Skip to main content
U.S. flag

An official website of the United States government

Ibuprofen reduces Aβ, hyperphosphorylated tau and memory deficits in Alzheimer mice


Year of Publication:
Contact PI Name:
Alpaslan Dedeoglu
Contact PI Affiliation:
Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, USA
Ann C. McKee, Isabel Carreras, Lokman Hossain, Hoon Ryu, William L. Klein, Salvatore Oddo, Frank M. LaFerla, Bruce G. Jenkins, Neil W. Kowall
Primary Reference (PubMED ID):
Funding Source:
National Institute on Aging (NIA)
United States Department of Veterans Affairs (VA)
Study Goal and Principal Findings:

This study examined the effects of ibuprofen on cognitive deficits, Aβ and tau accumulation in young triple transgenic (3×Tg-AD) mice. 3×Tg-AD mice were fed ibuprofen-supplemented chow between 1 and 6 months. Untreated 3×Tg-AD mice showed significant impairment in the ability to learn the Morris water maze (MWM) task compared to age-matched wild-type (WT) mice. The performance of 3×TgAD mice was significantly improved with ibuprofen treatment compared to untreated 3×Tg-AD mice. Ibuprofen-treated transgenic mice showed a significant decrease in intraneuronal oligomeric Aβ and hyperphosphorylated tau (AT8) immunoreactivity in the hippocampus. Confocal microscopy demonstrated co-localization of conformationally altered (MC1) and early phosphorylated tau (CP-13) with oligomeric Aβ, and less co-localization of oligomeric Aβ and later forms of phosphorylated tau (AT8 and PHF-1) in untreated 3×Tg-AD mice. These findings show that prophylactic treatment of young 3×Tg-AD mice with ibuprofen reduces intraneuronal oligomeric Aβ, reduces cognitive deficits, and prevents hyperphosphorylated tau immunoreactivity. These findings provide further support for intraneuronal Aβ as a cause of cognitive impairment, and suggest that pathological alterations of tau are associated with intraneuronal oligomeric Aβ accumulation. 

Therapeutic Agent

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

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:
Model Type:
Strain/Genetic Background:

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
Neurofibrillary Tau Tangles
Fibrillar beta Amyloid Deposits
Dense-core/Compact Plaques
Brain-beta Amyloid Oligomers
Tau Protein
Brain-beta Amyloid Peptides