Cocaine & Molly's correlation to Alzheimer's & Parkinsons

[Yellowfishmate]

I have spoken to a variety of individuals who have developed long term to permanent twitches/tics/Fasiculations (myself included) through the use of Molly and Coke. A damaged CNS. I am getting an understanding of the subject area.

Various Neurotransmittor operate within the brain nerves we know this. Cocaine/MDMA, the drug we too heavily indulged in releases Dopamine & Seretonin. Dopamine controls pleasure, motivation, movement, addiction. Seretonin controls happiness, sleep cycle, digestive regulation. When either of these neurotransmittors are producing a reduced amount in the brain, the most common Neurotransmittor, Acetylcholine is produced in excess amount to compensate and balance brain chemistry.


Acetylcholine Neurotransmittor is responsible for activating the muscles (movement) in the body as well as thought, learning and cognitive activities involved in the brain.


With Parkinson's patients, when dopamine reserves are depleted to 80%, this is when smyptoms of twitches and the shakes occur. The reduced dopamine in the brain allows for the Acetylcholine to flood the brains synapses. Which in turn creates Parkinsons extreme exaggerated movement.


I believe we have mildly damaged DAT/ D2 receptors in the brain which is causing excess Acetylcholine between the Synapse cleft. This is causing our nerves (over excited) to fire signals down to our muscles without our permission. Whether or not DAT/ D2 receptors can regenerate/regulate back to normal is another matter.


Would an increase in the likes of Acetylcholine or other compensatory neurotransmittors cause mental health issues like Alzheimer's or Parkinsons later down the line?

 

[asecin]

twitches turn me on maybe its related to my high abuse of coke and crack but twitching is severely perm dotted in my membrane as good

 

[Cotcha Yankinov]

One thing to remember is that many people develop tics while on Dopaminergic medications/drugs, but that doesn't necessarily mean that damage has been done. Dopamine is important for movement and generally too much dopamine means too much movement, I would look at the movement disorders associated with the L-dopa.

MDMA might possibly have a correlation to dementia (time will tell how significant) but not to Parkinson's. Cocaine users seem to be doing just fine from what other blue lighters have said.

There is a solid connection between anticholinergics and dementia, so I think excess acetylcholine would be okay. Not that I'm sure excess acetylcholine is the problem. If that were the case I would assume people on acetylcholinesterase inhibitors or colouracetam and such would have problems with excess movement, which I haven't heard about.

The pathology of fasciculations is probably different than tics though by the way.

 

[AlphaMethylPhenyl]

Acetylcholline is usually a pro-cognitive neurotransmitter. It's not really associated with impaired thinking at almost all of its binding regions (muscarinic1 and nicotinic receptor areas), and I believe lower amounts are pretty well-associated with Alzhemiers Disease. Muscarinic2 is perhaps a different story. The nicotinic receptor is pretty heavily associated with nootropic activity, and it tends to at lowish doses cause the release of dopamine and nor/epinephrine, which also facilitate thought.

I don't doubt that somewhere in the brain, if there's a deficit of dopamine and serotonin, somehow more aetylcholline is produced and released, but it's not a general rule to say the least.

Cocaine can be toxic to the brain, but the toxicity is probably mostly dopaminergic, and people tend to recover after six months or so of abstinence. MDMA is basically a neurotoxin to serotonergic neurons, as far as I know.

 

[MeDieViL]

Amphetamines work for parkinson which is completely independent of their da release, i dont remember where ive read the study, there also are case reports of mdma temporary curing parkinson so i long hypothised that MDAI could potentialkly even be a long term cure.

 

[Cotcha Yankinov]

There was one person on here who had very treatment refractory essential tremor, whose tremor completely disappeared while he was on MDMA. I was banging my head against my keyboard trying to figure it out because no other drugs (and he tried many illicit drugs) did this

 

[MeDieViL]

Ive long been a proponemt of long term therapeutic use of MDAI, ive written a article about but cant find, sure its unresearched but its a far more effective way to trreat things like depression trough serotonin, also by not inhibitng emotions or causing apathy but doing the opposite.

 

[Nagelfar]

One thing to remember is that many people develop tics while on Dopaminergic medications/drugs, but that doesn't necessarily mean that damage has been done. Dopamine is important for movement and generally too much dopamine means too much movement, I would look at the movement disorders associated with the L-dopa.

I was hit in the hospital (hearing voices after shooting a big shot of meth several hours previous) with a big green shot of Zyprexa (DA-R antagonist) and had a speech impediment for the whole next day, I couldn't enunciate my words.

 

[MeDieViL]

Antipsychotics are awefull, i used zyprexa for a while, at first i liked how it modulated amphetamine, then it blocked the anti anhedonic effect off stims and allways took 2 days before i could enjoy anything again when i took stims, but kept on going back to it for sleep, then randomly it chronically induced some state of meh i want to the time to pass, instead oh im enjoying this, i want it to last longer, i recovered my enjoyment for music with nsi198 but still in that constant neutral non enjoyment state, the internet is full of reports of aps randomly inducing long term anhedonia ajnd other isses over random ammounts of time, a few days even, its not really neurotoxic damage, they just shift the brain in a differened state.

 

[Cotcha Yankinov]

^I wonder if the long term anhedonia is related to induction of deltafosb by anti-psychotics... Any other theories? Diminished neurotrophic effects of dopamine or something random like that? No idea if dopamine has neurotrophic effects, I just recall cocaine increased BDNF I think so maybe that's mediated by dopamine? I mean serotonin can do it and as I recall 5HT2A agonists induce BDNF so maybe the atypical antipsychotics like zyprexa are suppressing a neurotrophic effect of either serotonin/dopamine/NE?

I like APs at low doses but holy fucking tits does real dopaminergic blockade suck ass through a bendy straw

 

[Cotcha Yankinov]

Ive long been a proponemt of long term therapeutic use of MDAI, ive written a article about but cant find, sure its unresearched but its a far more effective way to trreat things like depression trough serotonin, also by not inhibitng emotions or causing apathy but doing the opposite.

Care to take a guess at how sustainable daily MDAI use is? Maybe it would be superior to SSRIs as far as life after the drug and post acute withdrawal symptom dragging on for years (yes I'm talking about you survingantidepressants.com) possibly because of avoiding compensations of having no SERTs?

But I think its very interesting the differences between DRIs and DRAs, I suppose SRIs and SRAs must be fairly different as well?

 

[MeDieViL]

Im prettu sure it would be sustainable long term, but like with most substances i advice to add the use of memantine for long term use, like with amphetamine it would prevent receptor downregulation, you cant use memantine with ssris as receptors need to downregulate for them to work, and yes im also quite sure they wont have those severe aftereffects, especially as those long laqsting side effects dont occur with ssra occur in the first place.

dris are acutely effective so you can combine them with memantine to prevent long term receptor downregulation, ssris cause sexual dysfumctioning, anhedonia, emotional blunting and other severe side effects not seen with releasing agents.