• N&PD Moderators: Skorpio | thegreenhand

PARKINSON'S! First hand experience.

How about low dosed Ibogaine on long term, or maybe derivates with less side effects? The motor neuron degeneration only appears at very high doses (over 3-5g of Ibogaine), but I don't know about the QT-interval prologtion at low doses.
 
But the intracerrebral injections of GDNF showed a significant improve, and I think that Ibogaine raises GDNF levels in the whole brain, not only the striatal region.
Not in controlled trials. Open label trials aren't really all that useful for proving something is effective because they can't establish that the effect was actually specifically due to the treatment. It is great that the open label trial showed an effect, but if the same effect can't be reproduced in a controlled trial then that pretty much means the treatment is viewed as being ineffective. Don't forget that a placebo can often produce a therapeutically significant effect for many diseases.
 
How about low dosed Ibogaine on long term, or maybe derivates with less side effects? The motor neuron degeneration only appears at very high doses (over 3-5g of Ibogaine), but I don't know about the QT-interval prologtion at low doses.

I suppose you could try to isolate the portion of Ibogaine's neurotrophic effects and differentiate them from the undesired hallucinogenic, arrhythmic and neurodegenerative effects, as well as the tremor causing effects of ibogaine, assuming they can be separated like the anti-addictive effect (see 18-MC). Ibogaine is rather promiscuous when it comes to what receptors it binds to.

I assume you could do low doses with less risk of arrhythmia and much less risk of neurodegeration, but I fear that in elderly Parkinson's patients who are very vulnerable to neurodegeneration and who already have movement issues, there could be increased risk of adverse effects while a normal young person would probably do just fine with a moderate dose of ibogaine. The Parkinson's patient is already going to be in a state of compensation when it comes to the dopamine cell death as well, so who knows what the entails in differentiating a healthy brain's response to ibogaine and a Parkinson's disease brain's response.

It is certainly worth investigating though.
 
Damn. I neglected this post.
After a week of dopamine agonists, she is more cognitive, but going to hospice on Thursday. It's strange how I had that experience and now the knowledge ive found on bluelight and through other means has truly been reflected. She only recognises me and seems that no matter the case dopamine activity or not, theres always a lowering threshold of what can and can't be comprehended in the final stages. Morphine seems to stimulate somewhat (2mg IV seems to make her more aware of what's happening, for obvious reasons to my junkie brothers). The final statement is, dopamine action in the brain slowly stops, and no way of reversing that exists yet. It's merely an insight to what might cause (psychologically) more awareness in Parkinson's patients.
 
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