As a drug, marijuana has certain effects and, depending on why you’re taking it, some side effects. And not everyone wants the whole package. New research finds that for patients who consider weed’s buzz an unwanted side effect, the answer might be as simple as taking an ibuprofen with their tetrahydrocannibinol (or THC).

A study published Thursday in the journal Cell both demonstrates and explains why common anti-inflammatory drugs, including ibuprofen and the prescription analgesics indomethacin and celecoxib (marketed as Celebrex), appear to kill marijuana’s buzz and suppress its negative effects on cognition. In so doing, the research may clear the way for marijuana to play a growing role in treating Alzheimer’s disease and other neurodegenerative conditions.

If you want to get high, weed’s ability to mellow you out is the desired effect. But with regular use, marijuana stunts the growth of the tendrils that lash brain cells together and impairs memory and cognitive processing speed. That package of effect-and-side-effect appears to be inseparable.

But marijuana also has a not-so-widely known effect: it calms inflammation in the brain — a hallmark of several neurodegenerative diseases, including Alzheimer’s dementia, multiple sclerosis and Parkinson’s disease. The problem is that for patients who might benefit from marijuana’s inflammation-dampening effect, both the high and its downstream impact on brain cells and memory are distinctly unhelpful.

That package of effect-and-side-effect, it turns out, can be separated, and the unwanted side effect can be suppressed by inhibiting the induction of cyclooxygenase-2 (COX-2), a complex neurochemical process usually set off by inflammation. To their surprise, the researchers found that the THC in marijuana actually increases the COX-2 process — a finding that would suggest it has both inflammatory and anti-inflammatory effects on the brain.

Add a COX-2 inhibitor to the mix — or even a non-selective COX inhibitor such as ibuprofen — and the anti-inflammatory effects of THC remain. The “buzz,” the lethargy and negative cognitive effects of long-term use, however, are extinguished.

While marijuana is approved for medicinal use in 20 U.S. states and the District of Columbia, THC — marketed as Marinol — is approved for marketing by the Food & Drug Administration only to patients with nausea and vomiting resulting from chemotherapy. The federal agency cites its potential for abuse and its intoxicating side effects as limiting its effectiveness for a wider array of medicinal indications.

The researchers, all from the Louisiana State University’s School of Medicine, conducted a series of experiments on cells in the lab and in mice. To demonstrate the buzz-killing effects of suppressing the COX-2 process, they used mice bred without the gene that enables it, and also suppressed the process with medications.

They also used mice to establish that the mechanics of THC’s anti-inflammatory effects are different from those of its intoxicating effects. Mice bred to develop the beta-amyloid plaques of Alzheimer’s disease were given THC and a COX inhibitor over many days, and the researchers watched as the mix of medications reduced amyloid plaques. In the process, they noted the absence of the usual lethargy seen in stoned mice, and of the memory-impairing effects on brain cells that come with chronic use of THC.

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