Aging, Postmenopause
Conditions
Brief summary
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
Interventions
DIETARY_SUPPLEMENTMitoquinone (MitoQ)
MitoQ is a biochemically modified form of ubiquinol Other Names: Mitoquinol
DIETARY_SUPPLEMENTPlacebo
Each placebo capsule contains inert excipient and is identical in appearance
Sponsors
Colorado State University
National Heart, Lung, and Blood Institute (NHLBI)
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
TRIPLE (Subject, Investigator, Outcomes Assessor)
Eligibility
Sex/Gender
FEMALE
Age
60 Years to No maximum
Healthy volunteers
No
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.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Change from baseline in cerebrovascular conductance at 3 months | 3 months | Middle cerebral artery blood velocity in response to hypercapnia normalized for changes in end-tidal carbon dioxide and blood pressure |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Change from baseline in cerebrovascular reactivity at 3 months | 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 | 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 | 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 | 3 months | Cerebrovascular endothelium-dependent dilation |
| Change from baseline in mitochondrial oxidative stress-mediated suppression of internal carotid artery dilation at 3 months | 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 |
| Change from baseline in total cerebral blood flow at 3 months | 3 months | The amount of blood flow feeding the brain at rest |
| Change from baseline in cerebrovascular stiffness at 3 months | 3 months | Resting middle cerebral artery pulsatility index |
| Change from baseline in carotid artery compliance at 3 months | 3 months | Change in diameter of carotid artery for a given change in pressure |
| Change from baseline in mitochondrial oxidative stress-mediated suppression of carotid artery compliance at 3 months | 3 months | Carotid artery compliance following administration of a supratherapeutic dose of MitoQ (160 mg) known to scavenge mitochondrial reactive oxygen specie |
Countries
United States
Contacts
CONTACTKevin Murray, PhD
Outcome results
None listed