Estrogen
Therapy
Summary:
Scientists believe that estrogen may be neuroprotective, which would explain
why pre-menopausal women have a lower incidence of Parkinson’s disease than
do post-menopausal women who are not on estrogen replacement therapy, and
why men have a higher incidence than women.
While there is no proven mechanism for estrogen’s neuroprotection , one theory
is that it may inhibit mitochondrial failure and oxidative stress thought to
play a part in Parkinson’s disease. Scientists believe estrogen prevents cell
death in large measure by ensuring that mitochondrial membranes remain
functionally intact. Cells that are protected from sudden mitochondrial failure
are also protected from the gradual mitochondrial dysfunction associated with
Parkinson’s disease.[1]
Because
estrogen’s anti-oxidative abilities protect the brain, estrogen deprivation
is likely to initiate or enhance degenerative changes caused by oxidative
stress. Oxidative stress reduces the brain's ability to maintain synaptic
connectivity, leading to the cognitive decline seen in individuals who are
elderly and disease-afflicted.[2]
Potential benefits:
-
Neuroprotection
-
Slower disease
progression
-
Anti-oxidative abilities
-
Improved cognitive function
Risks:[3]
- Estrogen
combined with levodopa
is sometimes associated
with dyskinesias
- Higher
incidence of uterine cancer
- Blood
clots
- Nausea
- Edema
- Weight
gain
Obstacles:
-
Oral treatments in
men may produce unwanted feminizing side effects
Current
research:
MIGENIX’s
17a-estradiol sodium sulfate (“17a-estradiol”), designated MX-4509, is being
considered for the treatment of neurodegenerative diseases associated with
mitochondrial failure, including Alzheimer’s disease, Parkinson’s disease,
and Friedreich’s ataxia. This estrogen compound should be suitable for
chronic treatment of degenerative diseases in both men and women because
it has minimal feminizing consequences.[4]
The Parkinson Study Group (PSG) is
conducting a study in postmenopausal women with Parkinson’s Disease to
measure the safety and tolerability of estrogen replacement therapy (ERT).
The study includes how ERT affects daily activities, thinking and behavior,
and motor fluctuations and dyskinesias. Thirty participants will be
enrolled at six US sites. Enrollment began in 2003.[5]
[1]
Mitochondria Play a Central Role in Estrogen-Induced Neuroprotection
James W. Simpkins, Jian Wang, Xiaofei Wang, Evelyn Perez, Laszlo Prokai and James A. Dykens,
Current Drug Targets - CNS & Neurological Disorders, Volume 4, No. 1, 2005 |
