141 replies to this topic

[kikai93]

And regarding our old friend piracetam, a not-so-happy finding:

[Effects of piracetam and meclofenoxate on the brain NMDA and nicotinic receptors in mice with different exploratory efficacy in the cross maze test]
Kovalev GI, Firstova IuIu, Salimov RM.

A population of outbred mice of the ICR strain was divided into two subpopulations according to their high (EH mice) or low (EL mice) exploratory efficacy in the closed cross maze test. In addition, the EH and EL mice differed in the number of binding sites of (i) [G-3H]-MK-801 with NMDA receptors from hippocampus and (ii) [G-3H]-nicotine with nicotine cholinoreceptors (nACh) from neocortex. A subchronic administration of the cognition enhancer piracetam (200 mg/kg, once per day for 5 days) increased by 70% the number of binding sites of NMDA receptors in the EL mice. At the same time, this treatment decreased the density of neocortical nACh receptors in both EL and EH mice (by 55% and 40%, respectively). A subchronic administration of the cognition enhancer and anti-oxidant meclofenoxate (100 mg/kg, once per day for 5 days) also decreased the density of neocortical nACh receptors in both EL and EH mice (by 48% and 20%, respectively). However, meclofenoxate also increased by 41% the number of binding sites of NMDA receptors in the EH mice.

PMID: 18365480 [PubMed - indexed for MEDLINE]

What suggests to you that this is an unhappy finding? What, in your own words, do you think this means?

[Rational Madman]

Although I was initially deterred by what appears now to be isolated examples of suicide or psychological deterioration, I think Varenicline still might be a good candidate. But it still needs to emerge out of one of several trials, because as of now, it has proven itself only as a smoking cessation aid.

[aLurker]

Although I was initially deterred by what appears now to be isolated examples of suicide or psychological deterioration, I think Varenicline still might be a good candidate. But it still needs to emerge out of one of several trials, because as of now, it has proven itself only as a smoking cessation aid.

I agree that I would like to see at least one trial in which it shows great promise. I'd hold it to a higher standard than most drugs because of the side effects and not only the ones you mention; it recently "won" first prize among drugs correlated to violence. Especially impressive when you consider that it's meant to treat something as mundane as smoking and not more serious mental health issues or ADHD where the underlying condition itself is linked to more aggressive behaviour. *golf clap*

[kikai93]

Although I was initially deterred by what appears now to be isolated examples of suicide or psychological deterioration, I think Varenicline still might be a good candidate. But it still needs to emerge out of one of several trials, because as of now, it has proven itself only as a smoking cessation aid.

I agree that I would like to see at least one trial in which it shows great promise. I'd hold it to a higher standard than most drugs because of the side effects and not only the ones you mention; it recently "won" first prize among drugs correlated to violence. Especially impressive when you consider that it's meant to treat something as mundane as smoking and not more serious mental health issues or ADHD where the underlying condition itself is linked to more aggressive behaviour. *golf clap*

Anyone know the mechanism that influences the violent behavior?

[chrono]

What suggests to you that this is an unhappy finding? What, in your own words, do you think this means?

Well, my understanding is that, to be very general, nicotinic activation enhances cognition. That's the premise underlying most of this thread. Deficiency in the nicotinic system is implicated in AD, and may even play a role in its etiology by modulating amyloid toxicity. Granted, the small amount of data available (the one paper I cited) is highly inconclusive, the effects in humans may be different, may be mitigated with chronic usage, may be compensated for by homeostatic mechanisms or other MOAs of piracetam, or loss of nicotinic function in certain brain areas may not necessarily have a negative impact. But in general, I would say that halving nicotinic receptor density is not a very promising quality for a cognitive enhancer. Don't get me wrong: I still take piracetam every day right now, but I have no illusions of it being without flaw.

I'm always curious about drugs which are said to make people violent. I've seen documentaries about steroids that suggest it's usually an amplification of an existing trait. Though we certainly discuss medications here which I believe are capable of altering one's mood much more fundamentally. I'm also curious about the mechanism...dopamine, maybe? Regardless, another potentially beneficial mechanism for us ADD kids. Sounds pretty promising; I'll have to get around to looking into it, one of these days.

Edited by chrono, 19 January 2011 - 07:59 PM.

[chrono]

although piracetam seems to give me focus and clarity I've long suspected it to be very slightly de-motivational or in best case neutral in my own subjective experience.

I found this very interesting when you posted it, but forgot to respond (though I may have elsewhere...damn my post count!). I think this is the case for me, as well. Though piracetam gives me the ability to read about neuroscience all day, I am seldom able to transfer that ability to something I (quote-unquote emphasized) "should" be doing. Though it's off-topic for this thread, I wanted to show you this abstract I found quite by accident:

Effects of piracetam on retention and biogenic amine turnover in albino rats.
Nalini K, Karanth KS, Rao A, Aroor AR.

The chronic effects of orally administered 2-pyrrolidone acetamide (piracetam) on one-trial, passive avoidance task were studied in albino rats. The effects on the contents of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) in the brain and on the levels of their metabolites both in the brain and urine were also assessed. Significant improvement was observed in the retention ability compared with saline-administered controls. The contents of NE, DA, and 5-HT and their metabolites in the brain were significantly decreased after piracetam administration. The urinary metabolite levels were also significantly decreased except total 3-methoxy-4-hydroxyphenyl glycol (MHPG). These data indicate that piracetam causes an overall decrease in the turnover of central monoamines. Thus, the results of this study implicate the involvement of NE, DA, and 5-HT systems in learning and memory processes. Piracetam did not exert any GABAergic effect as shown by the absence of change in the brain GABA levels.

PMID: 1513869 [PubMed - indexed for MEDLINE]

As we've discussed, dopamine and NE are the two primary candidates for the neurochemical modulators of motivation, so this might be a pretty clear reason for the effect we've observed. And like the nicotinic receptor issue I just mentioned, another example of (possible) unintended detrimental effects.

Edited by chrono, 19 January 2011 - 07:51 PM.

[Rational Madman]

although piracetam seems to give me focus and clarity I've long suspected it to be very slightly de-motivational or in best case neutral in my own subjective experience.

I found this very interesting when you posted it, but forgot to respond (though I may have elsewhere...damn my post count!). I think this is the case for me, as well. Though piracetam gives me the ability to read about neuroscience all day, I am seldom able to transfer that ability to something I (quote-unquote emphasized) "should" be doing. Though it's off-topic for this thread, I wanted to show you this abstract I found quite by accident:

Effects of piracetam on retention and biogenic amine turnover in albino rats.
Nalini K, Karanth KS, Rao A, Aroor AR.

The chronic effects of orally administered 2-pyrrolidone acetamide (piracetam) on one-trial, passive avoidance task were studied in albino rats. The effects on the contents of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) in the brain and on the levels of their metabolites both in the brain and urine were also assessed. Significant improvement was observed in the retention ability compared with saline-administered controls. The contents of NE, DA, and 5-HT and their metabolites in the brain were significantly decreased after piracetam administration. The urinary metabolite levels were also significantly decreased except total 3-methoxy-4-hydroxyphenyl glycol (MHPG). These data indicate that piracetam causes an overall decrease in the turnover of central monoamines. Thus, the results of this study implicate the involvement of NE, DA, and 5-HT systems in learning and memory processes. Piracetam did not exert any GABAergic effect as shown by the absence of change in the brain GABA levels.

PMID: 1513869 [PubMed - indexed for MEDLINE]

As we've discussed, dopamine and NE are the two primary candidates for the neurochemical modulators of motivation, so this might be a pretty clear reason for the effect we've observed. And like the nicotinic receptor issue I just mentioned, another example of (possible) unintended detrimental effects.

As for the monamines, I think you're quite right, but another problem might be an imbalance between the behavior of AMPA an NMDA receptors. So I think co-administration with an agent like Sarcosine or glycine is important to maintain a balance. But the proper balance is difficult to broadly define, and is perhaps best determined by self-calibration.

[aLurker]

although piracetam seems to give me focus and clarity I've long suspected it to be very slightly de-motivational or in best case neutral in my own subjective experience.

I found this very interesting when you posted it, but forgot to respond (though I may have elsewhere...damn my post count!). I think this is the case for me, as well. Though piracetam gives me the ability to read about neuroscience all day, I am seldom able to transfer that ability to something I (quote-unquote emphasized) "should" be doing. Though it's off-topic for this thread, I wanted to show you this abstract I found quite by accident:

Effects of piracetam on retention and biogenic amine turnover in albino rats.
Nalini K, Karanth KS, Rao A, Aroor AR.

The chronic effects of orally administered 2-pyrrolidone acetamide (piracetam) on one-trial, passive avoidance task were studied in albino rats. The effects on the contents of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) in the brain and on the levels of their metabolites both in the brain and urine were also assessed. Significant improvement was observed in the retention ability compared with saline-administered controls. The contents of NE, DA, and 5-HT and their metabolites in the brain were significantly decreased after piracetam administration. The urinary metabolite levels were also significantly decreased except total 3-methoxy-4-hydroxyphenyl glycol (MHPG). These data indicate that piracetam causes an overall decrease in the turnover of central monoamines. Thus, the results of this study implicate the involvement of NE, DA, and 5-HT systems in learning and memory processes. Piracetam did not exert any GABAergic effect as shown by the absence of change in the brain GABA levels.

PMID: 1513869 [PubMed - indexed for MEDLINE]

As we've discussed, dopamine and NE are the two primary candidates for the neurochemical modulators of motivation, so this might be a pretty clear reason for the effect we've observed. And like the nicotinic receptor issue I just mentioned, another example of (possible) unintended detrimental effects.

Yeah I've kind of given up on piracetam by now.

While it does seem to induce a pleasant feeling of clarity of mind and alertness I never get around to doing anything important while on piracetam. Looking back I can't remember ever doing anything worthwhile when taking piracetam. I have issues with motivation and goal oriented behaviour in the first place and piracetam seems to exacerbate these issues. My actual behaviour on piracetam seems to indicate a certain aimlessness. This is in stark contrast to my initial goal-oriented hyperproductivity on nicotine (judging from the studies quoted here the effects upon nAChRs, DA and NE seem to be the opposite as well).

Of course this is just my subjective experience and opinion about how I react to piracetam. Thanks for posting these studies about nAChRs, DA, NE and piracetam since they feed my confirmation bias that it might not be all in my head.

[Rational Madman]

Although I was initially deterred by what appears now to be isolated examples of suicide or psychological deterioration, I think Varenicline still might be a good candidate. But it still needs to emerge out of one of several trials, because as of now, it has proven itself only as a smoking cessation aid.

I agree that I would like to see at least one trial in which it shows great promise. I'd hold it to a higher standard than most drugs because of the side effects and not only the ones you mention; it recently "won" first prize among drugs correlated to violence. Especially impressive when you consider that it's meant to treat something as mundane as smoking and not more serious mental health issues or ADHD where the underlying condition itself is linked to more aggressive behaviour. *golf clap*

Violent and erratic behavior can easily arise during withdrawal periods of addictive substances, and given Varenicline's mechanism, I don't think there's sufficient reason to be overly concerned. The greatest risk is probably during the early stages of cessation therapy, which if true, should add doubt to suggestions of there being a causal relationship between the administration of the agent, and behavioral disturbances. But even assuming that there is a causal relationship, an examination of the macro picture of the data---and not extreme incidents---seems to suggest that the risks have been the subject of sensationalist treatment.

Edited by Rol82, 26 January 2011 - 05:27 PM.

[aLurker]

Effects of CDP-choline and the combination of CDP-choline and galantamine differ in an animal model of schizophrenia: Development of a selective α7 nicotinic acetylcholine receptor agonist strategy
The regionally selective reduction of expression of the α7 nicotinic acetylcholine receptor (α7 nAChR) in schizophrenia underlies impaired sensory inhibition, a possible endophenotype of the disorder. This ligand-gated ion channel receptor has been proposed as a pharmacotherapeutic target in schizophrenia. The current study examined the effect of CDP-choline alone and the combination of CDP-choline and galantamine, administered acutely and once-daily for five consecutive days, in an animal model of NMDA receptor hypofunction that is relevant to schizophrenia. The results support the allosteric modulatory influence of galantamine on CDP-choline; however, individual doses of CDP-choline and galantamine must be carefully titrated in order to achieve optimal levels of α7 nAChR “agonism” that may be necessary for the desired therapeutic effect.

Galantamine alone didn't do much for me personally but I haven't tried CDP-choline yet. Interesting study nevertheless, especially the discussion part. Has anyone tried CDP-choline with galantamine?

[medievil]

Although I was initially deterred by what appears now to be isolated examples of suicide or psychological deterioration, I think Varenicline still might be a good candidate. But it still needs to emerge out of one of several trials, because as of now, it has proven itself only as a smoking cessation aid.

I agree that I would like to see at least one trial in which it shows great promise. I'd hold it to a higher standard than most drugs because of the side effects and not only the ones you mention; it recently "won" first prize among drugs correlated to violence. Especially impressive when you consider that it's meant to treat something as mundane as smoking and not more serious mental health issues or ADHD where the underlying condition itself is linked to more aggressive behaviour. *golf clap*

Violent and erratic behavior can easily arise during withdrawal periods of addictive substances, and given Varenicline's mechanism, I don't think there's sufficient reason to be overly concerned. The greatest risk is probably during the early stages of cessation therapy, which if true, should add doubt to suggestions of there being a causal relationship between the administration of the agent, and behavioral disturbances. But even assuming that there is a causal relationship, an examination of the macro picture of the data---and not extreme incidents---seems to suggest that the risks have been the subject of sensationalist treatment.

Such events arent documented with wellbutrin tough, it likely acts on a nicotinic receptor wich causes the associated negative effects, not essentially related to the smoking cessation itself.

[Rational Madman]

Effects of CDP-choline and the combination of CDP-choline and galantamine differ in an animal model of schizophrenia: Development of a selective α7 nicotinic acetylcholine receptor agonist strategy
The regionally selective reduction of expression of the α7 nicotinic acetylcholine receptor (α7 nAChR) in schizophrenia underlies impaired sensory inhibition, a possible endophenotype of the disorder. This ligand-gated ion channel receptor has been proposed as a pharmacotherapeutic target in schizophrenia. The current study examined the effect of CDP-choline alone and the combination of CDP-choline and galantamine, administered acutely and once-daily for five consecutive days, in an animal model of NMDA receptor hypofunction that is relevant to schizophrenia. The results support the allosteric modulatory influence of galantamine on CDP-choline; however, individual doses of CDP-choline and galantamine must be carefully titrated in order to achieve optimal levels of α7 nAChR "agonism" that may be necessary for the desired therapeutic effect.

Galantamine alone didn't do much for me personally but I haven't tried CDP-choline yet. Interesting study nevertheless, especially the discussion part. Has anyone tried CDP-choline with galantamine?

Since product grade is frequently suspect, I would go the pharmaceutical route for better results. But it should be noted that the effects of acetylcholinesterase inhibitors vary with pathology, and since you're almost certainly not suffering from accelerated apoptosis, I would expect the results would be limited. For normal subjects, the most pronounced improvement would be in the domain of episodic memory, but I wouldn't expect anything spectacular. I know it must be frustrating, because the number of pathways for pervasive disorders are enough to compel a reluctant and bitter defeat, but you owe it to yourself to sustain your efforts. Anyway, since I---like many others---have sacrificed an embarrassing number of hours reading a broad spectrum of medical literature, I suppose I could list what I deem to be the most noteworthy recurring correlates in many disorders:

1. NMDA receptor hypoactivity.
2. A disruption in COMT activity, and by extension, a reduction frontal catecholamine volume.
3. Reduced reelin protein levels.
4. An aberrant inflammatory response, and consequentially, a disconcerting rate of programmed cellular death.
5. A reduction of a7 nAChR expression.
6. Changes in choline transferase and acetylcholinesterase enzymatic activity.
7. An imbalance in D1 and D2 receptor expression.
8. A adverse change in glucose metabolism.
9. Phosphodiesterase mediated changes in vasodilation (especially PDE4).
10. A mysterious change in MAO-A enzymatic activity.
11. A disruption in the circadian rhythm.
12. Mitochondrial dysfunction, especially in terms of the synthesis of Adenosine Triphosphate.
13. A multi-causal reduction in neurotrophic factors and neuroplasticity.
14. Multiple areas of gastrointestinal dysfunction.
15. And the list goes exhaustingly on and on....

Presently, I think it's abundantly clear to me now that many pervasive disorders have similar correlates and etiologies, and differ primarily in terms of symptom presentation. But despite the parallels, I doubt there's a panacea treatment, because this cascade of symptoms is probably owing to either inherited genetic traits, or a DNA mutation that may be irreversible once a disorder progresses to a certain stage. So I'm afraid to say that afflicted subjects can probably only hope to attenuate the intensity of their symptoms, which unfortunately, is a reduction functionally related to the amount of money one is willing to pay. And since each subject is unique, I'm reluctant to render narrow medical advice, and only feel comfortable with providing a list of possible treatments---so that the algorithm can be individually determined.

Possible treatments
1. SSRIs (Fluvoxamine, Sertraline, Escitalopram, and Citalopram).
2. Psychostimulants (Amphetamine salts, Modafinil, Methylphenidate, Freeze Dried Coffee, and Transdermal Nicotine).
3. MAO Inhibitors (Nardil, Selegiline, and Rasagiline),
4. Mood Stabilizers (Valproate and Lamotrigine).
5. Antipsychotics (Aripiprazole, Ziprasidone, and Amisulpride).
6. COMT Inhibitors (Tolcapone, Entacapone, and Adenosyl Methionine).
7. Anxiolytics (Buspirone, Baclofen, Theanine, Sceletium Toruousum, and Hypericum Perfortum).
8. Flavonoids, Catechins, and Phenols (Resveratrol---NitroMx, Luteolin, Pycnogenol, Green Tea Extract, and Grape Seed Extract).
9. Essential Fatty Acids (Olive Oil, Fish Oil, Flax Seed Oil, Chia Seeds, and Hemp Oil).
10. Alcohol (Cabernet Sauvignon, Malbec, Pinot Noir, Champagne, Rhone, Bordeaux, and Burgundy).
11. Essential Vitamins (Multivitamin, Methylcobalamin, Methylfolate, Vitamin A, Vitamin D, and Vitamin K2).
12. Antibiotics (Minocycline, Rifampicin, and Doxycycline)
13. Antiviral (Valaciclovir).
14. NSAID (Celecoxib and Naproxen),
15. Antihyperintensive (Nimodipine, Clonidine, Guanfacine, Propanolol, and Losartan)
16. Antifungal (Diflucan)
17. Antihyperlipidemic (Atvorastatin, Simvastatin, and Cholestyramine).
18. Antidementia (Donepezil, Galantamine, and Rivastigmine).
19. Immunosuppressants (Rapamycin and Cyclosporine).
20. Hormones (Testosterone Undecanoate, Triiodothyronine, and Thyroxine).
21. Anti-Parkinson's (Apomorphine, Bromocriptine, and Cabergoline)
22. Tricyclic Antidepressants (Amineptine)
23. Phosphodiesterase Inhibitor (Tadalafil, Sildenafil, Propentofylline, and Roflumilast)
24. Anti-Emetic (Ondansetron and Tropisetron)
25. Hallucinogen (Psilocybin and Cannabis)
26. Anti-Diabetic (Metformin, Pioglitazone, and Rosiglitazone).
27. Bronchodilator (Salbutamol)
28. SARI (Trazadone and Nefazadone)
29. Tetracyclic (Mirtazapine)
30. Opiate (Buprenorphine)
31. Nootropic (Ortho Mind, Oxiracetam, Pramiracetam, and Pregnenolone)

To save yourself from the heartbreak of discovering that your hopes in an ostensibly broad spectrum "holy grail" of a supplement was lamentably misplaced, I encourage a preference for more psychoactive agents---which almost universally require a prescription. But if you can manage to procure any of these desired drugs through conventional means, then you should do so, and spare yourself the potential consequences of erring. Additionally, although some of the exotic drugs have a certain amount of allure, usually they're ineffectual or impractical. Instead, place your faith in the study outcomes, and the quantity of research publications----which is an excellent indicator of an agent's therapeutic potential. Indeed, the behavior of market participants may be bounded by the flow and quality of information, but given the capital at the disposal of major players, it's rare that significant opportunities are overlooked. Which means that if an exotic drug is not being sponsored by a leading pharmaceutical company or undergoing a sizable clinical trial, then it probably has a limited utility.

Edited by Rol82, 18 March 2011 - 12:45 AM.

[aLurker]

A very interesting article I read a while back about some new research:
Tobacco-Derived Compound Prevents Memory Loss in Alzheimer's Disease Mice

excerpts:

Cotinine, a compound derived from tobacco, reduced plaques associated with dementia and prevented memory loss in a mouse model of Alzheimer's disease, a study led by researchers at Bay Pines VA Healthcare System and the University of South Florida found.

The Bay Pines VA/USF team decided to look at the effects of cotinine, the major byproduct of nicotine metabolism, in Alzheimer's disease mice. Cotinine is nontoxic and longer lasting than nicotine. Furthermore, its safety has already been demonstrated in human trials evaluating cotinine's potential to relieve tobacco withdrawal symptoms.
The researchers administered cotinine daily for five months to young adult (2-month-old) mice genetically altered to develop memory problems mimicking Alzheimer's disease as they aged. At the end of the five-month study, the Alzheimer's mice treated with cotinine performed better on tasks measuring their working memory and thinking skills than untreated Alzheimer's control mice. Long-term cotinine treatment appeared to provide the Alzheimer's mice complete protection from spatial memory impairment; their performance in this area of testing was identical to that of normal mice without dementia.

Btw: cotinine is a weak agonist at nAChR alpha 7 so it seems highly relevant to this thread.

Looks very promising, I'd definitely switch from nicotine to cotinine if there was a product available but I guess it has a more limited market (pathologies and possibly cognitive enhancement) than nicotine replacement therapy. Let me know if you know how to include it in my regimen since something similar to nicotine but with less side effects sounds pretty awesome to me.

Edited by aLurker, 04 May 2011 - 02:06 PM.

[angus]

Cotinine appears to have been marketed under the name Scotine by Unimed as an antidepressant but i can't find any sellers on the web.
Anybody have more info on scotine?

At least for AD, cotinine seems very promising, and as usual w/ some AD drugs could be a great nootropic for healthy people.

[kevinseven11]

http://www.sigmaaldr...ng=en&region=US
Here is a promising source of cotinine.

[scibor]

Some substances which are readily available nicotinic receptor agonist alpha-7, in terms of Europe, it might also be available on prescription medication ...?

[medievil]

nefiracetam is a alpha7 PAM, add in nicotine and bam there you go A7 is active.

[scibor]

Nicotine is very little work on the alpha receptor -7, working hard on other nicotinic receptors

nefiracetam writing? piracetam and pramiracetam only cause annoyance, adding choline did not help ...

galantamiina makes me insomnia, are there any other options for response to novel compounds alpha-7 nicotinic receptor?

[warmin]

I want alpha-7 nicotinic receptors tested, which preparations you recomennds? any new substances?

[Erebus]

Anabaseine and anabasine are very potent agonists at alpha-7. They also happen to be natural. As to whether or not they're safe: The dose makes the poison... But of course they should be handled with extreme caution...

GTS-21 is a synthetic derivative of anabaseine, and it appears to be completely a(7)-selective. It's a true nootropic for all practical intents and purposes.

...I'm not so sure about cotinine. It looks like it's weak at best, actively harmful at worst: http://www.ncbi.nlm..../pubmed/9833639

[Reformed-Redan]

Great thread. Im wondering about the relation between AMPAkines and nACH alpha7 receptor. I already know that the alpha 7 receptor has great nootropic and therapeutic potential. However agonists of this receptor is AFAIK not the best way to go. PAMs are much better for these purposes.

If much stronger AMPAkines than piracetam lead to downregulation of the nACHa7 receptor, id rather pass.

[warmin]

Where can I buy anabaseine in Europe?

Ampakines upregulate or downregulate alpha-7? Which ampakines?


yadayada PAM is good idea? any supplements. drugs?

Edited by warmin, 27 April 2013 - 06:31 AM.

[Reformed-Redan]

Where can I buy anabaseine in Europe?

Ampakines upregulate or downregulate alpha-7? Which ampakines?

you dont want to jump onto that right away. I really think PAMs are the way to go

[Reformed-Redan]

Awesome seems likely that PRL-8-53 works on the nACHa7 receptor.

[warmin]

prl-8-53?
what is this?
It works also PAM ?

[warmin]

where buy nicotinic alpha-7 agonists? any labs adress?

[medievil]

any labs adress?

The news agent close by, the rc name is marlboro cigarettes.

In all serieusness galantamine and nefiracetam.

I could give you my lab adress but only synth XTC atm.

[prunk]

Does anybody have any experiences on Red yeast rice?

[scibor1]

does lovastatine, mestinon works on alpha-7 nicotinic?
prl 8-53 ?

[Nattzor]

does lovastatine, mestinon works on alpha-7 nicotinic?
prl 8-53 ?

From the research I've found, PRL is most likely a muscarinic acetylcholine receptor agonist, but I might ofc be wrong. Never got any feedback on it.