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Behavioral improvement after chronic administration of coenzyme Q10 in P301S transgenic mice


Year of Publication:
Contact PI Name:
Magali Dumont
Contact PI Affiliation:
Weill Cornell Medical College, Department of Neurology and Neuroscience, New York, New York, USA
Ceyhan Elipenahli, Cliona Stack, Shari Jainuddin, Meri Gerges, Lichuan Yang, Anatoly Starkov, M. Flint Beal
Primary Reference (PubMED ID):
Funding Source:
National Institute on Aging (NIA)
Tau Consortium
Study Goal and Principal Findings:

Coenzyme Q10 is a key component of the electron transport chain which plays an essential role in ATP production and also has antioxidant effects. Neuroprotective effects of coenzyme Q10 have been reported in both in vitro and in vivo models of neurodegenerative diseases. However, its effects have not been studied in cells or in animals with tau induced pathology. In this article, was reported administered coenzyme Q10 to transgenic mice with the P301S tau mutation, which causes frontotemporal dementia in man. These mice develop tau hyperphosphorylation and neurofibrillary tangles in the brain. Coenzyme Q10 improved survival and behavioral deficits in the P301S mice. There was a modest reduction in phosphorylated tau in the cortex of P301S mice. There was also examined the effects of coenzyme Q10 treatment on the electron transport chain enzymes, the mitochondrial antioxidant enzymes, and the tricarboxylic acid cycle. There was a significant increase in complex I activity and protein levels, and a reduction in lipid peroxidation. Our data show that coenzyme Q10 significantly improved behavioral deficits and survival in transgenic mice with the P301S tau mutation, upregulated key enzymes of the electron transport chain, and reduced oxidative stress. 

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Dietary Interventions & Supplements
Therapeutic Agent:
Coenzyme Q10
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
Open Field Test
Tau Pathology
Isocitrate Dehydrogenase (ICD)
Superoxide Dismutase (SOD)
Glutathione Reductase (GR)
Glutathione (GSH)
Malondialdehyde (MDA)
Mitochondrial Respiratory Complex II/Succinate Dehydrogenase (SDH)
Aconitase (ACO)
Citrate Synthase
Electron Transport Chain
Lipid Peroxidation
Cytochrome C
Mitochondrial Respiratory Complex I
Drug Concentration-Brain
Drug Concentration-Organs