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
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;
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;
Parallel
Mitoquinone (MitoQ)
Dietary supplementMitoQ is a biochemically modified form of ubiquinol Other Names: Mitoquinol
Placebo
Dietary supplementEach placebo capsule contains inert excipient and is identical in appearance
Change from baseline in cerebrovascular conductance at 3 months
Middle cerebral artery blood velocity in response to hypercapnia normalized for changes in end-tidal carbon dioxide and blood pressure
Change from baseline in cerebrovascular reactivity at 3 months
Middle cerebral artery blood velocity in response to hypercapnia normalized to changes in end-tidal carbon dioxide
Change from baseline in mitochondrial oxidative stress-mediated suppression of cerebrovascular conductance at 3 months
Cerebrovascular conductance to hypercapnia following administration of a supratherapeutic dose of MitoQ (160 mg) known to scavenge mitochondrial reactive oxygen species
Change from baseline in mitochondrial oxidative stress-mediated suppression of cerebrovascular reactivity at 3 months
Cerebrovascular reactviity to hypercapnia following administration of a supratherapeutic dose of MitoQ (160 mg) known to scavenge mitochondrial reactive oxygen species
Change from baseline in internal carotid artery dilation in response to hypercapnia at 3 months
Cerebrovascular endothelium-dependent dilation
Change from baseline in serum exposure-induced arterial endothelial function at 3 months
Donor mouse arterial endothelium-dependent dilation after treatment with serum from subjects
Change from baseline in serum exposure-induced arterial stiffness at 3 months
Donor mouse arterial elastic modulus after treatment with serum from subjects
Change from baseline in circulating oxidized low-density lipoprotein at 3 months
Blood marker of oxidative stress
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Colorado State University
Lead sponsor
National Heart, Lung, and Blood Institute (NHLBI)
Collaborator
This trial is not recruiting at the moment. You can still explore other options:
