Salicylic Acid prevented Methamphetamine-induced dopaminergic toxicity

[Madrus]

Check out this paper: http://docdro.id/Da90276

Methamphetamine caused significant generation of reactive oxygen species and decreased complex-I activity leading to dopamine depletion. Striatal dopamine depletion led to significant behavioral changes associated with movement disorders. Sodium salicylate (50 & 100mg/kg) significantly scavenged reactive oxygen species, blocked mitochondrial dysfunction and exhibited neuroprotection against methamphetamine-induced neurotoxicity.

Given this information, how much aspirin should I take with my meth?

 

[Seppi]

Given that meth and aspirin both can induce acute renal failure (kidney injury) or intracranial hemorrhage (bleeding in the brain) when taken in overdose, I'd very strongly recommend that you don't take more than the recommended maximum daily dose of aspirin.
Salicylic acid and aspirin are both antipyretics, which likely is the mechanism of action of those drugs which mediates the reduction in ROS production and impairments in cellular protein function from a methamphetamine overdose (as described in the reference you linked), since methamphetamine-induced hyperpyrexia (a core body temperature ≥ 40 °C) markedly enhances methamphetamine's neurotoxic effects through the facilitation of ROS production, impairment of cellular protein function in the brain, and transient enhancement of blood-brain barrier permeability (this is also based upon animal models of methamphetamine neurotoxicity).†

A better alternative would be to use the recommended dose of aspirin, keep yourself well hydrated, and use chemical/frozen ice packs and/or take cold showers to lower your core body temperature. A better long-term alternative would be to use amphetamine instead of methamphetamine since, when taken in overdose, it acts on fewer cellular mechanisms that induce neurotoxicity than methamphetamine. Both drugs cause hyperpyrexia when taken at sufficiently high doses though.


† See the following review:
Bowyer JF, Hanig JP (November 2014). "Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity". Temperature (Austin). 1 (3): 172–182. doi:10.4161/23328940.2014.982049. PMC 5008711

. PMID 27626044. "Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia (≥40°C) are minimally neurotoxic. Hyperthermia likely enhances AMPH and METH neurotoxicity directly through disruption of protein function, ion channels and enhanced ROS production. Forebrain neurotoxicity can also be indirectly influenced through the effects of AMPH- and METH- induced hyperthermia on vasculature. The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier (BBB) resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals. ... In animal models that evaluate the neurotoxicity of AMPH and METH, it is quite clear that hyperthermia is one of the essential components necessary for the production of histological signs of dopamine terminal damage and neurodegeneration in cortex, striatum, thalamus and hippocampus."

 

[Dresden]

Taking melatonin which also lowers body temperature, is also helpful in reducing methamphetamine neurotoxicity.