Coenzyme Q10 Attenuates β-Amyloid Pathology in the Aged Transgenic Mice with Alzheimer Presenilin 1 Mutation


Year of Publication: 
Contact PI Name: 
Xifei Yang
Contact PI Affiliation: 
The Jockey Club MRI Center, The University of Hong Kong, Hong Kong, China
Ying Yang & Geng Li & Jianzhi Wang & Edward S. Yang
Primary Reference (PubMED ID): 
Funding Source:
Study Goal and Principal Findings: 

One of the neuropathological features of Alzheimer’s disease (AD) is the deposition of senile plaques containing β-amyloid (Aβ). There is limited evidence for the treatment to arrest Aβ pathology of AD. In the present study, they tested the effect of coenzyme Q10 (CoQ10), an endogenous antioxidant and a powerful free radical scavenger, on Aβ in the aged transgenic mice overexpressing Alzheimer presenilin 1-L235P (leucine-to-proline mutation at codon 235, 16–17 months old). The treatment by feeding the transgenic mice with CoQ10 for 60 days (1,200 mg kg−1 day−1) partially attenuated Aβ overproduction and intracellular Aβ deposit in the cortex of the transgenic mice compared with the age-matched untreated transgenic mice. Meanwhile, an increased oxidative stress reaction was detected as evidenced by elevated level of malondialdehyde (MDA) and decreased activity of superoxide dismutase (SOD) in the transgenic mice relative to the wild-type mice, and supplementation of CoQ10 partially decreased MDA level and upregulated the activity of SOD. The results indicate that oxidative stress is enhanced in the brain of the transgenic mice, that this enhancement may further promote Aβ42 overproduction in a vicious formation, and that CoQ10 would be beneficial for the therapy of AD.

Therapeutic Agent

Therapeutic Information: 
Therapy Type:

Animal Model

Model Information: 
Model Type:
Strain/Genetic Background: 
C57BL/6J× A2G

Experimental Design

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


Outcome MeasuredOutcome Parameters
  • Congophillic amyloid deposits
  • Biochemical
  • Brain-formic acid soluble beta amyloid peptide 40
  • Brain-formic acid soluble beta amyloid peptide 42
  • Brain-Lipid Peroxidation
  • Superoxide Dismutase (SOD)
  • Malondialdehyde (MDA)
  • Immunochemistry
  • Brain-beta amyloid peptide 42