| pubmed-article:18615177 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18615177 | lifeskim:mentions | umls-concept:C0006864 | lld:lifeskim |
| pubmed-article:18615177 | lifeskim:mentions | umls-concept:C0027746 | lld:lifeskim |
| pubmed-article:18615177 | lifeskim:mentions | umls-concept:C0208757 | lld:lifeskim |
| pubmed-article:18615177 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:18615177 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:18615177 | pubmed:dateCreated | 2008-7-10 | lld:pubmed |
| pubmed-article:18615177 | pubmed:abstractText | Endocannabinoids are released following brain injury and may protect against excitotoxic damage during the acute stage of injury. Brain injury also activates microglia in a secondary inflammatory phase of more widespread damage. Most drugs targeting the acute stage are not effective if administered more than 6 hours after injury. Therefore, drugs targeting microglia later in the neurodegenerative cascade are desirable. We have found that cannabinoid CB2 receptors are up-regulated during the activation of microglia following brain injury. Specifically, CB2-positive cells appear in the rat brain following both hypoxia-ischemia (HI) and middle cerebral artery occlusion (MCAO). This may regulate post-injury microglial activation and inflammatory functions. In this paper we review in vivo and in vitro studies of CB2 receptors in microglia, including our results on CB2 expression post-injury. Taken together, studies show that CB2 is up-regulated during a process in which microglia become primed to proliferate, and then become fully reactive. In addition, CB2 activation appears to prevent or decrease microglial activation. In a rodent model of Alzheimer's disease microglial activation was completely prevented by administration of a selective CB2 agonist. The presence of CB2 receptors in microglia in the human Alzheimer's diseased brain suggests that CB2 may provide a novel target for a range of neuropathologies. We conclude that the administration of CB2 agonists and antagonists may differentially alter microglia-dependent neuroinflammation. CB2 specific compounds have considerable therapeutic appeal over CB1 compounds, as the exclusive expression of CB2 on immune cells within the brain provides a highly specialised target, without the psychoactivity that plagues CB1 directed therapies. | lld:pubmed |
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| pubmed-article:18615177 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18615177 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18615177 | pubmed:status | PubMed-not-MEDLINE | lld:pubmed |
| pubmed-article:18615177 | pubmed:issn | 1570-159X | lld:pubmed |
| pubmed-article:18615177 | pubmed:author | pubmed-author:GlassMichelle... | lld:pubmed |
| pubmed-article:18615177 | pubmed:author | pubmed-author:AshtonJohn... | lld:pubmed |
| pubmed-article:18615177 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18615177 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:18615177 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18615177 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18615177 | pubmed:pagination | 73-80 | lld:pubmed |
| pubmed-article:18615177 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:18615177 | pubmed:articleTitle | The cannabinoid CB2 receptor as a target for inflammation-dependent neurodegeneration. | lld:pubmed |
| pubmed-article:18615177 | pubmed:affiliation | Department of Pharmacology & Toxicology, University of Otago, PO Box 913, Dunedin, New Zealand. john.ashton@stonebow.otago.ac.nz | lld:pubmed |
| pubmed-article:18615177 | pubmed:publicationType | Journal Article | lld:pubmed |
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