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Phenolic anti-inflammatory antioxidant reversal of Aβ-induced cognitive deficits and neuropathology


Year of Publication:
Contact PI Name:
Sally A. Frautschy
Contact PI Affiliation:
Departments of Medicine and Neurology, UCLA, California, USA
W. Hu, P. Kim, S.A. Miller, T. Chu, M.E. Harris-White, G.M. Cole
Primary Reference (PubMED ID):
Funding Source:
UCLA Pilot Center on Aging
National Institute on Aging (NIA)
The Elizabeth and Thomas Plott Family Foundation
United States Department of Veterans Affairs (VA)
Study Goal and Principal Findings:

This study investigated effects of NSAID ibuprofen and dietary curcumin on Aβ neuropathology and cognitive deficits in aged Sprague-Dawley  rats given an intracerebroventricular infusion of Abeta peptides. Oxidative damage has been hypothesized to play a central role in AD pathogenesis. Although CNS inflammation may contribute to oxidation, aspects of inflammation unrelated to oxidation, such as complement activation, are likely to contribute to AD pathogenesis. Therefore intervention strategies for AD may require targeting both oxidation and inflammation. Curcumin is both a potent antioxidant and an effective antiinflammatory agent. In this study, dietary curcumin (2000 ppm), but not ibuprofen, suppressed oxidative damage (isoprostane levels) and synaptophysin loss. Both ibuprofen and curcumin reduced microgliosis in cortical layers, but curcumin increased microglial labeling within and adjacent to Aβ -ir deposits. In a second group of middle-aged female SD rats, 500 ppm dietary curcumin prevented Aβ -infusion induced spatial memory deficits in the Morris Water Maze and post-synaptic density (PSD)-95 loss and reduced Aβ deposits. Because of its low side-effect profile and long history of safe use, curcumin may find clinical application for AD prevention.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Natural Product
Therapeutic Agent:
Therapeutic Target:
Multi Target
Therapy Type:
Small Molecule
Therapeutic Agent:
Therapeutic Target:
Cyclooxygenase 1 (COX 1)
Therapeutic Target:
Cyclooxygenase 2 (COX 2)

Animal Model

Model Information:
Model Type:
beta Amyloid Peptide Injection
Strain/Genetic Background:
Not Applicable

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
Morris Water Maze
Activated Microglia
beta Amyloid Deposits
beta Amyloid Load
F2 Isoprostanes
Brain-beta Amyloid Peptide-Total
Postsynaptic Density Protein 95 (PSD95)
Activated Microglia