Nonsteroidal anti-inflammatory drugs repress beta-secretase gene promoter activity by the activation of PPARgamma. - Wikidata - wikimedia - TriplyDB

Nonsteroidal anti-inflammatory drugs repress beta-secretase gene promoter activity by the activation of PPARgamma.

Nonsteroidal anti-inflammatory drugs repress beta-secretase gene promoter activity by the activation of PPARgamma.

http://www.wikidata.org/entity/Q34249625

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Docosahexaenoic acid-derived neuroprotectin D1 induces neuronal survival via secretase- and PPARγ-mediated mechanisms in Alzheimer's disease models The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies Signaling effect of amyloid-beta(42) on the processing of AbetaPP An overview on therapeutics attenuating amyloid β level in Alzheimer's disease: targeting neurotransmission, inflammation, oxidative stress and enhanced cholesterol levels Glial cells in (patho)physiology Inflammatory process in Alzheimer's Disease TREM2 and the neuroimmunology of Alzheimer's disease BACE1 expression and activity: relevance in Alzheimer's disease Depletion of GGA1 and GGA3 mediates postinjury elevation of BACE1 The normal and pathologic roles of the Alzheimer's β-secretase, BACE1 Short-term treatment with tolfenamic acid improves cognitive functions in Alzheimer's disease mice Chronic administration of R-flurbiprofen attenuates learning impairments in transgenic amyloid precursor protein mice.Temporal-logic analysis of microglial phenotypic conversion with exposure to amyloid-β.Selective modulation of amyloid-beta peptide degradation by flurbiprofen, fenofibrate, and related compounds regulates Abeta levels.Influence of drug transporters and stereoselectivity on the brain penetration of pioglitazone as a potential medicine against Alzheimer's disease AlzPlatform: an Alzheimer's disease domain-specific chemogenomics knowledgebase for polypharmacology and target identification research.Modulation of microglial innate immunity in Alzheimer's disease by activation of peroxisome proliferator-activated receptor gamma.Metabolic stress modulates Alzheimer's β-secretase gene transcription via SIRT1-PPARγ-PGC-1 in neurons.Inhibition of amyloidogenesis by nonsteroidal anti-inflammatory drugs and their hybrid nitrates Neuroprotectin D1 induces neuronal survival and downregulation of amyloidogenic processing in Alzheimer's disease cellular models.Why pleiotropic interventions are needed for Alzheimer's disease.Tracking neuroinflammation in Alzheimer's disease: the role of positron emission tomography imaging.Presenilin/gamma-Secretase and Inflammation.Microglia activation and anti-inflammatory regulation in Alzheimer's disease Docosahexaenoic acid signalolipidomics in nutrition: significance in aging, neuroinflammation, macular degeneration, Alzheimer's, and other neurodegenerative diseases.Beta-secretase: structure, function, and evolution.Activation of TRPML1 clears intraneuronal Aβ in preclinical models of HIV infection.Decrease in the production of β-amyloid by berberine inhibition of the expression of β-secretase in HEK293 cells.Proteases and proteolysis in Alzheimer disease: a multifactorial view on the disease process.Pilot data on telmisartan short-term effects on glucose metabolism in the olfactory tract in Alzheimer's disease.Obovatol improves cognitive functions in animal models for Alzheimer's disease.Two novel DNA motifs are essential for BACE1 gene transcription Synaptic and cognitive improvements by inhibition of 2-AG metabolism are through upregulation of microRNA-188-3p in a mouse model of Alzheimer's disease.Nuclear receptors in neurodegenerative diseases.Differential regulation of BACE1 expression by oxidative and nitrosative signals Pan-PPAR modulation effectively protects APP/PS1 mice from amyloid deposition and cognitive deficits Aging is associated with an increase in T cells and inflammatory macrophages in visceral adipose tissue Differential peroxisome proliferator activated receptors activity in a rodent model of amyotrophic lateral sclerosis Amyloid-beta vaccination, but not nitro-nonsteroidal anti-inflammatory drug treatment, increases vascular amyloid and microhemorrhage while both reduce parenchymal amyloid Alzheimer's Disease: Fatty Acids We Eat may be Linked to a Specific Protection via Low-dose Aspirin.

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P2860

Nonsteroidal anti-inflammatory drugs repress beta-secretase gene promoter activity by the activation of PPARgamma.

http://www.wikidata.org/entity/Q34249625

description

2006 nî lūn-bûn

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2006 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2006 թվականի հունվարին հրատարակված գիտական հոդված

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2006年の論文

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Nonsteroidal anti-inflammatory ...... y the activation of PPARgamma.

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Nonsteroidal anti-inflammatory ...... y the activation of PPARgamma.

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Nonsteroidal anti-inflammatory ...... y the activation of PPARgamma.

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Nonsteroidal anti-inflammatory ...... y the activation of PPARgamma.

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Nonsteroidal anti-inflammatory ...... y the activation of PPARgamma.

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Nonsteroidal anti-inflammatory ...... y the activation of PPARgamma.

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Nonsteroidal anti-inflammatory ...... y the activation of PPARgamma.

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Proceedings of the National Academy of Sciences of the United States of America

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Bernd O Evert

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Dietmar R Thal

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Evan Rosen

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Fred van Leuven

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Gary Landreth

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Jochen Walter

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Lucia Dumitrescu-Ozimek

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Magdalena Sastre

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Michael T Heneka

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Nenad Bogdanovic

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P2860

Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE

Amyloid beta peptide load is correlated with increased beta-secretase activity in sporadic Alzheimer's disease patients

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

Inflammation and Alzheimer's disease

Differential expression and activation of a family of murine peroxisome proliferator-activated receptors

Stimulation of adipogenesis in fibroblasts by PPAR gamma 2, a lipid-activated transcription factor

Astrocytic expression of the Alzheimer's disease beta-secretase (BACE1) is stimulus-dependent.

Nonsteroidal anti-inflammatory drugs for the prevention of Alzheimer's disease: a systematic review.

BACE1 (beta-secretase) knockout mice do not acquire compensatory gene expression changes or develop neural lesions over time.

Stereoselective disposition of ibuprofen enantiomers in human cerebrospinal fluid.

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103

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Thomas Klockgether

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