PARKINSON'S! First hand experience.

[LordOfTabs]

As anyone who wants to look it up or simply already knows dopamine gives you reward. But that's not all. My grandmother has final stage Parkinson's, now she lived a sad life before, but as I read more and spoke to her neurologist he explained that when your brain starts degrading, it's all about that dopamine.

To test this theory , first off less than 3 days ago she had mild tremors and severe ataxia. After discontinuing what I was told to be rotigotine, a patch that realeased dopamine agonists as to help alieve the tremors and bring back cognition.

After hearing this I tried to tell her rewarding things, even if it was Bull. Because she would respond to my presence best, I felt maybe I could influence a natural, temporary rise in cognition and awareness.
Long story short, it worked. Criticism? ?

 

[Cotcha Yankinov]

You mean to say that she isn't on any medication for "final stage Parkinson's"?

Anyways of course there is more to the brain than just dopamine (or just dopamine in the substantia nigra region), but if there was severe enough dopaminergic cell death or if she was on a dopamine antagonist, the response to your encouragements would have been quite different I'm sure. The other thing is that there is a difference between dopaminergic cell regions, the cells in the substantia nigra degenerate the fastest.

People can get pretty profound anhedonia from strong dopamine receptor antagonism.

On the other hand, dopamine agonists can sensitize dopamine receptors as well as prevent some of the cellular changes that occur with a dopamine drought that contribute to Parkinson's.

The brain is indeed also remarkably plastic and will try to compensate for the cell death seen in Parkinson's https://www.ncbi.nlm.nih.gov/pubmed/7847868

 

[d1nach]

Why isnt she on her medication parkinsons is a serious progressive disease if she has side effects maybe you can ask her about then because parkinsons may cause her issues with the planning focusing and complexities of getting her issues heard and addressed

 

[d1nach]

You can influence dopamine in the short term and actually just talking to her keeeps her brain going and may improve her in the long term. But without medication the issue isnt the now its a increase in the progression of her state getting worse think of it like if you stopped a blood thinner for someone with blood clots they might seem fine but over time the odds of a obstruction increases

 

[Cotcha Yankinov]

^The decrease in functioning that you will see with a chronic dopamine deficit is really an issue. The brain cells undergo changes when there is a chronic dopamine deficit and this can lead to a worsening of movement disorders.

 

[cdin]

ibogaine is an effective treatment for parkinsons. including late stage

 

[DotChem]

^ source?

 

[Cotcha Yankinov]

^ source?

same

 

[d1nach]

Ibogaine seems to hold alot of promis however, if my loved had parkinsons id not try to reinvent the wheel on my own and use standard interventions like l dopa comt inhibitors and maois until more research is done. Hope and miracles of a full magical recovery might make you feel good but would most likely rob you of what few years you could have left with them with the depressing but strongly researched clearly significant effects of standard treatments

 

[Amml]

same

https://www.ncbi.nlm.nih.gov/m/pubmed/17023388/
https://www.ncbi.nlm.nih.gov/m/pubmed/17691299/

Ibogaine increases GDNF-Levels, therefore the survival of dopaminergic and motor neurons and the reinnervation of the remaining, not destroyed neurons.

Also curcumin is actually a helpful substance (https://www.ncbi.nlm.nih.gov/m/pubmed/22211691/) due it's neuroprotective function, Catechins may help (https://www.ncbi.nlm.nih.gov/m/pubmed/26092629/) and supplementation with antioxidants like alpha-Lipoic-Acid should be worth a chance to prevent further progression of the Parkinson's.

 

[Amml]

^The decrease in functioning that you will see with a chronic dopamine deficit is really an issue. The brain cells undergo changes when there is a chronic dopamine deficit and this can lead to a worsening of movement disorders.

This sounds interesting! Do you have a source/study how different neurotransmitter levels change brain cells?

 

[d1nach]

I think we are missing the main issue here someone has final stage parkinsons, may or may not be in a healthy enough state to advocate for them self, and isnt on any medication. Tumeric or green tea may of prevented them from getting parkinsons or like ibogaine might offer improvents but right now they have zero drug interventions for the acute phase of a progressive brain disease

 

[Cotcha Yankinov]

Interesting. I would think that using ibogaine itself could be very different than GDNF injection into the brain though.

Since we're on the subject of Parkinson's https://www.ncbi.nlm.nih.gov/pubmed/20590830 "In Parkinson's disease, dopamine depletion blocks autoinhibition of acetylcholine release through muscarinic autoreceptors, leading to excessive acetylcholine release which eventually prunes spines of the indirect-pathway projection neurons of the striatum and thus interrupts information transfer from motor command centers in the cerebral cortex"

 

[Amml]

I think we are missing the main issue here someone has final stage parkinsons, may or may not be in a healthy enough state to advocate for them self, and isnt on any medication. Tumeric or green tea may of prevented them from getting parkinsons or like ibogaine might offer improvents but right now they have zero drug interventions for the acute phase of a progressive brain disease

As direct therapy L-Dopa, dopamine agonists and deep brain stimulation is used, but those therapies only treat the symptoms, and can't stop the neurodegeneration.
Those therapies combined with the mentioned substances may stop or even reverse to some point the progression of the illness.

 

[Amml]

Interesting. I would think that using ibogaine itself could be very different than GDNF injection into the brain though.

Since we're on the subject of Parkinson's https://www.ncbi.nlm.nih.gov/pubmed/20590830 "In Parkinson's disease, dopamine depletion blocks autoinhibition of acetylcholine release through muscarinic autoreceptors, leading to excessive acetylcholine release which eventually prunes spines of the indirect-pathway projection neurons of the striatum and thus interrupts information transfer from motor command centers in the cerebral cortex"

The reduced dopamine in the striatum also causes general lower activation of cortical regions, therefore symptoms of dementia. Animal studies showed a high success rate with stem cells, they believe that some of the regenerative effects come from increased GDNF levels, which cause the dopaminergic fibers to reinnervate in the survived cells. Although getting GDNF directly into the brain is very difficult (injection of GDNF directly into the brain), substances that directly induce GDNF production (such as Ibogaine) could be a promising treatment due their lower costs and easier ways of administration (oral, i.v.)

Also in a study I mentioned before, direct GDNF injections reduce symptoms massively in a span of a few months. And together with neuroprotective agents (curcumin, CBD?) and plaque protecting substances (EGCG, other flavonoids, maybe in liposomal form?) it should stop the progression of Parkinson's and may reverse it.

 

[serotonin2A]

https://www.ncbi.nlm.nih.gov/m/pubmed/17023388/
https://www.ncbi.nlm.nih.gov/m/pubmed/17691299/

Ibogaine increases GDNF-Levels, therefore the survival of dopaminergic and motor neurons and the reinnervation of the remaining, not destroyed neurons.

Also curcumin is actually a helpful substance (https://www.ncbi.nlm.nih.gov/m/pubmed/22211691/) due it's neuroprotective function, Catechins may help (https://www.ncbi.nlm.nih.gov/m/pubmed/26092629/) and supplementation with antioxidants like alpha-Lipoic-Acid should be worth a chance to prevent further progression of the Parkinson's.

The findings you posted do not actually show that ibogaine is an effective treatment for Parkinson's disease. Even if ibogaine increases GDNF levels in humans -- which has yet to be established -- that doesn't appear to be an effective treatment for Parkinson's disease because the controlled trial of intra-striatal GDNF infusion failed to show clinical benefit.

 

[Amml]

I know that there are only a few closer examinations about the use of Ibogaine in Parkinson's disease, but it may be promising if further studies are made.

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.

 

[Cotcha Yankinov]

I think we are missing the main issue here someone has final stage parkinsons, may or may not be in a healthy enough state to advocate for them self, and isnt on any medication. Tumeric or green tea may of prevented them from getting parkinsons or like ibogaine might offer improvents but right now they have zero drug interventions for the acute phase of a progressive brain disease

The issue with preventative therapies is that Parkinson's related dopamine cell death is fairly asymptomatic (especially if it occurs slowly, giving the brain time to adapt) until more than 80% of the relevant cells have died. Taking antioxidants as a preventative wouldn't be a huge deal but regular ibogaine on the other hand can have many side effects, including degeneration of purkinje (motor) cells in the cerebellum https://www.ncbi.nlm.nih.gov/pubmed/10966515

I think there are some cases where dopamine replacement and deep brain stimulation can actually treat underlying pathology to some degree and slow progression but its definitely not a cure. Deep brain stimulation of the hippocampus in Alzheimer's for example can help reverse hippocampal atrophy, and I believe that neurotrophic effects of DBS are thought to play some role in DBS for Parkinson's as well.

 

[Cotcha Yankinov]

This sounds interesting! Do you have a source/study how different neurotransmitter levels change brain cells?

I tried to edit my post to answer this better earlier but bluelight isn't fond me lately

But some of the most recognized forms of neuroplasticity mediated by receptor activity are LTP and LTD, see for example the role of AMPA and NMDA receptors in LTP.

There are various neuroplastic changes associated with drugs of abuse, for example enlargement of dendritic spines https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669702/

 

[Cotcha Yankinov]

I know that there are only a few closer examinations about the use of Ibogaine in Parkinson's disease, but it may be promising if further studies are made.

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.

Further studies definitely need to be made, I think Serotonin2A is throwing caution to the wind especially in light of this "Based on our 6-month results, a randomized controlled clinical trial was conducted to confirm the open-label results, however, GDNF infusion over 6-months did not confer the predetermined level of clinical benefit to patients with PD despite increased 18F-dopa uptake surrounding the catheter tip."

So even straight GDNF may not help and ibogaine may only indirectly raise GDNF while it has risks of fatal arrhythmias and neuronal degeneration in motor areas.

Its unfortunately not uncommon to see something in one study that looks really promising but is difficult for others or different trials to replicate.