Abstract：
:Microglial cells killed neurons damaged following incubation with sub-lethal concentrations of peptides derived from either the human prion protein (HuPrP82-146) or amyloid-beta1-42 (a peptide found in Alzheimer's disease). HuPrP82-146 or amyloid-beta1-42 induced phenotypic changes in neurons that caused them to bind a CD14-IgG chimera. In co-cultures microglial cells produced interleukin (IL)-6 in response to HuPrP82-146 or amyloid-beta1-42 damaged neurons. The binding of the CD14-IgG chimera to HuPrP82-146 or amyloid-beta1-42 damaged neurons was reduced by pre-treatment with cyclo-oxygenase (COX)-1 inhibitors and in co-cultures, COX-1 inhibitors significantly increased neuronal survival. Studies with individual prostaglandins demonstrated that the addition of prostaglandin D2, or prostaglandin E2, but not other prostaglandins (F2alpha, H2, I2 or 15-dJ2), mimicked the effects of amyloid-beta1-42 on neurons. Thus, prostaglandin D2 or E2 damaged neurons bound the CD14-IgG chimera, and in co-cultures prostaglandin D2 damaged neurons activated microglial cells. These effects were mediated via the DP prostanoid receptor; DP receptor agonists BW245C or SQ27986 induced neuronal damage, while the DP receptor antagonist BWA868C was neuroprotective in co-cultures. These results indicate that prostaglandin D2, produced following activation of COX-1 by sub-lethal concentrations of HuPrP82-146 or amyloid-beta1-42, causes phenotypic changes in neurons that activates microglial cells and leads to neuronal loss.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Bate C,Kempster S,Williams Adoi
10.1016/j.neuropharm.2005.09.008subject
Has Abstractpub_date
2006-02-01 00:00:00pages
229-37issue
2eissn
0028-3908issn
1873-7064pii
S0028-3908(05)00351-5journal_volume
50pub_type
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pub_type： 杂志文章,随机对照试验
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abstract：:Despite evidence from psychiatry and psychology clinics pointing to altered cognition and decision making following the consumption of cannabis, the effects of cannabis derivatives are still under dispute and the mechanisms of cannabinoid effects on cognition are not known. In this study, we used effort-based and dela...
journal_title：Neuropharmacology
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更新日期：2018-05-01 00:00:00
