β-Amyloid exacerbates inflammation in astrocytes lacking fatty acid amide hydrolase through a mechanism involving PPAR-α, PPAR-γ and TRPV1, but not CB₁ or CB₂ receptors.

β-Amyloid exacerbates inflammation in astrocytes lacking fatty acid amide hydrolase through a mechanism involving PPAR-α, PPAR-γ and TRPV1, but not CB₁ or CB₂ receptors.

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http://www.wikidata.org/entity/Q42272971
Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?Treatment of chronic regional pain syndrome type 1 with palmitoylethanolamide and topical ketamine cream: modulation of nonneuronal cells.Glial Modulation by N-acylethanolamides in Brain Injury and NeurodegenerationPalmitoylethanolamide, a neutraceutical, in nerve compression syndromes: efficacy and safety in sciatic pain and carpal tunnel syndromeRole of transient receptor potential ankyrin 1 channels in Alzheimer's diseaseAlzheimer's disease: relevant molecular and physiopathological events affecting amyloid-β brain balance and the putative role of PPARs.PPAR agonists as therapeutics for CNS trauma and neurological diseasesTransient receptor potential vanilloid 1-immunoreactive signals in murine enteric glial cells.Cannabinoids for treatment of Alzheimer's disease: moving toward the clinic.Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications.The anti-inflammatory compound palmitoylethanolamide inhibits prostaglandin and hydroxyeicosatetraenoic acid production by a macrophage cell lineMetabolic and Inflammatory Adaptation of Reactive Astrocytes: Role of PPARs.Increased levels of palmitoylethanolamide and other bioactive lipid mediators and enhanced local mast cell proliferation in canine atopic dermatitis.Dual role of PPAR-γ in induction and expression of behavioral sensitization to cannabinoid receptor agonist WIN55,212-2.Clinical studies and anti-inflammatory mechanisms of treatments.The Effect of Sea Buckthorn ( L.) Seed Oil on UV-Induced Changes in Lipid Metabolism of Human Skin Cells
P2860

β-Amyloid exacerbates inflammation in astrocytes lacking fatty acid amide hydrolase through a mechanism involving PPAR-α, PPAR-γ and TRPV1, but not CB₁ or CB₂ receptors.

Item
http://www.wikidata.org/entity/Q42272971
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
β-Amyloid exacerbates inflamma ...... but not CB₁ or CB₂ receptors.
@en
β-Amyloid exacerbates inflamma ...... but not CB₁ or CB₂ receptors.
@nl
type
label
β-Amyloid exacerbates inflamma ...... but not CB₁ or CB₂ receptors.
@en
β-Amyloid exacerbates inflamma ...... but not CB₁ or CB₂ receptors.
@nl
prefLabel
β-Amyloid exacerbates inflamma ...... but not CB₁ or CB₂ receptors.
@en
β-Amyloid exacerbates inflamma ...... but not CB₁ or CB₂ receptors.
@nl
P1433
P1476
P2093
P2860
P304
P31
P356
P407
P433
P478
P50
P577
P5875
P698
P921
P932
P356
P1433
P1476
β-Amyloid exacerbates inflamma ...... but not CB₁ or CB₂ receptors.
@en
P2093
P2860
P304
P31
P356
10.1111/J.1476-5381.2012.01889.X
P407
P433
P478
P50
P577
P5875
P698
P921
P932