connieb wrote:My neuro is actually recommending that I take estriol in addition to Copaxone-- he believes that estriol, which is apparently widely used in HRT in Europe, may actually protect against breast cancer (I'll try and get some of his references for us all later), but I am very nervous about starting on it.
I never suspected that hormones and steroids were similar, and I look forward to Sharon's response to your comments.
These findings suggest that an increase in steroidogenesis is part of an overall mechanism used by the nervous tissue to cope with neurodegenerative conditions. Neural steroidogenesis is the result of a coordinated interaction of neurons and glia.
In the central nervous system, the steroids produced by glia regulate synaptic function, affect anxiety, cognition, sleep and behavior, and exert neuroprotective and reparative roles.
the only currently recommended pharmacotherapy is high-dose methylprednisolone, which has limited efficacy.
Estrogen is a multi-active steroid that has shown antiinflammatory and antioxidant effects, and estrogen may modulate intracellular Ca(2+) and attenuate apoptosis
Treatment of SCI rats with estrogen reduced edema and decreased inflammation and myelin loss in the lesion and penumbral areas, suggesting its potential as a therapeutic agent.
CONCLUSIONS: Our data indicate that the neurotoxic effects of glutamate can be inhibited differentially by various equine estrogens.
estrogens may provide compounds that are useful for preventing neurodegenerative diseases in both women and men.
The potent feminizing hormone, 17 beta-estradiol (E2), has shown cytoprotective activities in a host of cell and animal models of stroke, myocardial infarct and neurodegenerative diseases.
The cytoprotective and mitoprotective potencies for 14 of these analogs are significantly correlated, suggesting that these compounds prevent cell death in large measure by maintaining functionally intact mitochondria. This therapeutic strategy is germane not only to sudden mitochondrial failure in acute circumstances, such as during a stroke or myocardial infarction, but also to gradual mitochondrial dysfunction associated with chronic degenerative disorders such as AD, PD and HD.
Maintaining membrane integrity is critical to mitochondrial function, where loss of impermeability of the inner membrane initiates both necrotic and apoptotic pathways. Thus, by serving as a mitoprotectant, 17alpha-E2 forestalls cell death and could correspondingly provide therapeutic benefit in a host of degenerative diseases, including AD, PD, Friedreich's ataxia, and amyotrophic lateral sclerosis,
Accumulating evidence from basic science studies demonstrates that estrogens exert profound protective actions against various forms of neurodegenerative diseases and injury.
recent work demonstrating that estradiol may additionally enhance the ability of the adult brain to undergo repair by influencing the production of new neurons under neuropathological conditions, as well as by promoting an anti-inflammatory response.
we increasingly appreciate that the mechanisms by which estrogens achieve these effects are diverse and complex.
work that we have done during the past 6 yr that strongly suggests that low levels of estradiol therapy exert dramatic protective actions in the adult injured brain.
Our results reveal that 17beta-estradiol slows the progression of this injury and diminishes the extent of cell death by suppressing apoptotic cell death pathways and enhancing expression of genes that optimize cell survival. Furthermore, we have found that estrogen receptors play a pivotal functional role in neuroprotection. Together, these results carry broad implications for the selective targeting of estrogen receptors in the treatment of neurodegenerative conditions resulting from disease or injury, particularly for aging, postmenopausal women.
Furthermore, we have shown that the lack of estradiol increases the vulnerability of the brain to injury and neurodegeneration.
From early embryonic life to death, estrogen is a primary regulator of brain neurogenesis and cell number, synaptogenesis and synaptolysis, multiple cognitive and autonomic functions, vascular function, immune responses and defense measures against brain lesions and dystrophy.
While the mechanisms of this potent neuroprotection are currently unresolved, a mitochondrial mechanism is involved
Collectively, results of these animal and tissue culture models suggest that the loss of both estrogens and progestins at the menopause makes the brain more vulnerable to acute insults and chronic neurodegenerative diseases.
To investigate the influence of methylprednisolone therapy on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the ON, we used a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced EAE.
Methylprednisolone treatment significantly increased RGC apoptosis during MOG-EAE.
we provide evidence for negative effects of steroid treatment on neuronal survival during chronic inflammatory autoimmune disease of the CNS, which should result in a reevaluation of the current therapy regimen
connieb wrote:I think my neuro was talking about HRT with estriol only, which is bioidentical and the weakest of estrogens, whereas these studies looked at various combined therapies with other, synthetic estrogens.
When I wrote about cognitive decline in PM women using estrogens I forgot to mention that they usually experience great emotional disturbances,
New research suggests that hormone therapy taken soon after menopause may help protect against the mental decline of dementia,
the latest evidence suggests that timing of treatments may be key, at least for heart attacks and now for dementia
drugs do not raise the risk of heart attack for women ages 50-to-59, and they seem to survive longer with the drug.
for women who took hormones before age 65: Dementia risk was reduced by nearly half.
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