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β—Amyloid exacerbates inflammation in astrocytes lacking fatty acid amide hydrolase through a mechanism involving PPAR-α, PPAR-γ and TRPV1, but not CB(1) or CB(2) receptors
BACKGROUND AND PURPOSE: The endocannabinoid system may regulate glial cell functions and their responses to pathological stimuli, specifically, Alzheimer's disease. One experimental approach is the enhancement of endocannabinoid tone by blocking the activity of degradative enzymes, such as fatt...
Tallennettuna:
| Päätekijät: | , , , , , , , , |
|---|---|
| Aineistotyyppi: | Artigo |
| Kieli: | Inglês |
| Julkaistu: |
Blackwell Publishing Ltd
2012
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| Aiheet: | |
| Linkit: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3417461/ https://ncbi.nlm.nih.gov/pubmed/22321194 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/j.1476-5381.2012.01889.x |
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