Abstract

Abstract

Friday, August 19, 2016

Pipe dream?


Over the last twenty years, half of all state legislatures have legalized marijuana for medical purposes, such as controlling nausea among cancer patients. But recently I came across a notion about marijuana that struck me as counterintuitive: The drug’s active ingredient in marijuana, THC, may benefit people with Alzheimer’s.
I was not much of a pot smoker as a teen, but I partook enough times to learn that, unlike alcohol, the effect could be unpredictable. In April 1979, a couple of friends and I drove the 90 miles to Seattle for the day, and I was driving my dad’s gas-guzzling Chevrolet Malibu. Driving under the influence, be it alcohol or marijuana, is never a good idea, but my timing was especially bad. When I noticed that we were low on gas, I found my way to a gas station, but it was nothing like I had ever seen. There were multiple lines of at least a half-a-dozen cars ahead of us, and the lines showed little sign of advancing. I was seventeen, the second energy crisis was at its peak, and I interpreted the unmoving line of cars as an omen that civilization, like Jimmy Carter’s presidency, was collapsing.
If I were to smoke pot these days, or, more likely, to absorb the THC orally, I imagine it would be an act of piling mild confusion on top of mild confusion. It is not unusual for me to forget why I entered a room by the time I get there. But according to a press release earlier this summer from the San Diego-area Salk Institute, THC can promote “the cellular removal of amyloid beta”—also known as plaque, and assumed to be a key element in the progression of Alzheimer’s. “Cellular” is the key word.
The Salk team studied nerve cells altered to produce high levels of amyloid beta to mimic aspects of the disease. “The researchers found that higher levels of amyloid beta were associated with cellular inflammation,” the press release noted. While the tests involved neurons grown in laboratories, “they may offer insight into the role of inflammation”—a much-discussed topic among Alzheimer’s researchers. While other studies have suggested that cannabinoids, THC in particular, offer protection from the symptoms of the disease, “We believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells,” according to David Salk.
A postdoctoral researcher working on the project, Antonio Currais, was quoted as saying, “Inflammation is a major component of the damage associated with Alzheimer’s, but it has always been assumed that this response was coming from immune-like cells in the brain, not the nerve cells themselves [my italics]. When we were able to identify the molecular basis of amyloid beta, it became clear that THC-like nerve cells may be involved in protecting the cells from dying.”
This was treated as good news, and I assume that in some abstract way, it is. But as I was reading through my notes, I was hoping for something less ambiguous than Currais’s cogent but not particularly promising remark. The deflating word is “may.” So broad in implication. So unlikely to be fulfilled through a cure anytime soon.

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