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Curcumin structure-function, bioavailability, and efficacy in models of neuroinflammation and Alzheimer's disease


Year of Publication:
Contact PI Name:
Sally A. Frautschy
Contact PI Affiliation:
Departments of Medicine/Neurology UCLA, Greater Los Angeles Healthcare System, Sepulveda, California, USA
Aynun N. Begum, Mychica R. Jones, Giselle P. Lim, Takashi Morihara, Peter Kim, Dennis D. Heath, Cheryl L. Rock, Mila A. Pruitt, Fusheng Yang, Beverly Hudspeth, Shuxin Hu, Kym F. Faull, Bruce Teter, Greg M. Cole
Primary Reference (PubMED ID):
Funding Source:
National Institute on Aging (NIA)
United States Department of Veterans Affairs (VA)
Study Goal and Principal Findings:

The purpose of this study was to examine the antioxidant, anti-inflammatory and anti-amyloidogenic properties of dietary curcumin, and its metabolite tetrahydrocurcumin (TC). Curcumin was administered chronically to aged Tg2576 mice, or acutely LPS treated wild type mice. Despite dramatically higher drug plasma levels after TC dosing, compared with curcumin gavage, the resulting brain levels of the two compounds were similar. Treatment with either drug or TC resulted in a reduction in LPS-stimulated inducible nitric-oxide synthase, nitro tyrosine, F2 isoprostanes, and carbonyls. In both the acute (LPS) and chronic inflammation model (Tg2576), TC and curcumin similarly reduced interleukin-1β. Both drugs reduced Tris-buffered saline soluble Aβ and phospho-c-Jun NH2-terminal kinase (JNK). However, despite these similarities, only curcumin was effective in reducing amyloid plaque burden, insoluble β-amyloid peptide (Aβ).  These data indicate that the dienone bridge present in curcumin, but not in TC, is necessary to reduce plaque deposition and protein oxidation in an Alzheimer’s model.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Natural Product
Therapeutic Agent:
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:
Model Type:
Strain/Genetic Background:
Not Reported

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest


Outcome Measured
Outcome Parameters
beta Amyloid Load
Activated Astrocytes
Oxidized Proteins
Interleukin 1 beta (IL-1 beta)
Inducible Nitric Oxide Synthase (iNOS/NOS2)
F2 Isoprostanes
phospho-c-Jun N-terminal Kinase (phospho-JNK)
Brain-beta Amyloid Peptide-Total
Drug Concentration-Plasma
Drug Concentration-Brain
Metabolite Concentration-Plasma
Metabolite Concentration-Brain
Brain/Plasma Ratio
Drug Metabolites