| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10762835 | Biochemical and Biophysical Research Communications | 2011 | 7 Pages |
Abstract
⺠AD brain tissue has enhanced CXCL8 levels. ⺠Neurons also produce CXCL8 upon Aβ-injury or stimulation by TNF-α. ⺠CXCL8 protects neurons from Aβ-induced toxicity and enhances BDNF levels. ⺠Capacity of self-protection in neurons against Aβ has implications in AD.
Keywords
DAPITNFNon-dementedHuman neuronCXCL8dsDNAAmyloid-β (Aβ)GFAPterminal deoxynucleotidyltransferase-mediated dUTP nick end labelingSTSMAP-2AβNIH3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide4′,6-diamidino-2-phenylindoleBDNFMTTamyloid-βstaurosporineAlzheimer’s diseaseAlzheimer’s disease (AD)ANOVAone-way analysis of varianceEnzyme-linked immunosorbent assayELISATUNELstandard error of meanCNScentral nervous systemTumor necrosis factor-α (TNF-α)Brain-derived neurotrophic factortumor necrosis factorNational Institutes of HealthCSFCerebrospinal fluidNeuroprotectionSEMGlial fibrillary acidic proteinmicrotubule-associated protein 2
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Authors
Ashutosh Ashutosh, Wei Kou, Robin Cotter, Kathleen Borgmann, Li Wu, Raisa Persidsky, Namita Sakhuja, Anuja Ghorpade,