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02-01-2018, 06:31 PM | #1 | ||
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02-02-2018, 05:04 PM | #2 | ||
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Thanks BF,
Hopefully this will lead to something useful for all of us in the short/mid term.... Eric |
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02-03-2018, 01:53 PM | #3 | ||
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This is fascinating research, but I'm not sure that I see how regulating the signaling of dopamine-secreting neurons helps us except as to perhaps mitigating side effects of sinemet like dyskensias.
If researchers are right and PWP have lost a large number of their dopamine-secreting neurons, then how will managing how frequently those neurons secret dopamine help? Seems like we still have the fundamental issue of not enough dopamine to begin with, because we've lost so many of those neurons. Or maybe they aren't seeing this as a cure, but rather a possible treatment to help make the most of the dopamine we make and get externally from sinemet. What am I missing? |
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02-04-2018, 05:57 AM | #4 | ||
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The article pointed to says:
"Our data suggest that dopamine is released in very specific locations, with incredible spatial precision and speed, whereas before it was thought that dopamine was slowly and promiscuously secreted." I always thought that this was likely because: - taking levodopa, which is metabolized into dopamine, never gives a complete relief from the symptoms of PD (though for some people it does an excellent job for a number of years); - levodopa gives better relief in the early years of the illness when there are still large numbers of dopaminergic neurons present. Not only do these produce dopamine, but they also store dopamine in vesicles. The indirect access to exogenously sourced dopamine via existing vesicles gives better relief than having dopamine spread out across the whole brain. John
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Born 1955. Diagnosed PD 2005. Meds 2010-Nov 2016: Stalevo(75 mg) x 4, ropinirole xl 16 mg, rasagiline 1 mg Current meds: Stalevo(75 mg) x 5, ropinirole xl 8 mg, rasagiline 1 mg |
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