New research suggests certain cannabis compounds may be able to protect the brain from damage brought on by methamphetamine use.

Italian researchers from the University of Cagliari recently published a study in the journal PLOS One entitled, “9-Tetrahydrocannabinol Prevents Methamphetamine-Induced Neurotoxicity,” which indicates that marijuana, specifically the psychoactive compound THC, is able to prevent brain damage sustained from the consumption of methamphetamine.

“In the present study, we showed that THC, the principal constituent of cannabis, attenuates the neurotoxic effect of meth by reducing two markers of neuronal damage,” according to the study authors.

To formulate these results, researchers injected over a hundred rats with a steady regimen of methamphetamine, followed by doses of THC, which researchers say showed significant promise in offering protection to the brain. This phenomenon is due to the way THC pathways called CB2 receptors react with immune cells and prevent inflammation. “A neuroprotective effect of cannabinoid was likely mediated, at least in part, by their anti-inflammatory properties.”

The authors of the study conclude their findings provide the first scientific evidence that THC has the ability to reduce brain damage induced as the result of frequent meth binges, which, as researchers point out, provides addition fuel to the argument for medical marijuana.

“Several studies have provided compelling evidence for the neuroprotective effects of cannabinoid CB1 receptor in several models of neuronal injury. Extensive in vitro and in vivo studies have shown that natural cannabinoids, e.g. tetrahydrocannabinol (THC) and cannabinol, and synthetic CB1 receptor agonists, can attenuate experimentally-induced neurotoxicity in multiple pathological conditions, such as glutamate excitoxicity, hypoxia, ischemic stroke, brain trauma, and oxidative stress. The neuroprotective effects of natural and synthetic cannabinoids have been also shown animal models of Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. Indeed, a local and temporary increase of 2-arachidonoylglycerol (2-AG) level in response to traumatic brain injury has also been established.