Kathryn Whitehead

Alexander Wells

The human body is difficult territory to conquer, even for medicine: Many drugs have to enter the bloodstream, bypass the immune system, and arrive at a precise location within a designated cell. That’s why Kathryn Whitehead, a chemical engineer at Carnegie Mellon University, is searching for the perfect vehicle: a nanoparticle that can shuttle new therapies directly to where they’re most needed.

Whitehead is focused on double-stranded bits of nucleic acid called small interfering RNAs (siRNAs). These molecules can block the production of many proteins that cause disease, and so can potentially treat everything from genetic disorders to viral infections. But siRNAs are unstable and difficult to deliver. While many researchers have tried encapsulating them with nanoparticles, they’ve struggled to find one that works successfully.

"People look at me like I’m crazy when I say I tested thousands of materials."

To identify the ideal delivery system, Whitehead employed a labor-intensive approach: Rather than tweaking the structure of a single nanoparticle bit by bit, she and her colleagues generated 5,000 novel ones, then tested the most promising in mice. “It sounds like a lot of work, and I suppose it was,” she says. But the strategy enabled Whitehead to find nanoparticles she might have otherwise missed. “You just never know what’s going to work well,” she says.

By comparing the successes and failures, the team developed a model to predict the best particles. And they’re now using their top candidate to develop therapies for non-Hodgkin lymphoma—drugs that target only cancer cells with specific mutations, hopefully ridding the body of disease with fewer harmful side effects.

Whitehead credits much of her scientific success to plain old perseverance; her lab’s mascot is the honey badger, an animal known for its determination. “People look at me like I’m crazy when I say I tested thousands of materials,” she says. “I think some others would have given up.”

Every year, Popular Science honors the 10 brightest young minds who are reshaping science, engineering, and the world. Check out the rest of this year’s Brilliant 10 here.

Naloxone

Wikimedia User intropin

Mega-pharmacy chain CVS announced Wednesday that it will start selling naloxone without a prescription in 12 new states. Previously, only customers in Rhode Island and Massachusetts had over-the-counter privileges for the drug, which treats overdoses from opioids like heroin, morphine, and prescription pain medications like Oxycontin and Vicodin.

When someone overdoses on an opioid, the drug attaches to receptors in their brain and blocks signals that control their breathing. Naloxone works by knocking the opioids off the brain’s receptors, allowing an overdose victim to start breathing again within minutes.

The drug comes in an injectable form and a nasal spray, which vary in price per state. In Pennsylvania, one of the new states added to CVS’s list, the injectable form will sell for $52.99 and the nasal spray for $40.69.

“Over 44,000 people die from accidental drug overdoses every year in the United States and most of those deaths are from opioids, including controlled substance pain medication and illegal drugs such as heroin,” said Tom Davis, Vice President of Pharmacy Professional Practices at CVS, in a statement. “Naloxone is a safe and effective antidote to opioid overdoses and by providing access to this medication in our pharmacies without a prescription in more states, we can help save lives.”

The new states in which CVS will be selling naloxone without a prescription are Arkansas, California, Minnesota, Mississippi, Montana, New Jersey, North Dakota, Pennsylvania, South Carolina, Tennessee, Utah and Wisconsin.

CVS hopes to grow that list even more. “While all 7,800 CVS/pharmacy stores nationwide can continue to order and dispense naloxone when a prescription is presented, we support expanding naloxone availability without a prescription and are reviewing opportunities to do so in other states,” said Davis.

Some smaller independent pharmacies and other large chains, such as Walgreens, are also selling naloxone without a prescription.

Toxoplasma gondii

Totodu74/Wikimedia Commons CC By SA 2.0

According to the CDC, more than 60 million people in the United States may be infected with the Toxoplasma parasite, which is spread through cat feces (as well as soil and uncooked meat). Most peoples' immune systems are able to fend off illness. But in people with compromised immune systems, such as pregnant women, toxoplasmosis can damage the brain, eyes, and other organs. Symptoms include blurred vision, muscle aches, and flu-like symptoms. Prevention: Change your cat's litter box daily. Use gloves, and wash your hands afterwards. Keep your cat indoors, and don't touch stray cats.

If someone offered you a drug that would save your life, what would you be willing to pay for it? Could you even put a number on it?

Let’s start at $750 per pill. It’s a large number, but when you consider its benefit — your health — it certainly seems manageable. And think about what else that number buys. Along with curing you, that money pays for scientists who will design even better drugs, which might work faster and have fewer side effects. What’s more, your insurance provider or Medicare might cover much of the bill.

Now imagine, after being quoted that price, you heard a neighbor with the same illness only paid $13.50 per dose last week. What do you think of that $750 figure now? Does it seem wildly unfair? Who decides these numbers, anyway?

This is the situation that set up a major firestorm this week over drug prices, with a company called Turing Pharmaceuticals at the center. Turing Pharmaceuticals is a startup operated by a former hedge fund manager, Martin Shkreli (who is no stranger to controversy).

Last month Turing purchased the intellectual property right to a drug developed in 1953 called Daraprim (also known by its scientific name, pyrimethamine), which treats a parasitic disease called toxoplasmosis. You might recognize that as “crazy cat-lady syndrome,” because it can be transmitted through cat litter, among other ways.

It can cause blindness, neurological problems and even death, but is easily treated with a six-week course of Daraprim taken twice a day. That treatment used to cost about $1,130. After Turing bought the drug in August, treatment shot to $63,000, according to a joint statement from the Infectious Diseases Society of America and the HIV Medicine Association. The statement pointed out that for some vulnerable people like AIDS patients (who often take the drug as a preventative measure), annual treatment would now be $634,000.

When the news hit major media outlets, outrage spread across the web, with many members of the public and journalists calling for Shkreli to lower his company's price. After a couple days of raging debate, Shkreli told news stations Tuesday night that the company would indeed bring the cost down, but he hasn’t said to how much yet.

“There were mistakes made with respect to helping people understand why we took this action; I think that it makes sense to lower the price in response to the anger that was felt by people,” Shkreli told NBC News.

But this debate is about much more than Daraprim. Some drugs are just astronomically expensive, including lifesaving treatments for cancer, hepatitis C, and other ailments. It's such a common problem that medical societies offer tips to help doctors get drugs for their patients. There's an entire cottage industry of Patient Assistance Programs that offset the cost of certain drugs, operated by private foundations and some drug companies. Doctors, patients, and pharmaceutical companies have been arguing about this for years, but in recent months it’s been getting more contentious as prices have been on the rise. Pharmaceutical prices were up 13.6 percent last year, compared to about 8 percent over the previous five years, according to Topher Spiro, vice president for health policy at the progressive-leaning Center for American Progress.

"There was a big spike last year, and I think that's what’s fueling a lot of the current debate. It’s increasing health insurance premiums and Medicare premiums," Spiro told Popular Science. "A big portion of the premium rate [insurers] are seeking is a direct result of pharmaceutical costs, so it is starting to explode."

In August, for example, 117 doctors from around the country signed a commentary in the journal Mayo Clinic Proceedings calling for a complete overhaul of cancer drug prices. In 2014, all new FDA-approved cancer drugs were priced above $120,000 per year, the doctors pointed out. It’s a situation that literally leaves people choosing between paying their mortgage and paying for their lifesaving cancer drugs.

The Mayo Clinic Proceedings letter recommends allowing importation of cancer drugs across the border; laws that prevent companies from delaying access to generic versions of their drugs; letting Medicare negotiate drug prices; and even forming price oversight committees that would review new drugs and propose prices based on their potential benefit.

“The good news is that effective new cancer therapies are being developed by pharmaceutical and biotechnology companies at a faster rate than ever before,” the letter reads. “Drug companies should be rewarded with reasonable profits for these efforts. The unfortunate news, also acknowledged by some of the pharmaceutical leadership, is that the current pricing system is unsustainable and not affordable for many patients.”

As the Turing price-test showed, this is hardly limited to cancer. Members of Congress (including Sen. Bernie Sanders, the Vermont independent vying for the Democratic presidential nomination) earlier this summer sent a letter requesting data from a company called Valeant Pharmaceuticals after it raised the prices of two heart medications. Isuprel and Nitropress went up by about 525 percent and 212 percent, respectively, immediately after Valeant bought the drugs from Marathon Pharmaceuticals. Before the sale, Marathon itself had already jacked up the prices by nearly 400 percent over their 2013 cost, according to Sanders’ office.

“It is unacceptable that Americans pay, by far, the highest prices in the world for prescription drugs,” he said in a statement.

Doctors who have cried foul have pointed out that the Turing price hike would actually mean fewer patients can access Daraprim. Dr. Wendy Armstrong, professor of infectious diseases at Emory University in Atlanta, told The New York Times her hospital has not had access to the drug in several months and that toxoplasmosis was not a disease where physicians have been crying out for better therapies. Spiro said many drugs like Daraprim are simply being marketed differently with little or no change to the way they work.

Pharmaceutical companies are quick to point out that the promise of profits is part of what sparks innovation in the first place. And some of their revenues are re-invested in research and development, they add. It takes about 10 years for a new medicine to reach the marketplace, including about seven years for clinical trials, according to PhRMA, the main trade group for drug industry. PhRMA says a new drug costs about $2.6 billion to develop.

"Conversations on the cost of medicines often fail to acknowledge the competitive biopharmaceutical market that exists in the U.S., which helps to control costs while encouraging the development of innovative new therapies," Holly Campbell, a spokesperson for PhRMA, told Popular Science.

In some cases, new and very expensive drugs are indeed better therapies for which people have been clamoring for some time. One notable example is Sovaldi, which cures the liver-wasting disease hepatitis C. In 2014, the pharmaceutical company Gilead Life Sciences came under fire for charging about $84,000 for Sovaldi (a Best of What’s New winner). It cures hepatitis C in three months with practically no side effects.

When I talked to John McHutchison, Gilead’s vice president of clinical research, he said Sovaldi took years and considerable effort to develop because it’s a very precise, targeted virus attacker called a nucleotide polymerase inhibitor. Instead of working with the immune system, like many other drugs, Sovaldi works against the hepatitis virus, attaching itself to the mechanism the virus uses to replicate. Its developers had to find just the right enzymes to make it work without harming other cells in the body, McHutchison explained to me last year. Gilead also notes that most people who need Sovaldi can get it at deep discounts through insurance companies.

Gilead Sciences Sovaldi

Courtesy Gilead Sciences

This first-of-its-kind drug cures Hepatitis C in weeks. Wow.

Sovaldi was one of the first high-priced drugs to hit the market, and other companies have followed suit, Spiro said.

"It happens to be a coincidence that a lot of these drugs are coming onto the market now. Some of the newer ones cost $10,000 a month. We’re seeing a lot of new drugs that cost thousands of dollars," he said.

This is not to say that it ought to be this way, and that insurance companies (and taxpayers) should be on the hook for pricey treatments. The Mayo commentators argue that high prices don’t help anyone, noting that money diverted as profit doesn't necessarily contribute to better health outcomes or novel therapies. Given this climate, the Mayo co-signers said there is "no relief in sight" because drug companies keep challenging the market by raising prices higher and higher. "This raises the question of whether current pricing of cancer drugs is based on reasonable expectation of return on investment or whether it is based on what prices the market can bear,” they wrote.

But the market didn't even have a chance to bear a $750-per-pill treatment for toxoplasmosis, as Turing Pharmaceuticals learned. The people would not go for it. Might that mean people are ready for some kind of price cap, or at least a new type of regulation? The Mayo cosigners call for a few incremental steps in that direction. In a new report for CAP, Spiro and his coauthors also call for new executive actions and congressional legislation to address costs. And the Democratic presidential contenders are beating this drum, too.

Former secretary of state Hillary Clinton's plan includes a per-patient spending cap, a requirement that drug makers spend a certain percentage of their profits on research and development, and a way to enable Americans to import drugs from other countries. Sanders' plan, announced earlier in September, also calls for importing drugs from Canada and for allowing Medicare to negotiate drug prices, something that was expressly barred under the law that created Medicare drug benefits. The Republican contenders have been much less specific (although Donald Trump did say the Turing price increase was "disgusting").

Unsurprisingly, the pharmaceutical industry is skeptical. “The policy proposals they recommend would, if adopted, send a chilling signal to the marketplace that risk-taking will no longer be rewarded, stopping innovation in its tracks and halting decades of progress in cancer care,” PhRMA said in response.

Regardless of who wins the White House next year, any sweeping changes would take Congressional action. That means it could be years before any meaningful change takes place, if it ever does — but, Spiro says, that doesn't mean things can't get better.

"You could bring public pressure to bear," he said, "and we’ve seen already how that can be effective. Public shaming is a very effective strategy, and again, there's no congressional action needed."

At least it seems to work some of the time.

Platelets under a scanning electron microscope

Perelman School of Medicine, University of Pennsylvania

It’s notoriously difficult to direct cancer drugs to only the cells you want to target—they often kill many healthy cells in the process, making the patient feel sicker, or the body attacks them assuming that they are invaders. For the past few years, researchers have been devising new ways to disguise drug molecules so that they will reach cancerous cells more efficiently. Now a team of researchers from the University of North Carolina, Chapel Hill may have found the best cloaking mechanism yet, masking drugs as blood cells, according to a study published yesterday in the journal Advanced Materials.

Platelets, a type of blood cell, are a good disguise for drugs because blood cells naturally stick to cancer cells, so the drugs can go directly to tumors or destroy cancer cells in the blood stream before they colonize new organs. Plus, since the platelets are derived from the patient’s own body, the immune system doesn’t immediately try to destroy them, allowing the drugs to stay in the system for longer, the study authors tell Science Beta.

A schematic of the cancer-fighting drug coated in platelet membrane

Quanyin Hu et al, Advanced Materials, 2015

In this study, the researchers tested their method on 231 mice with tumors. They first separated the platelets from the blood drawn from each mouse, then removed the platelet membranes and combined them with two cancer-fighting drugs. The result was a sphere with a drug on the inside, surrounded by the platelet membrane. The researchers then injected the spheres into the mice’s bloodstream. They found that the particles stayed in the bloodstream for 30 hours, 24 hours longer than the particles not coated with platelet membranes, and that the coated molecules killed cancer cells and stopped tumor growth much more effectively.

Since this is a study in mice, this technology isn’t yet ready to be used in humans. And while it makes sense that blood cells would be a good disguise for drugs because of blood’s relationship with tumor cells, it’s unclear if the platelet membranes work better than similar efforts to camouflage drugs as innocuous viruses or bacteria. The researchers plan to answer some of these questions in future studies. They also anticipate that this method could be used to send other types of drugs to targeted places in the body to heal leaky veins or combat conditions like heart disease.

Painkillers: are they really working, or is your brain just telling you they are?

Eric Norris via Flickr, CC by 2.0

Painkiller manufacturers are confused. Their drugs have maintained the same efficacy at relieving symptoms for the past 25 years, but the placebo effect has gotten stronger in drug trials conducted in the U.S., according to an analysis of 35 experiments published online ahead of print in the journal Pain. In 1996, a painkiller relieved symptoms in 27 percent more patients than a placebo; in a similar trial in 2013, it was only 9 percent, as Nature News reports. As a result, the drugs are appearing less effective during clinical trials, which means that fewer of them have been approved by the Food and Drug Administration; over the past 10 years, more than 90 percent of drugs designed to treat pain have failed in late stages of testing.

The real question, of course, is: why? Why has the placebo effect gotten stronger, and why only in the United States? The study authors have a few ideas. Drug companies in the U.S. market directly to consumers, a practice illegal in much of the rest of the world, which might raise patient’s expectations for how well a drug should work. But a more likely reason, the study authors suspect, is that the glossy setting of an expensive, large-scale clinical trial—with professional nurses taking patients’ vitals and administering drugs—may raise patients’ expectations and convince them of the pill’s efficacy, even if it doesn’t have any active ingredient. Historically, trials in Europe weren’t as large and didn’t last as long, which may have offset the effects of the placebo. But it still doesn’t fully explain the difference in outcomes across the Atlantic, especially because the two systems are now more alike than ever before.

The study, as Nature News points out, raises a question about one of the basic assumptions we make to evaluate drugs: that they should show a stronger effect than placebo. And while a stronger placebo effect clearly isn’t good for getting new drugs approved, maybe it’s not so bad in practice—it could mean that patients could take lower doses of a drug and still experience a clinical benefit. And though the researchers didn’t address it in this study, placebo could boost the efficacy of other drugs with physiological effects that are difficult to measure, like those to treat psychological conditions. But for drug companies looking to get their products on the market, they may have to find a different way to conduct clinical trials, like making them shorter and smaller.

Loïc Samuel/Rice University

Molecular Submarine

In the nearly 400 years since the first submarine was invented, these underwater machines have become incredibly sophisticated. They're armed and they're really stealthy. We're even planning on sending subs to oceans on distant moons. Trippy.

But now, a submarine is going where no submarine has gone before. To the molecular level. In a paper published this month in NanoLetters, researchers announced that they've invented a submarine so small that it's made out of a single molecule.

The submarine is made of just 244 atoms, and can move through fluids with molecules of approximately the same size all around it.

“This is akin to a person walking across a basketball court with 1,000 people throwing basketballs at him,” co-author James Tour said in a statement. Several years ago, Tour built nanocars, extremely tiny cars with rolling wheels.

Not only can the tiny sub move through that difficult solution, it can also move relatively quickly. One inch per second isn't especially fast for us, but for a single molecule, it's really quick. The submarine is powered by UV light hitting the submarine's motors, which whip the submarine through the water, similar to this bacterium's flagella:

The scientists can't steer the submarine yet, but they hope that one day the nanosub could be used to carry tiny items like medical treatments through liquids.

© Science Photo Library/Alamy Stock Photo

This past August, Stanford bioengineer Christina Smolke announced a first: Her team used brewer’s yeast—the stuff in beer—to produce a precursor to oxycodone and the active ingredient in Vicodin, two of the world’s most popular painkillers. By splicing 23 genes from plants, animals, and microbes into yeast DNA, she says, “We created a chemical assembly line.”

Predictably, the achievement caused a stir. On the one hand, it was a significant breakthrough. Opiates are useful and highly sought-after painkillers. Yet their manufacture still begins with physically scraping sap from the seedpods of opium poppies. That makes them expensive and limited. Smolke’s method breaks that process open in a big way.

—Christina Smolke, Stanford bioengineer

On the other hand, democratizing drug manufacture sounds scary. “People are trying to figure out potential abuses of this powerful technology,” says Kenneth Oye, a political scientist at MIT. “It is hard to put stuff back in bottles after the fact.” In theory, once Smolke refines the process, anyone with an undergraduate biology degree could start an underground dope lab. Picture Breaking Bad but with yeast. Drug agencies, Oye says, are not remotely prepared to handle a flood of synthetic opiates.

The truth is, they don’t have to worry for some time. In its current form, Smolke’s yeast is still proof-of-principle. The yield is so low that you’d need 4,400 gallons of it to make a single Vicodin pill. That said, the process will become more efficient, as every process does, and when that happens some regulation needs to be in place. “We don’t want to get caught flat-footed and suffer a moratorium on exciting research,” says John Dueber, a synthetic biologist at the University of California at Berkeley.

In the meantime, scientists will continue to coax painkillers and other drugs from yeast. Synthetic biologists already have a target list of thousands. They will also try to improve and customize the drugs we have. By modifying yeast, scientists could in theory use it to produce less-addictive painkillers, resistance-proof antibiotics, and even drugs to combat cancer. “Plants have never made the ideal medicine; humans just adapted them,” Smolke says. “Now we can go beyond that to build better medicines.”

This article was originally published in the December 2015 issue of Popular Science, under the title, "How To Brew A Better Painkiller".

Fernando Soto, Aida Martin, Stuart Ibsen, Mukanth Vaidyanathan, Victor Garcia-Gradilla, Yair Levin, Alberto Escarpa, Sadik C. Esener, and Joseph Wang

Microcannon

Pills are a clumsy way to deliver drugs. Digestion is a messy process, and making sure the right drug enters the body the right way in enough amounts to matter after digestion is at best inefficient. What if, instead, the drugs could be delivered directly to the part of the body that needs them? Think “topical anesthetic”, only instead of a cotton swab numbing part of a mouth, it’s tiny cannons that use sonic force to fire drugs into organs.

Let me back up a bit. A paper entitled “Acoustic Microcannons: Toward Advanced Microballistics,” published late last month in the journal ACSNano, details the creation of tiny powerful cannons that could some day deliver targeted dosages of medicine into tissues in the body.

The cannon’s barrel itself is 5 micrometers long. To make it, researchers first punctured a membrane (such as pores on skin), and then spraycoated the holes with graphene before adding a coating of gold to further reinforce the tiny boomstick. Gizmodo then describes the tiny cannon firing like this:

Then they had to “load” the cannon with 1-micrometer nanobullets (about the size of the HIV virus) made of silica and encased in a liquid gel. That gel also contained a perfluorocarbon (PFC) as a propellant — because without a propellant, how do you shoot the cannon? PFC starts to vaporize when you blast it with an ultrasonic pulse, and this produces teensy gas bubbles that expand rapidly. It’s that rapid expansion that “fires’ the nanobullets out of the microcannon. Without the PFC, the microcannon just won’t fire.

The cannons haven’t delivered medicine yet, but they did fire deep into tissue, proving themselves as a possible mechanism for drug delivery in the future. As Gizmodo notes, ultrasound has become increasingly attractive for drug delivery as it's pretty non-invasive and can be easily targeted to very specific areas on the body.

It wouldn’t be the first time researchers looked to putting tiny cannons inside people. Last summer, researchers tested small, water-borne railguns, designed to someday travel the bloodstream and, with the aid of an MRI machine, precisely administer drugs.

[Gizmodo]

National Cancer Institute via Wikimedia Commons

Cell death

A cancer cell undergoing the first stage of scheduled cell death. White blood cells with the BCL-2 protein resist this, building up in the body.

Every year, more than 14,000 Americans are diagnosed with chronic lymphocytic leukemia (CLL), a cancer that starts in the bone marrow and creates a lot of white blood cells that stick around in the body too long. It often doesn’t respond well to conventional treatments like chemotherapy and radiation, and the prognosis can be bleak for patients once this first line of treatment has been exhausted. But a new drug called Venetoclax seems like a promising candidate to change that.

In its first phase of a clinical trial, nearly 80 percent of patients responded to the drug (doctors detected fewer leukemic cells than before), and 20 percent went into complete remission, according to a study published last week in the New England Journal of Medicine. Those results are even more impressive because cancers are much harder to treat after the first round of treatments has failed.

Venetoclax works by targeting a protein called BCL-2, which in healthy people, helps regulate when cells should die. In CLL patients, though, a mutated gene generates a different form of the protein, causing cells to stick around longer than they should in the blood, getting in the way of the body’s typical functions. Venetoclax doesn’t kill the cancerous white blood cells; instead, it stops them from producing BCL-2, enabling them to die as they usually would, as Forbes writes.

Venetoclax is the most recent of a number of drugs that might offer promising treatments for CLL. And it’s not the first to treat conditions with small molecules, either. But it’s making scientists excited because it’s so far proven to be the most effective, having shown such amazing results in clinical trials. “This is a powerful drug. It’s like we’ve got a tiger by the tail,” Andrew Schorr, the founder of two patient advocacy non-profits, told Forbes. “This is more like a knock-out punch to the tumor.”

The drug worked best in patients with a mutation that makes CLL resistant to most other types of treatment, which would make Venetoclax particularly useful in the growing field of precision medicine.

But it’s not on the market quite yet; Venetoclax needs to go through several more rounds of clinical trials, and researchers need to figure out the right dose of the potent drug (several patients in the last trial showed signs of tumor lysis syndrome, which results from a chemical imbalance in the blood if too many tumor cells die in a short period). If it does receive FDA approval, it could be used to treat other conditions caused by a mutation in the BCL-2 gene, including several other types of leukemia or cancers of the skin, breast, prostate, or lungs.

Further research into inhibiting or increasing BCL-2 may also reveal new ways to treat schizophrenia or autoimmune or degenerative diseases in which cells die too quickly.

DEA Drug Enforcement Agency via Wikimedia Commons

Researchers trained mice to associate a particular space with cocaine, a highly addictive drug, shown above.

Combatting an addiction is far more complicated than stopping the chemical cravings—a person can associate places or other people with drug use, making the habit much harder to kick. Now a team led by neuroscientists from the University of Oxford have used light to alter mice's memories so that they no longer associate particular locations with cocaine, according to a study published this week in Nature Neuroscience. Eliminating that association might present a whole new way to treat drug addiction.

In the study, the researchers trained mice to associate a particular space with cocaine. Over time, they preferred to hang out in that space over the other places that were associated with a simple saline solution. They suspected that neurons in the hippocampus, a seahorse-shaped part of the brain that is essential for long-term memory and spatial navigation, were responsible for that association, but they didn’t know exactly which neurons were responsible.

To figure it out, the researchers injected the mice with a chemical that caused the neurons to produce a light-sensitive protein when the mouse was in the cocaine-associated area. They found 133 neurons that lit up and implanted light-transmitting fibers near the neurons in the mice’s brains. When the researchers used light to turn off those spatial mapping neurons in the hippocampus, the mice no longer preferred the cocaine-associated area. To the study authors, that meant that the mice’s memories had been altered to forget the drug-related association.

This isn’t the first study to suggest that altering memories and making the brain forget could reduce addiction in humans. And this one isn’t exactly the most feasible—it wouldn’t be very practical for people to walk around with optical cables implanted in your brain. But the researchers do believe that their findings show that altering the spatial memories associated with drug use could be a good way to reverse drug addiction, or other compulsive and harmful habits. If the researchers could use their findings to discover a less invasive way to limit neuron function in the hippocampus, the technique could someday be useful in clinical practice.