S-Equol in Alzheimer's Disease (SEAD) Trial
| Status: | Recruiting |
|---|---|
| Conditions: | Alzheimer Disease |
| Therapuetic Areas: | Neurology |
| Healthy: | No |
| Age Range: | 60 - 90 |
| Updated: | 4/21/2016 |
| Start Date: | July 2014 |
| End Date: | December 2016 |
| Contact: | Rebecca Bothwell |
| Email: | rbothwell@kumc.edu |
| Phone: | (913) 945-5033 |
The purpose of this study is to determine if S-equol could benefit persons with Alzheimer's
Disease (AD).
Disease (AD).
Alzheimer's disease (AD) is a progressive brain disorder which causes memory and thinking
problems. The exact cause of AD is unknown. Researchers believe mitochondria (the part of
your cells that produces energy) might be linked to symptoms of AD. Some studies have shown
that patients with Alzheimer's disease have reduced mitochondrial activity or have fewer
mitochondria present in neurons. In this study, it is believed that by targeting
mitochondria, we might learn more about its influence on AD symptoms.
Mitochondria have a receptor site for estrogen (a hormone) called estrogen receptor β (ERβ).
When estrogen attaches to this site, it promotes mitochondrial function. Studies have also
suggested ERβ stimulation can cause cells to create new mitochondria. More mitochondria, or
increased activity of existing mitochondria, in the cell might have an impact on patients
with Alzheimer's disease. One way to measure this increase in function is to look for the
presence of an enzyme called COX in your blood. If a drug increases mitochondrial function,
there will be an increase in COX concentration in the bloodstream.
By doing this study we hope to learn if S-equol, a compound that acts like estrogen in the
body, causes such an increase in mitochondrial activity. We also hope to determine the
tolerability of a therapeutic dose of S-equol. It is our goal to advance the understanding
of AD, particularly in women.
problems. The exact cause of AD is unknown. Researchers believe mitochondria (the part of
your cells that produces energy) might be linked to symptoms of AD. Some studies have shown
that patients with Alzheimer's disease have reduced mitochondrial activity or have fewer
mitochondria present in neurons. In this study, it is believed that by targeting
mitochondria, we might learn more about its influence on AD symptoms.
Mitochondria have a receptor site for estrogen (a hormone) called estrogen receptor β (ERβ).
When estrogen attaches to this site, it promotes mitochondrial function. Studies have also
suggested ERβ stimulation can cause cells to create new mitochondria. More mitochondria, or
increased activity of existing mitochondria, in the cell might have an impact on patients
with Alzheimer's disease. One way to measure this increase in function is to look for the
presence of an enzyme called COX in your blood. If a drug increases mitochondrial function,
there will be an increase in COX concentration in the bloodstream.
By doing this study we hope to learn if S-equol, a compound that acts like estrogen in the
body, causes such an increase in mitochondrial activity. We also hope to determine the
tolerability of a therapeutic dose of S-equol. It is our goal to advance the understanding
of AD, particularly in women.
Inclusion Criteria:
- Very mild (CDR 0.5) or mild (CDR 1) AD at time of last KU ADC assessment
- Have a study partner
- Speak English as primary language
Exclusion Criteria:
- No viable study partner
- Report a potentially confounding, serious medical risk such as type 1 diabetes,
cancer, or a recent cardiac event (i.e. heart attack, angioplasty, etc.)
- Use any type of estrogen replacement therapy
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