NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease. - Wikidata - wikimedia - TriplyDB

NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease.

NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease.

http://www.wikidata.org/entity/Q37452311

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A Unified Hypothesis of Early- and Late-Onset Alzheimer's Disease Pathogenesis Neurodegenerative disease and adult neurogenesis Prostaglandin receptor EP2 in the crosshairs of anti-inflammation, anti-cancer, and neuroprotection Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis Pathological implications of cell cycle re-entry in Alzheimer disease.Reimagining Alzheimer's disease--an age-based hypothesis.Regulation of tau pathology by the microglial fractalkine receptor.Glutamine acts as a neuroprotectant against DNA damage, beta-amyloid and H2O2-induced stress.ATM and the epigenetics of the neuronal genome.DNA damage and cell cycle events implicate cerebellar dentate nucleus neurons as targets of Alzheimer's disease.Upregulation of TREM2 ameliorates neuropathology and rescues spatial cognitive impairment in a transgenic mouse model of Alzheimer's disease Nonsteroidal anti-inflammatory drug naproxen destabilizes Aβ amyloid fibrils: a molecular dynamics investigation.Multi-target action of the novel anti-Alzheimer compound CHF5074: in vivo study of long term treatment in Tg2576 mice.Binding of nonsteroidal anti-inflammatory drugs to Abeta fibril Neurovascular dysfunction, inflammation and endothelial activation: implications for the pathogenesis of Alzheimer's disease.Naproxen interferes with the assembly of Aβ oligomers implicated in Alzheimer's disease.Drug development for Alzheimer's disease: recent progress Alzheimer's Disease: Fatty Acids We Eat may be Linked to a Specific Protection via Low-dose Aspirin.Non-Neuronal Cells Are Required to Mediate the Effects of Neuroinflammation: Results from a Neuron-Enriched Culture System.Minocycline corrects early, pre-plaque neuroinflammation and inhibits BACE-1 in a transgenic model of Alzheimer's disease-like amyloid pathology.Quantitating the subtleties of microglial morphology with fractal analysis.Panel of Genetic Variations as a Potential Non-invasive Biomarker for Early Diagnosis of Alzheimer's Disease.Identification and modification of amyloid-independent phenotypes of APOE4 mice Microglial derived tumor necrosis factor-α drives Alzheimer's disease-related neuronal cell cycle events Untangling the Web: Toxic and Protective Effects of Neuroinflammation and PGE2 Signaling in Alzheimer's Disease.Therapeutic implications of the prostaglandin pathway in Alzheimer's disease.Beyond amyloid: getting real about nonamyloid targets in Alzheimer's disease.Mechanisms of action of non-steroidal anti-inflammatory drugs for the prevention of Alzheimer's disease.Neuroinflammatory processes in Alzheimer's disease.Therapeutic intervention for Alzheimer's disease with γ-secretase inhibitors: still a viable option?NSAIDs in the treatment and/or prevention of neurological disorders.The role of clusterin in Alzheimer's disease: pathways, pathogenesis, and therapy.Review: experimental manipulations of microglia in mouse models of Alzheimer's pathology: activation reduces amyloid but hastens tau pathology.Neuroinflammation in the pathogenesis of Alzheimer's disease. A rational framework for the search of novel therapeutic approaches.A comparative study of five mouse models of Alzheimer's disease: cell cycle events reveal new insights into neurons at risk for death Adult neurogenesis in neurodegenerative diseases.The Role of PGRN in Alzheimer's Disease.Potential Use of Flavopiridol in Treatment of Chronic Diseases.Role of Microglia in Neurological Disorders and Their Potentials as a Therapeutic Target.Re-imagining Alzheimer's disease - the diminishing importance of amyloid and a glimpse of what lies ahead.

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P2860

NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease.

http://www.wikidata.org/entity/Q37452311

description

2009 nî lūn-bûn

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年學術文章

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2009年學術文章

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2009年學術文章

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name

NSAIDs prevent, but do not rev ...... se model of Alzheimer disease.

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NSAIDs prevent, but do not rev ...... se model of Alzheimer disease.

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type

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NSAIDs prevent, but do not rev ...... se model of Alzheimer disease.

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NSAIDs prevent, but do not rev ...... se model of Alzheimer disease.

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prefLabel

NSAIDs prevent, but do not rev ...... se model of Alzheimer disease.

@en

NSAIDs prevent, but do not rev ...... se model of Alzheimer disease.

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Journal of Clinical Investigation

P1476

NSAIDs prevent, but do not rev ...... use model of Alzheimer disease

@en

P2093

Bruce T Lamb

http://www.w3.org/2001/XMLSchema#string

Karl Herrup

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Kiran Bhaskar

http://www.w3.org/2001/XMLSchema#string

Maria Z Kounnas

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Steven L Wagner

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Yan Yang

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P2860

Protective effects of NSAIDs on the development of Alzheimer disease

NSAIDs and enantiomers of flurbiprofen target gamma-secretase and lower Abeta 42 in vivo

Effect of non-steroidal anti-inflammatory drugs on risk of Alzheimer's disease: systematic review and meta-analysis of observational studies

Early correlation of microglial activation with enhanced tumor necrosis factor-alpha and monocyte chemoattractant protein-1 expression specifically within the entorhinal cortex of triple transgenic Alzheimer's disease mice

Inflammation and Alzheimer's disease

Diverse compounds mimic Alzheimer disease-causing mutations by augmenting Abeta42 production

Control of microglial neurotoxicity by the fractalkine receptor

Blood monocytes consist of two principal subsets with distinct migratory properties

BACE1 is the major beta-secretase for generation of Abeta peptides by neurons.

Chronic administration of R-flurbiprofen attenuates learning impairments in transgenic amyloid precursor protein mice.

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12

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Nicholas H Varvel

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19907078

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Alzheimer's disease

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2786797

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