of Aβ42 ameliorates cognitive deficits without brain inflammation in an Alzheimer's disease model.Aβ seeds resist inactivation by formaldehyde The role of ryanodine receptor type 3 in a mouse model of Alzheimer disease Contribution of reactive oxygen species to cerebral amyloid angiopathy, vasomotor dysfunction, and microhemorrhage in aged Tg2576 mice.Mapping synaptic glutamate transporter dysfunction in vivo to regions surrounding Aβ plaques by iGluSnFR two-photon imaging.LW-AFC, a new formula derived from Liuwei Dihuang decoction, ameliorates behavioral and pathological deterioration via modulating the neuroendocrine-immune system in PrP-hAβPPswe/PS1ΔE9 transgenic mice.Alzheimer's disease-linked mutations in presenilin-1 result in a drastic loss of activity in purified γ-secretase complexes.In vivo turnover of tau and APP metabolites in the brains of wild-type and Tg2576 mice: greater stability of sAPP in the beta-amyloid depositing mice Synaptic plasticity in the hippocampus of a APP/PS1 mouse model of Alzheimer's disease is impaired in old but not young mice.Reduced synaptic STIM2 expression and impaired store-operated calcium entry cause destabilization of mature spines in mutant presenilin mice.Distribution pattern following systemic mesenchymal stem cell injection depends on the age of the recipient and neuronal health T cells specifically targeted to amyloid plaques enhance plaque clearance in a mouse model of Alzheimer's disease Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection.Altered microglial response to Aβ plaques in APPPS1-21 mice heterozygous for TREM2.Immunoproteasome deficiency alters microglial cytokine response and improves cognitive deficits in Alzheimer's disease-like APPPS1 mice.Modeling familial Danish dementia in mice supports the concept of the amyloid hypothesis of Alzheimer's disease.

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P2860

Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology.

http://www.wikidata.org/entity/Q35016226

description

2006 nî lūn-bûn

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2006 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի օգոստոսին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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Abeta42-driven cerebral amyloi ...... ls early and robust pathology.

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Abeta42-driven cerebral amyloi ...... ls early and robust pathology.

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type

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Abeta42-driven cerebral amyloi ...... ls early and robust pathology.

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Abeta42-driven cerebral amyloi ...... ls early and robust pathology.

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Abeta42-driven cerebral amyloi ...... ls early and robust pathology.

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Abeta42-driven cerebral amyloi ...... ls early and robust pathology.

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Abeta42-driven cerebral amyloi ...... ls early and robust pathology.

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Bernardino Ghetti

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Dennis Lindau

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Fabienne Jäggi

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Hartwig Wolburg

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Janaky Coomaraswamy

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Lars Stoltze

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Michael E Calhoun

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Rebecca Radde

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Simon Gengler

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Stephan A Kaeser

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P2860

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

Presenilin clinical mutations can affect gamma-secretase activity by different mechanisms

Lack of the metabotropic glutamate receptor subtype 7 selectively impairs short-term working memory but not long-term memory

Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model

Mean age-of-onset of familial alzheimer disease caused by presenilin mutations correlates with both increased Abeta42 and decreased Abeta40.

Presenilin-1 mutations of leucine 166 equally affect the generation of the Notch and APP intracellular domains independent of their effect on Abeta 42 production

Abeta is targeted to the vasculature in a mouse model of hereditary cerebral hemorrhage with amyloidosis.

Abeta42 is essential for parenchymal and vascular amyloid deposition in mice.

Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease.

Comparison of neurodegenerative pathology in transgenic mice overexpressing V717F beta-amyloid precursor protein and Alzheimer's disease.

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940-946

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9

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6881599

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