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NCT Number: NCT07406243

Oral Antioxidant Therapy Targeted to the Mitochondria for Improving Brain Artery Health in Postmenopausal Women

The goal of this clinical trial is to learn if 3 months of taking the dietary supplement MitoQ [a mitochondria-targeted antioxidant that targets to reduce mitochondrial reactive oxygen species (mitoROS)] works to treat age- and menopause-related reductions in brain artery (cerebrovascular) function in postmenopausal women 60 years of age or older free of clinical disease. The main questions it aims to answer are:

Does MitoQ improve cerebrovascular function in postmenopausal women?

If so, does MitoQ improve cerebrovascular function by lowering mitoROS in these arteries?

Researchers will compare MitoQ to a placebo (a look-alike substance that contains no drug) to see if MitoQ can improve cerebrovascular function by lowering mitoROS in arteries involved in brain health and function.

Participants will:

Take MitoQ (20 mg/day) or a placebo every day for 3 months

Visit the research laboratory at baseline and then after 3 months for cerebrovascular testing; there is also a check-in visit at 6 weeks, which is the halfway point

Keep track of symptoms and events during their treatment period to report to the study team

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Key information

Conditions

Aging Postmenopause

Age range

60 year and older

Sex eligibility

Female

Study type

Interventional

Phase

Not applicable

Primary location

Translational Physiology Laboratory within the Food Science Clinical Research Laboratory

Fort Collins, Colorado, 80526, United States

Location contact

Kevin Murray, PhD

CONTACT

[email protected]

(970) 491-3663

Kevin Murray, PhD

PRINCIPAL_INVESTIGATOR

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Age 60 years or older;
  • Postmenopausal women defined as at least 1 year without menses as self-reported;
  • Estrogen-deficient; no hormone therapies (e.g., estrogen, progesterone, testosterone, DHEA, oral contraceptives, etc.) within the previous 6 months;
  • Ability to provide informed consent;
  • Willing to accept random assignment to condition;
  • Body mass index (BMI) ≤35 kg/m2;
  • Mini-mental state examination score ≥21;
  • Weight stable in the prior 3 months;
  • Abstinence from antioxidant or CoQ10 therapy for 3 months; and
  • Absence of clinical disease as determined by the physician of record following a medical history and blood chemistries

Exclusion criteria

  • History of uncontrolled hypertension;
  • Currently meeting aerobic exercise guidelines of ≥75 mins/week of vigorous or ≥150 mins/week of moderate intensity exercise as assessed by Modified Activity Questionnaire;
  • Current smoker;
  • Alcohol dependence or abuse;
  • Other chronic medical conditions; and
  • Subject report of blood donation within 8 weeks prior to enrolling.

Treatment and study plan

Mitoquinone (MitoQ)

Dietary Supplement

MitoQ is a biochemically modified form of ubiquinol

Other Names:

Mitoquinol

Placebo

Dietary Supplement

Each placebo capsule contains inert excipient and is identical in appearance

Primary outcomes

  1. Change from baseline in cerebrovascular conductance at 3 months

    Time frame: 3 months

    Middle cerebral artery blood velocity in response to hypercapnia normalized for changes in end-tidal carbon dioxide and blood pressure

Secondary outcomes

  1. Change from baseline in cerebrovascular reactivity at 3 months

    Time frame: 3 months

    Middle cerebral artery blood velocity in response to hypercapnia normalized to changes in end-tidal carbon dioxide

  2. Change from baseline in mitochondrial oxidative stress-mediated suppression of cerebrovascular conductance at 3 months

    Time frame: 3 months

    Cerebrovascular conductance to hypercapnia following administration of a supratherapeutic dose of MitoQ (160 mg) known to scavenge mitochondrial reactive oxygen species

  3. Change from baseline in mitochondrial oxidative stress-mediated suppression of cerebrovascular reactivity at 3 months

    Time frame: 3 months

    Cerebrovascular reactviity to hypercapnia following administration of a supratherapeutic dose of MitoQ (160 mg) known to scavenge mitochondrial reactive oxygen species

  4. Change from baseline in internal carotid artery dilation in response to hypercapnia at 3 months

    Time frame: 3 months

    Cerebrovascular endothelium-dependent dilation

  5. Change from baseline in mitochondrial oxidative stress-mediated suppression of internal carotid artery dilation at 3 months

    Time frame: 3 months

    Internal carotid artery dilation to hypercapnia following administration of a supratherapeutic dose of MitoQ (160 mg) known to scavenge mitochondrial reactive oxygen species

  6. Change from baseline in total cerebral blood flow at 3 months

    Time frame: 3 months

    The amount of blood flow feeding the brain at rest

  7. Change from baseline in cerebrovascular stiffness at 3 months

    Time frame: 3 months

    Resting middle cerebral artery pulsatility index

  8. Change from baseline in carotid artery compliance at 3 months

    Time frame: 3 months

    Change in diameter of carotid artery for a given change in pressure

  9. Change from baseline in mitochondrial oxidative stress-mediated suppression of carotid artery compliance at 3 months

    Time frame: 3 months

    Carotid artery compliance following administration of a supratherapeutic dose of MitoQ (160 mg) known to scavenge mitochondrial reactive oxygen specie

Other outcomes

  1. Change from baseline in serum exposure-induced arterial endothelial function at 3 months

    Time frame: 3 months

    Donor mouse arterial endothelium-dependent dilation after treatment with serum from subjects

  2. Change from baseline in serum exposure-induced arterial stiffness at 3 months

    Time frame: 3 months

    Donor mouse arterial elastic modulus after treatment with serum from subjects

  3. Change from baseline in circulating oxidized low-density lipoprotein at 3 months

    Time frame: 3 months

    Blood marker of oxidative stress

Study contacts

Contact information is provided by the study sponsor or research team.

Kevin Murray, PhD

CONTACT

[email protected]

(970) 491-3663

Sponsors and collaborators

Lead sponsor

Colorado State University

Other

Collaborators

  • National Heart, Lung, and Blood Institute (NHLBI)

Registry information

Official study title

Mitochondrial-Targeted Antioxidant Supplementation for Improving Cerebrovascular Function in Postmenopausal Women

Important dates

Study start
2026
Primary completion
2030
Study completion
2030
First posted
Feb 12, 2026
Registry last updated
Feb 12, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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