Neuroscience 2005 Abstract
| Presentation Number: | 14.10 |
|---|---|
| Abstract Title: | Curcumin and its metabolite block Aβ (1-42) oligomer-induced neuronal toxicity and apoptosis via inhibition of p-JNK activation. |
| Authors: |
Frautschy, S. A.*1,2,3
; Begum, A. N.1,2
; Lim, G. P.1,2
; Simmons, M. R.1,2
; Beech, W.1,2
; Kayed, R.
; Milton, S. C.
; Glabe, C.
; Cole, G. M.1,2,3
1Medicine , UCLA, Sepulveda, CA 2Neurology , UCLA, Sepulveda, CA 3Greater Los Angeles Healthcare System, GRECC, UCLA, Sepulveda, CA |
| Primary Theme and Topics |
Disorders of the Nervous System - Neurodegenerative and Movement Disorders -- Alzheimer's disease: APP and presenilin -- abeta |
| Secondary Theme and Topics | Disorders of the Nervous System<br />- Neurodegenerative and Movement Disorders<br />-- Dementia: Cognitive function |
| Session: |
14. Abeta I Slide |
| Presentation Time: | Saturday, November 12, 2005 3:15 PM-3:30 PM |
| Location: | Washington Convention Center - Room 151B |
| Keywords: |
Soluble Aβ oligomers are neurotoxins in AD, which correlate with its severity. p-JNK is one candidate implicated inβ-amyloid mediated neurodegeneration. Curcumin (curc) is a polyphenolic antioxidant known to be an AP-1 binding inhibitor which affects p-JNK. Curc also has anti-amyloidgenic activity. Therefore, we investigated Aβ oligomer induced p-JNK stimulation, co-localization and neuronal apoptosis. We also investigated the inhibitory effect of curc and its one known metabolite tetrahydrocurcumin (THC) on this Aβ oligomer induced p-JNK activation. We used high molecular weight oligomer (~35 mer) to conduct this study which is neurotoxic to human neuroblastoma cells (SY5Y) at 1μM and increases p-JNK. We also found soluble Aβ oligomer co-localized with p-JNK as determined by A11 and p-JNK antibody in vitro and in vivo. Our results suggest that curc and its metabolite significantly reduced Aβ oligomer induced neuronal toxicity from 1-2.5 μM and blocked p-JNK activation and co-localization through inhibition of neuronal apoptosis. In conclusion, curc or its metabolite exert anti-amyloidgenic and neuroprotective activity on Aβ oligomer-induced p-JNK . This supports curc as a therapeutic agent to block pJNK and neurodegeneration for Alzheimer’s diseases.
Supported by AG10685, AG021975 ,AG16793
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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