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Early vitamin E supplementation in young but not aged mice reduces Aβ levels and amyloid deposition in a transgenic model of Alzheimer's disease


Year of Publication:
Contact PI Name:
Domenico Praticò
Contact PI Affiliation:
Center for Experimental Therapeutics, Department of Pharmacology; University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Syuan Sung, Yuemang Yao, Kunihiro Uryu, Hengxuan Yang, Virginia M.-Y. Lee, John Q. Trojanowski
Primary Reference (PubMED ID):
Funding Source:
American Heart Association
National Institute on Aging (NIA)
Alzheimer's Association
Study Goal and Principal Findings:

Increased brain oxidative stress is a key feature of Alzheimer’s disease (AD) and manifests predominantly as lipid peroxidation. However, clinical evidence that antioxidants can affect the clinical course of the disease is limited. In the present study, they investigated the effect of the antioxidant Vitamin E on the AD-like phenotype when given to a transgenic mouse model (Tg2576) of the disease before or after the amyloid plaques are deposited. One group of Tg2576 received Vitamin E starting at 5 months of age until they were 13 months old, the second group started at 14 months of age until they were 20 months old. Brain levels of 8,12-iso-iPF2α-VI, a specific marker of lipid peroxidation, were significantly reduced in both groups of mice receiving Vitamin E compared with placebo. Tg2576 administered with Vitamin E at a younger age showed a significant reduction in Aβ levels and amyloid deposition. By contrast, mice receiving the diet supplemented with Vitamin E at a later age did not show any significant difference in either marker when compared with placebo. These results support the hypothesis that oxidative stress is an important early event in AD pathogenesis, and antioxidant therapy may be beneficial only if given at this stage of the disease process.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Dietary Supplement
Therapeutic Agent:
Vitamin E
Therapeutic Target:
Multi Target

Animal Model

Model Information:
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 Deposits
8,12-iso-isoprostane F2 alpha VI
Brain-Buffer Insoluble beta Amyloid Peptide 40
Brain-Buffer Insoluble beta Amyloid Peptide 42
Brain-Buffer Soluble beta Amyloid Peptide 40
Brain-Buffer Soluble beta Amyloid Peptide 42
Plasma-Triglyceride Profile
Brain-Lipid Peroxidation
Drug Concentration-Plasma
Target Engagement (Reduction Lipid Peroxidation-Brain)
Body Weight
General Behavior
Motor Function
General Activity
Food Intake
General Health
Physical Appearance