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Prevention of age-related spatial memory deficits in a transgenic mouse model of Alzheimer’s disease by chronic ginkgo biloba treatment


Year of Publication:
Contact PI Name:
Robert W. Stackman
Contact PI Affiliation:
Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, Oregon, USA
Felix Eckenstein, Balz Frei, Doris Kulhanek, Jessica Nowlin, and Joseph F. Quinn
Primary Reference (PubMED ID):
Funding Source:
Veteran’s Administration Career Development Award
Alzheimer’s Research Alliance of Oregon
National Institutes of Health (NIH)
Study Goal and Principal Findings:

Alzheimer’s disease (AD) is characterized by cognitive decline and deposition of β-amyloid (Aβ) plaques in cortex and hippocampus. A transgenic mouse AD model (Tg2576) that overexpresses a mutant form of human Aβ precursor protein exhibits age-related cognitive deficits, Aβ plaque deposition, and oxidative damage in the brain. They tested the ability of Ginkgo biloba, a flavonoid-rich antioxidant, to antagonize the age-related behavioral impairment and neuropathology exhibited by Tg2576 mice. At 8 months of age, 16 female Tg2576 and 15 female wild-type (wt) littermate mice were given ad lib access to tap water or Ginkgo biloba (70 mg/kg/day in water). After 6 months of treatment, all mice received Morris water maze training (4 trials/day for 10 days) to assess hippocampal dependent spatial learning. All mice received a 60-s probe test of spatial memory retention 24 h after the 40th trial. Untreated Tg2576 mice exhibited a spatial learning impairment, relative to wt mice, while Ginkgo biloba-treated Tg2576 mice exhibited spatial memory retention comparable to wt during the probe test. Spatial learning was not different between Ginkgo biloba-treated and untreated wt mice. There were no group differences in learning to swim to a visible platform. Soluble Aβ and hippocampal Aβ plaque burden did not differ between the Tg2576 groups. Brain levels of protein carbonyls were paradoxically elevated in Ginkgo biloba-treated mice. These data indicate that chronic Ginkgo biloba treatment can block an age-dependent decline in spatial cognition without altering Aβ levels and without suppressing protein oxidation in a transgenic mouse model of AD.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Natural Product
Therapeutic Agent:
Ginkgo Biloba Extract (EGb761)
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:
C57BL/6J x SJL

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
Spatial Learning Task
beta Amyloid Deposits
Brain-Buffer Insoluble beta Amyloid Peptide 42
Brain-Buffer Soluble beta Amyloid Peptide 40
Brain-Buffer Soluble beta Amyloid Peptide 42
Brain-Formic Acid Soluble beta Amyloid Peptide 40
Brain-Formic Acid Soluble beta Amyloid Peptide 42
Carbonyl Protein
Brain-beta Amyloid Deposits
Water Consumption
Body Weight