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Supplements for prevent neurotoxicity

N

Ne0

Bluelighter
Joined
May 24, 2008
Messages
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So I'd like to make list for supplements that will prevent stimulants (especially amphetamines & MDMA) and possible other substances induced neurotoxicity.

So far I know:
Magnesium - 600mg
Vitamin C (antioxidant, lot of fruits have it, so eat them, orange, apple,) - 100mg
l-tyrosine (?) - 2g
Omega3 & EPA + DHA
Acetyl-L-Carnitine
Alpha Lipoic Acid
COQ-10 or mitoquinone
Piracetam

If somebody knows more then please mention them and also recommendet dosage.

I think you should take the supplements before taking possible neurotoxic chemical. This is mainly for different stimulants.

e. list updated.
 
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Alpha Lipoic Acid
A single administration of 3,4-methylenedioxymethamphetamine (MDMA, 20 mg/kg, i.p.), induced significant hyperthermia in rats and reduced 5-hydroxytryptamine (5-HT) content and [3H]paroxetine-labeled 5-HT transporter density in the frontal cortex, striatum and hippocampus by 40-60% 1 week later. MDMA treatment also increased glial fibrillary acidic protein (GFAP) immunoreactivity in the hippocampus. Repeated administration of the metabolic antioxidant alpha-lipoic acid (100 mg/kg, i.p., b.i.d. for 2 consecutive days) 30 min prior to MDMA did not prevent the acute hyperthermia induced by the drug; however, it fully prevented the serotonergic deficits and the changes in the glial response induced by MDMA. These results further support the hypothesis that free radical formation is responsible for MDMA-induced neurotoxicity.
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Acetyl-L-Carnitine

3,4-Methylenedioximethamphetamine (MDMA, ecstasy) is a worldwide abused stimulant drug, with persistent neurotoxic effects and high prevalence among adolescents. The massive release of 5-HT from pre-synaptic storage vesicles induced by MDMA followed by monoamine oxidase B (MAO-B) metabolism, significantly increases oxidative stress at the mitochondrial level. l-Carnitine and its ester, acetyl-l-carnitine (ALC), facilitate the transport of long chain free fatty acids across the mitochondrial membrane enhancing neuronal anti-oxidative defense. Here, we show the potential of ALC against the neurotoxic effects of MDMA exposure. Adolescent male Wistar rats were assigned to four groups: control saline solution, isovolumetric to the MDMA solution, administered i.p.; MDMA (4x10 mg/kg MDMA, i.p.); ALC/MDMA (100 mg/kg 30 min of ALC prior to MDMA, i.p.) and ALC (100 mg/kg, i.p.). Rats were killed 2 weeks after exposure and brains were analyzed for lipid peroxidation, carbonyl formation, mitochondrial DNA (mtDNA) deletion and altered expression of the DNA-encoded subunits of the mitochondrial complexes I (NADH dehydrogenase, NDII) and IV (cytochrome c oxidase, COXI) from the respiratory chain. Levels of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) were also assessed. The present work is the first to successfully demonstrate that pretreatment with ALC exerts effective neuroprotection against the MDMA-induced neurotoxicity at the mitochondrial level, reducing carbonyl formation, decreasing mtDNA deletion, improving the expression of the respiratory chain components and preventing the decrease of 5-HT levels in several regions of the rat brain. These results indicate potential benefits of ALC application in the prevention and treatment of neurodegenerative disorders.
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What doses of Alpha Lipoic Acid and Acetyl-L-Carnitine should be consumed before taking MDMA? And also would it prevent other amphetamine-analogs neurotoxicity? I assume that it works with any other chemical that works in the same way as MDMA do. So I think it also helps with different beta kationes.
 
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Crankinit, what animal was used in the ALA study that you are quoting? 100 mg/kg sounds pretty high a dose for a human. The maximum (according to wiki) is 60 mg/kg before adverse effects may start to appear.

Am I right to assume that these are both from the same study and that rats were used? (Rats were used in the Acetyl-L-Caritine study).
 
Try Mitoquinone.

It works best for neurotoxicity, as a free radical scavenger 100x more potent than COQ-10.

Mafius
 
http://www.ncbi.nlm.nih.gov/pubmed/17854275

The mitochondria-targeted drug mitoquinone (MitoQ) has been used as an antioxidant that may selectively block mitochondrial oxidative damage; however, it has been recently suggested to increase reactive oxygen species (ROS) generation in malate- and glutamate-fueled mitochondria. [...] In light of these results, studies using mitoquinone as an antioxidant should be interpreted with caution.
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If you had actually read my post, you'd see that that article does nothing to respond to the one which I have referenced.

Mitoquinone's antioxidative properties are not being contested. It's ability to generate highly reactive oxides is what is being contested and that article offers no evidence to the contrary of that statement.
 
http://www.nature.com/npp/journal/v18/n1/full/1395108a.html

Neuropsychopharmacology (1998) 18 57-62.10.1038/sj.npp.1395108

Serotonergic Agents That Activate 5HT2A Receptors Prevent NMDA Antagonist Neurotoxicity

Nuri B Farber MD, Jennifer Hanslick BS, Charity Kirby BS, Laurie McWilliams BA and John W Olney MD
Department of Psychiatry, Washington University, St. Louis, Missouri

Correspondence: Dr Nuri B Farber, Washington University, Department of Psychiatry, 4940 Children's Place, St. Louis, MO 63110-1093

ABSTRACT

Phencyclidine, ketamine, and other agents that block NMDA glutamate receptors trigger a schizophrenia-like psychosis in humans and induce pathomorphological changes in cerebrocortical neurons in rat brain. Accumulating evidence suggests that a complex network disturbance involving multiple transmitter receptor systems is responsible for the neuronal injury, and it is proposed that a similar network disturbance is responsible for the psychotomimetic effects of NMDA antagonists, and might also be involved in the pathophysiology of schizophrenia. In the present study we present evidence that serotonergic agents possessing 5HT2A agonist activity prevent NMDA antagonist neurotoxicity in rat brain. It is proposed that 5HT2A agonists may also prevent the psychotomimetic effects of NMDA antagonists. Among the 5HT2A agonists examined and found to be neuroprotective are LSD and related hallucinogens. The apparent contradiction in proposing that these agents might have antipsychotic properties is resolved by evidence linking their hallucinogenic activity to agonist action at 5HT2C receptors, whereas antipsychotic activity would be attributable to agonist action at 5HT2A receptors.

...

DOI (n = 73), DOB (n = 48), DOM (n = 28) and LSD (n = 55), all 5HT2A/2C agonists, dose dependently prevented MK-801 neurotoxicity. DOB was the most potent with an ED50 of 0.36 mg/kg (Table 1). LSD, DOM, and DOI were also effective but slightly less potent with ED50s of 0.67 mg/kg, 0.81 mg/kg, and 0.98 mg/kg, respectively.
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Flacky,

I am just trying to highlight to you there will always be good and bad clinical trials done on all kinds of supplements/drugs.

And take note the studies you cited was from 2007.

Mafius
 
flacky said:
Sweet. Block drug toxicity by getting even higher =D
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It inspired me to try (R,S)-DOI prior to taking a large dose of 4-methoxy-PCP recently. In actuality, it reduced the high from both... so perhaps the neurotoxicity is part of an NMDA antagonist's dissociative/hallucinogenic method of action.
 
That's an interesting conjecture, but I have to ask: could it have been from the serotoninergic properties of the DOI "masking" the effects of the 4-MeO-PCP's high?
 
Piracetam? It's supposed to prevent neurotoxicity from all sorts of stuff. It's almost supposed to improve memory and it seems to potentiate a whole range of drugs. Search on google for more info.

I would try taking about 2g a day. That seems to be pretty safe, look online for more information on it's safety.
 
I found this from wikipedia:
http://en.wikipedia.org/wiki/Cotinine
There is some research being done on the effects of cotinine on memory and cognition. Some studies have suggested that cotinine (as well as nicotine) improves memory and prevents neuron death. For this reason it has been studied for effectiveness in treating schizophrenia, Alzheimer's and Parkinson's diseases[3]. There is research, however, which also suggests that nicotine and cotinine contribute to Alzheimer's disease in other ways which counter and maybe even negate the possible positive effects they might have, and as such, the matter is still debatable
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So would this mean that if one smokes while doing MDMA or meth it would prevent neurotoxicity on some degrees?
 
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