Eli Lilly and Company has spent nearly three decades and $3 billion in an Ahab-like quest to develop the world’s first effective drug to attack Alzheimer’s. The search has consumed the careers of Lilly scientists and staffers as they try to cure a disease that afflicts a new victim in the United States every 66 seconds. And this month—when the results of a milestone clinical trial are revealed in a top-secret room in the company’s Indianapolis headquarters—the world will find out whether they got it right.

A statuesque, soft-spoken statistician named Hong Liu-Seifert will arrive for work this month at Eli Lilly and Company’s grassy, sprawling corporate headquarters in downtown Indianapolis, descend deep into the core of Building 88, and approach a door marked “Restricted Access.” She will enter 31-C-RMC056, a small, windowless room that an exclusive circle of Lilly staffers have named “The Cave.” Inside, she will pass several rows of gray cubicles, then emerge in an even smaller windowless room, 31/C/B—“The Cave Within a Cave,” she calls it—past a sign that reads, “Put on your poker face.” There, under the drone of fluorescent lights at a table where she will sit with a team of statisticians, Liu-Seifert will lose track of time, as if she were in a casino. She and the others will be prepared to spend 12-hour stretches there without leaving, taking breaks only to use the bathroom.

Very few people ever get to see the inside of The Cave, which is shrouded in cloak-and-dagger secrecy and exists for only one purpose: Statisticians like Liu-Seifert and a handful of colleagues become some of the first people in the company to see raw data from clinical trials for drugs Lilly is developing. The results are revealed to Liu-Seifert and her cohorts in an almost holy ceremony that people in the pharmaceutical industry refer to in hushed tones as “The Unblinding”—a reference to the culmination of a double-blind scientific study. The data compares trial patients who took an active molecule against patients who received a placebo instead.

The work that goes on in The Cave is so top-secret, in fact, that not even the company’s CEO is allowed inside. A positive finding might boost the company’s stock price by as much as 20 percent, and a negative one could trigger a plummet; knowing either result too early could expose executives to charges of insider trading. The last time Liu-Seifert and her team gathered in The Cave, in 2012, Lilly performed extensive background checks on the housekeeping staff, weeding out recent hires to prevent corporate espionage; only one person, a friendly 70-year-old janitor named Charles, cleared the bar. With so much hanging in the balance, the otherwise staid Liu-Seifert let her “emotion run out” during her last trip to The Cave, a favorable unblinding she celebrated as if she were still a schoolgirl. Other times in The Cave, when statisticians have run up against negative results in an unblinding, typically stoic Lilly technicians have cried. Drugs have been born here, and drugs have died.

As years raced by without a drug, setbacks have turned bright-eyed, optimistic scientists into more measured, sober realists.

This month, when Liu-Seifert opens her laptop inside The Cave and pores over the thousands of rows of numbers and decimals, she will discover whether the iconic Indianapolis pharmaceutical company has solved one of the most difficult riddles in medicine: how to slow the cognitive decline caused by Alzheimer’s disease. In that instant—the moment carrying the fate of three decades and $3 billion worth of work, and the hopes of hundreds of researchers and thousands of patients—Liu-Seifert will know if Lilly has an answer, a drug.

Many in the small cadre of scientists, marketers, and executives working on this project describe it as their moonshot: a quest not to outer space but inner space, into the very thing that makes us human, gives us our identity. As years raced by without a drug, setbacks have turned bright-eyed, optimistic scientists into more measured, sober realists. Researchers on the project have retired and lost spouses. Their own parents have succumbed to the very illness they are trying to forestall. For patients, the undertaking represents a chance at salvation.

Soon, Liu-Seifert will emerge from The Cave knowing the outlook for a $90 billion company—what high-level executives at Lilly are calling a “binary” event that could result in bringing the drug to market by 2018, and windfall profits; or another blow to the field of Alzheimer’s research. The statistician will open the door of 31/C/B and return to 31-C-RMC056. She will face the small group of staffers who have spent much of their professional lives waiting for this moment. Her poker face will fall away.

“The moment I open the door, they will know,” Liu-Seifert says.

And soon, so will the world.

In 1901, a bespectacled German doctor named Alois Alzheimer visited Auguste Deter, one of his patients. At 51, Deter complained of lapses in memory. “I have lost myself,” she told the doctor. Alzheimer conducted a routine cognitive examination, which he recorded in his notes.

What is your name?

Auguste.

Last name?

Auguste.

What is your husband’s name?

Auguste, I think.

Your husband?

Ah, my husband …

Are you married?

To Auguste.

Mrs. D.?

Yes, to Auguste D.

Deter died a few years later. Examining her brain tissue under a microscope, Alzheimer discovered and recorded two abnormalities. The first was a plaque-like substance in the nerves—chains of proteins called amyloid beta that had folded in on themselves and accumulated rather than getting cleared away by the body. The second was a knot of a protein called tau. Each forms neurofibrillary tangles; imagine balled-up strands of spaghetti.

Scientists would later discover that all humans have both of the offending peptides—small proteins—present in our bodies. Our brains produce them from birth, and they float around until we die. In some individuals, at some point during their fourth or fifth decade, the system that removes the peptides begins to malfunction. The plaques and tangles erode the brain’s cortex, taking with them memories, basic cognitive function, and, eventually, lives.

Lilly entered the race to solve the Alzheimer’s problem in the 1980s. Founded by Colonel Eli Lilly after the Civil War, the Midwestern drugmaker had already gone all-in on molecular biology. Introduced in 1982, Lilly’s Humulin (human insulin) was the first genetically engineered or “recombinant DNA” product approved by the FDA. A few years later, Lilly made a big splash with the antidepressant Prozac, a sexier—and more profitable—drug than the likes of its earlier, more prosaic (but no less world-changing) penicillin. Prozac cemented Lilly’s status as a company focused on developing drugs for the central nervous system.

In 1987, a group of academic researchers cloned the Amyloid Precursor Protein. The breakthrough yielded the first clues that amyloid peptide, one of the primary culprits in the disease, included enzymes such as gamma-secretase and beta-secretase. If that was true, scientists might be able to fashion a drug that could target those enzymes. The discovery ushered in the modern era of Alzheimer’s research, and Lilly began positioning itself to be at the forefront.

In 1995, Lilly acquired Dr. Alzheimer’s original microscopes and purchased his childhood home in Marktbreit. They transformed the two-story structure, situated off a cobblestone sidewalk, into a conference center. For Lilly execs, the purchase was symbolic. Like the home, the drugmaker intended to own the field of Alzheimer’s research.

Almost a century after Dr. Alzheimer first observed the plaques and tangles in Auguste Deter’s brain, a Lilly scientist named Patrick May found himself gazing through the lens of the very same microscope. But it was a love of folk music that ultimately led May into the field of Alzheimer’s research. He grew up in Tulsa, Oklahoma, in the 1950s. His mother worked for a while as a technician in a clinical lab at a doctor’s office. As a child, the precocious May read one of her books, Microbe Hunters, about the scientists who discovered microorganisms in the 1800s. May was inspired by the account, as well as by favorite-son folk balladeer Woody Guthrie, who was ascendant at the time. May learned to play “This Land Is Your Land” on the piano, and when Guthrie died of Huntington’s disease in 1967, a condition similar to Alzheimer’s, May decided he would make it his life’s work to research age-related neurodegenerative illnesses.

May pursued two passions, medicine and music, but weekend gigs with his band threatened to derail his academic goals. He hopped from the University of Oklahoma to Oklahoma State before finally finding a home studying medical technology at the University of Tulsa. The program required work at a hospital, where he did routine tests on clinical samples. He met a clinical chemist named Donald Armstrong, who studied neurodegenerative diseases, and May stood out on the chemist’s rotation. He graduated, married his high school sweetheart, and attended graduate school while working with Armstrong.

After graduate school, May moved to Los Angeles to study under Caleb “Tuck” Finch at the University of Southern California Leonard Davis School of Gerontology, one of the first institutes of its kind devoted to the study of aging. May did seven years as a postdoctoral student and senior research associate and began his first Alzheimer’s experiments in 1985, generating a DNA library of genes from patients afflicted with the disease. The experiments were innovative but laborious: He was essentially doing it from scratch. Soon, he identified a gene he coded pADHC-9, short for Alzheimer’s Disease Hippocampus 9. A decade later, it would be recognized as one of the risk factors for the disease. May was one of the first researchers to apply molecular biology techniques to the study of Alzheimer’s, a pioneer in the field—a reputation that helped him get a foot in the door at Lilly.

May arrived in Indianapolis in 1989 for his first round of interviews. His recruiter, Paul Burnett, director of the molecular biology group, drove him by the company’s shiny downtown headquarters, up Meridian Street and out to Carmel, through neighborhoods where the houses looked like mansions but cost roughly the same as the 1,200-square-foot matchbox he shared with his wife and son in Pasadena. May was impressed. Burnett took him to a French restaurant, and after dinner, May retired to the tony Canterbury Hotel, where Lilly had put him up for the night. I could get used to this, May thought.

When he returned to California, May talked to his mentor about the move. Finch thought May would fit in well at Lilly, could put down roots. Unlike a lot of Big Pharma firms of the era, Lilly had a reputation as a scientist’s company. Researchers didn’t just work on a lab assembly line; they published papers in peer-reviewed scientific journals. Recruits received a booklet listing all of the recent publications by Lilly Research Lab scientists—debunking the notion among academics at the time that their peers at pharmaceutical companies didn’t get ink.

What’s more, Lilly had just forged a partnership with Athena Neurosciences, a private California company studying the pathology of Alzheimer’s disease. Athena scientists discovered that the amyloid peptide involved in Alzheimer’s was not unique to those afflicted with the disease, but was instead naturally secreted by everyone. With access to Athena’s research, Lilly scientists could now create cell-based assays, a lab test to screen for compounds that reduce the body’s production of amyloid peptide.

May signed on with Lilly and moved his family to Indianapolis in 1989. In 1992, as a major research conference in Italy approached, the Athena and Lilly researchers kept their cards close to the vest. As it turned out, three other companies that presented at the conference had already made a similar discovery. Now, scientists across the field could turn their attention to developing cell models to study the pathways that the peptides traced in the brain. The race was on.

After Lilly purchased Dr. Alzheimer’s childhood home, May made a pilgrimage to the site. A year later, his father was diagnosed with the disease. The intellectual problem that drove May’s work was suddenly personal.

Lilly terminated its partnership with Athena in 1997. The following year, a team of Lilly scientists including May broke Alzheimer’s research wide open: They discovered a molecule called semagacestat that seemed to block the secretion of damaging amyloid peptides. May thought he and his colleagues were closer than ever before to bringing an Alzheimer’s drug to market.

Meanwhile, May’s father’s condition was getting worse. Then he suffered a stroke. Doctors installed a pacemaker, and out of surgery, May’s father lay on the hospital gurney, rubbing his frail fingers over the new lump in his chest. “What’s that?” his father wondered. A pacemaker, his son explained. Ten minutes later, fingering the same spot, his father asked, “What’s that?” Every 10 or 15 minutes, the same question.

Ron Demattos stumbled into Alzheimer’s research by accident. Before he became Lilly’s chief scientific officer for neurobiologics, the amiable University of Michigan grad had landed an internship at Parke-Davis, a subsidiary of the pharmaceutical company Pfizer. He worked as a lab tech among the group of scientists behind the cholesterol-lowering wonder drug Lipitor. They urged DeMattos to go to graduate school, and at Stony Brook University in Long Island, DeMattos intended to study atherosclerosis, the buildup of cholesterol and fats in the arteries. On his first day in the lab, DeMattos met Dave Williams, a leader in the field. Williams promptly told DeMattos that given his background, he shouldn’t focus on atherosclerosis, but rather a new protein called ApoE, short for Apolipoprotein E. A year before DeMattos arrived, in 1993, another breakthrough in Alzheimer’s research had shown that the presence of a certain type of ApoE, a protein once linked to atherosclerosis, predisposed patients to develop Alzheimer’s. It was the first discovered genetic risk factor for the disease. Before that, researchers thought some cases of the disease were genetic, and had no explanation for the cases that weren’t. Williams told DeMattos he should study the ApoE molecule’s link to Alzheimer’s.

DeMattos was pissed. I came halfway across the country to study under you for atherosclerosis, and you’re talking about Alzheimer’s? That’s neuroscience. I’m a biochemist. DeMattos agreed to at least read the literature behind the research. What he found, he recalls, was “the Wild West.” No one in the field knew why the disease caused neurons to die. He had found a mystery worth investigating.

DeMattos earned his Ph.D in molecular and cellular biochemistry in 1998, the same year Alzheimer’s researchers at Lilly identified semagacestat. As a postdoctoral fellow at Washington University School of Medicine, DeMattos conducted the original laboratory studies that led to the creation of an antibody known as solanezumab and sparked the idea that soluble amyloid in the brain could be removed. At the time, most scientists in the field presumed that once the amyloid peptide descended on a diseased brain, it was intractable—that removing it would be like clearing concrete from the interstices and crevices of a sponge.

With this marquee discovery, though, that thinking changed. Instead of concrete, the peptide was more like sugar: It started out as soluble—meaning it could be dissolved. In essence, solanezumab, or “sola,” as scientists began to call it, worked like a chaperone at a high school dance, finding free-floating pieces of soluble amyloid plaques that were bumping and grinding with other plaque structures—and then escorting the amyloid out of the brain to the bloodstream, where it could be broken down in the body.

Already using DeMattos’s research to advance their own search for an Alzheimer’s drug, in 2002 Lilly scientists wooed the cherub-cheeked 32-year-old to Indianapolis.

Lilly was recruiting some of the best scientists and doctors working in the field, and soon the company would have nearly 400 people around the world, as far away as England and China, working on a possible Alzheimer’s drug. Along with May and DeMattos, there was Richard Mohs, the brilliant vice president of neuroscience clinical development, in charge of early-phase drug development. Sharp business minds like Phyllis Barkman Ferrell, the DePauw grad, Stanford MBA, and Proctor & Gamble alum. And then–senior medical director of the Alzheimer’s Disease Global Development Team Eric Siemers, an Indiana University neurologist who, with his easy, affable manner, became known as “The Country Doc” around the Lilly complex. As May, DeMattos, and others worked in the lab, Siemers designed and organized massive clinical trials to test their work.

Within a short time after DeMattos’s arrival, two promising molecules were already brewing in Building 88 in Indianapolis, the nerve center of Lilly’s global Alzheimer’s research and development. In 2004, solanezumab, which investigators hoped would remove the Alzheimer’s-causing amyloid, and semagacestat, thought to lower the amyloid’s production, went into their first clinical trials. Aimed at measuring the effectiveness and toxicity of a potential drug, trials take years and hundreds of millions of dollars to conduct. To get a drug to a phase III trial, the last one before federal regulators decide whether to approve a product for market, Lilly spends roughly $900 million.

CEO John Lechleiter choked up when he heard the results. You moved science, DeMattos thought to himself.

The trials for semagacestat, called Identity, came first, and in the summer of 2010, a handful of top-level staffers descended into The Cave to find out whether the molecule was working. Lilly needed a win. The previous year, the company had agreed to pay a record $1.4 billion to settle a class-action lawsuit over its marketing of the anti-psychotic drug Zyprexa. Meanwhile, patents on some of its most profitable drugs, notably Cymbalta and Evista, were on the verge of expiring. Folks at Lilly hoped semagacestat would be the company’s next big score.

No one at Lilly needed good news more than Patrick May. As the semagacestat trials neared completion, his father, afflicted with the disease May was trying to remedy, died from an unrelated renal tumor. In March 2010, after silencing his cell phone at an all-day conference, May returned to his office to find seven voicemails, all from his wife’s Pilates instructor. His wife, Elaine, had suffered a stroke while exercising. She died the next day.

Then in August, as the final phase of the semagacestat Identity trials unfolded, May’s colleague Eric Siemers received an email. An external data-monitoring committee wanted to review more information from the Identity trial. Normally, as a drug trial unfolds, if everything is going well, Siemers receives a one-line email from the committee: Continue the study without modification. Anything more—or less—is always a bad sign.

After he received the email, Siemers and a small group of Lilly staffers studied the data over the course of the next week and saw the same pattern flagged by the committee. Semagacestat appeared to be making patients worse, not better—hastening their cognitive decline rather than stalling it. At the same time, they were showing higher occurrences of skin cancer. The Lilly research team reeled.

The company issued a press release announcing the bad news. “This is a setback, but Lilly’s commitment to beating Alzheimer’s will not waver,” said Jan M. Lundberg, president of Lilly Research Laboratories. On the same day, Lilly instructed clinical trial investigators in 31 countries, spanning thousands of patients, to “contact study participants as soon as possible and tell them to immediately stop taking the study drug they have received.”

“There were people crying,” Siemers recalls of his colleagues’ reaction. “You go into this business to make people better.” He had delivered the news personally to May before the announcement. Coming on the heels of his wife’s death, the setback hit May particularly hard. I’m so glad that she isn’t around to see this, May thought. It feels like my whole life has been for naught.

May and a few colleagues, including DeMattos, walked to a steakhouse in downtown Indianapolis to commiserate over meat and gin and tonics. After dinner, May found himself walking to The Canterbury, where Lilly had put him up 21 years earlier when he was in town for his job interview. He had dedicated his entire career to finding a cure for Alzheimer’s, and his best effort made patients worse. He checked into the hotel and went to the bar, where DeMattos joined him. At some point, May switched from gin and tonics to martinis.

“It’s like every day I try to go to work and do something noble, and try and make people’s lives better,” May recalls. “This is all we want to do is make lives better, solve this problem, and then we end up with this terrible result. It was just devastating.”

The following morning, even as a headline in The Wall Street Journal blared “Lilly Ends Work on Alzheimer Treatment,” May showed up at the office and got back to work.

For most of her life, 45-year-old Hong Liu-Seifert has been accustomed to arriving at answers before her colleagues. In China, when she was a high school student in Shanxi Province, she would pretend to be sick so she could spend the day at home solving pages of advanced mathematical problems, unfettered by slower peers. Later, she breezed through undergraduate studies in applied mathematics at Nankai University, then a master’s degree in biostatistics and a Ph.D. in statistics at Tulane University in New Orleans. She came to Lilly in 2001.

In the wake of the semagacestat failure, Liu-Siefert busied herself trying to figure out what went wrong. Amid the wreckage, there were a few pieces of debris to which disappointed Lilly staffers could cling. By this time, the company’s other promising Alzheimer’s molecule, solanezumab, discovered in DeMattos’s lab, had been in human trials for nearly six years, dating back to 2004. In the same press release announcing the termination of clinical trials for semagacestat, Lilly noted that phase III trials for solanezumab were proceeding on schedule. Outside analysts and investors gave the drug only a 20 percent chance of affecting patients.

In 2012, DeMattos’s wife managed to coax him away from Lilly for a summer getaway with their children, and they rented a six-bedroom beach house in North Carolina. DeMattos hoped to stay offline and keep his mind off of work. But that would be tough: The data on solanezumab would be streaming in while he was on vacation.

Liu-Siefert went to The Cave to study the results from the latest solanezumab trial, called ExpeditionII. Normally reserved, she and fellow statistician Wei Zhou jumped up and down like little kids when they saw the data: The drug seemed to be working among patients with mild cognitive decline. “Guys, we have a drug,” said Phyllis Ferrell, the global Alzheimer’s team leader.

The study just missed statistical significance, however, meaning the gap in cognition levels between the test and placebo groups wasn’t wide enough. Siemers concluded that a larger study would likely have been positive. (ExpeditionIII, the current trial, was built to include a much larger sample size of 2,100 patients.) Later that night, DeMattos, still on vacation, received an email that an announcement would be made the next morning. Ten years after donning his first Lilly lab coat, DeMattos found himself hundreds of miles away from Indianapolis as the results of his life’s work were about to go public. “It’s happening,” he told his wife. “I can’t believe I’m not there.”

DeMattos woke up at 5 a.m. and began mainlining coffee. In his inbox, he found a press release with the headline, “Eli Lilly and Company Announces Top-Line Results on Solanezumab Phase 3 Clinical Trials in Patients with Alzheimer’s Disease.” He read that the study had missed its target of statistical significance. But the second and third sentences of the release caught his attention: Both trials showed statistically significant slowing of cognitive decline in the overall study population of patients with mild-to-moderate Alzheimer’s disease. In addition … both studies showed a statistically significant slowing of cognitive decline in patients with mild Alzheimer’s disease.

DeMattos received a congratulatory call at the beach house from Lilly CEO John Lechleiter, who had choked up when he heard the results. You moved science, DeMattos thought to himself.

At 75, Patient 12765 was still a capable man. He had led a good life, built a solid business, loved the same woman for 51 years. He had been an engineer, a career his father had nudged him into, though he’d always wanted to be an artist. He would find farmers planning to clear Indiana Black Walnut trees from their property and buy the specimens, then turn the trees into sculptures in his backyard workshop. He never sold the pieces—each one was reserved for his wife.

Patient 12765 was able to answer most of the questions on the Mini-Mental State Examination, a commonly used test to determine dementia, with little trouble. But he stumbled on questions designed to determine the depth of his cognitive decline, scoring a -4. On attention and calculation questions, he scored a -2. On recall, a -1. Overall, he scored 23 out of a possible 30 points, a sign of mild cognitive decline. Inside his brain, plaques and tangles were killing neurons.

About 10 years ago, he began to fumble over the names of longtime clients: He couldn’t remember them. He grew frustrated and saw his family doctor. The doctor suggested joining one of Lilly’s Alzheimer’s trials, and he jumped at the chance. So a couple of years ago, he made an appointment at the Indiana University Alzheimer’s Center in Indianapolis. He read a 21-page document that informed him the goal of the study was to determine “whether solanezumab will slow the rate of mental (thinking and remembering) decline of Alzheimer’s disease as compared with placebo (a substance that looks like the study drug, but has no medicine).” He learned that monkeys who had 35 times as much sola in their bloodstreams as the amount he would receive had experienced no bad effects. He read warnings about potential side effects, which included ailments ranging from abdominal pain to vomiting. He was undeterred.

On a warm and clear day this past June, more than a year into the trial, Patient 12765 lay on a gurney, as 70 milliliters—roughly five tablespoons—of a clear liquid dripped from a pouch into his left arm. By now, he was out of the double-blind phase and into the open-label phase of the trial, meaning he knew he was receiving solanezumab and not the placebo.

What if it doesn’t work? After three decades of Alzheimer’s research, “We have nothing to show for it,” says Lechleiter, but adds that, “We’re not a one-trick pony.”

He wore a chambray shirt tucked into his jeans, his silver hair matted against his head. One time during an infusion, he thinks he remembers a few women from Lilly stepping into his room to observe. He wanted to thank them, but the words didn’t come. Next to him lay a photo of his sculptures, skinny, angular totems that look like they were fashioned by an ancient civilization. He brought the photo in that day to show the doctors. Lately, the sculptures had been taking him longer to make. He long ago turned management of his business over to his wife and adult children, hoping to spend more time on his art.

On most days, Patient 12765 would wake up and amble out to his shop, tinker around. But the formerly lit pathways between neurons in his brain had darkened. He knew how all this could end, of course. Remembered how his mother, who lived with him and his wife near the end of her life, would disappear during the night, in the middle of summer, with her winter coat on, wandering the streets, searching for something known only to her. A neighbor would see her, bring her home. Eventually, they had to put her in a nursing home.

“Loss is loss,” his wife said, as more clear liquid dripped into him. “But we’ve had a good life.”

“We still do,” he told her.

Thirty minutes later, the infusion was over. He had four sessions left, one every four weeks, until he and the rest of the world would find out whether solanezumab was working.

He believed it was. He felt sharper since the infusions. Still, he didn’t want friends or former clients to know about his disease. He feared they’d abandon him, would treat him differently, pity him. His wife was less certain the drug was working. Sometimes, she thought it had leveled off the disease’s progression; sometimes she just couldn’t tell.

“The drug works,” he said. “I’ll get up and scream it from the mountaintops.”

If the results of this latest solanezumab trial—which Liu-Siefert and company will review for the first time this month—are positive, Lilly’s investment of $3 billion over 27 years will pale in comparison to the revenue it stands to generate with such a drug, which could register in the billions each year.

But for many of those engaged in Lilly’s Alzheimer’s project, the financial stakes for the company are a secondary concern. They swap tearful stories about relatives—a mother, a father, an in-law—who recently contracted the disease, and how they tried to enroll them in the solanezumab trials.

When Phyllis Ferrell, the global Alzheimer’s team leader, begins a presentation, she asks the room for a show of hands of people who know an Alzheimer’s patient. Without fail, about 80 percent do. Six months after Ferrell joined the Alzheimer’s team in 2011, her own father showed signs of dementia. “There’s going to be a time in my life when I know I’m not going to be able to garden when I want to garden, when I’m not going to swim when I want to swim, or do the elliptical when I want to do the elliptical,” Ferrell says. “But you never believe there’s going to be a time when you believe you’re going to lose your memories. If you think about it, your memories are who you are. This disease doesn’t take what you expect to lose, it takes your identity. That’s why it’s so personal.”

In the best-case scenario, if solanezumab does work, it won’t cure the disease, but only slow the cognitive decline by 30 to 40 percent. And what if it doesn’t work? After three decades of Alzheimer’s research, “We have nothing to show for it,” outgoing CEO Lechleiter says, but adds that, “We’re not a one-trick pony.” At any given time across the company, Lilly can have as many as 70 different molecules in development.

But a lot is riding on the outcome of the solanezumab trial. ExpeditionIII is not only testing a drug, but a hypothesis about how Alzheimer’s functions—that amyloid beta plaques in the brain lead to the development of the disease. And as of October, 2,100 patients around the world were receiving the last doses of solanezumab or a placebo in the largest-ever Alzheimer’s drug trial in history. Every four weeks, for 18 months, they have wondered if the drug was working. Hoped the drug was working.

In March, Lilly announced it was changing the statistical analysis plan it was using to evaluate the solanezumab study. The primary measurement changed from cognition and function to only cognition. The company’s shares fell by 8 percent. Lilly pushed back on the perception it was moving the goalposts for its study, arguing in a press release that “emerging scientific evidence supports the idea that cognitive decline precedes and predicts functional decline in Alzheimer’s disease, particularly in earlier stages of the disease. Thus, Lilly has decided to amend the ExpeditionIII trial to include a single primary endpoint of cognition.”

At one point in 2016, across multiple pharmaceutical companies, as many as 20 Alzheimer’s drugs were in development. In July, Biogen, a biotech firm in Massachusetts, announced that a sola-like drug called aducanumab was successful in ridding the brain of amyloid deposits during a 54-week study of 165 patients. Johnson & Johnson, Merck & Co., and Pfizer are all racing toward their own drugs, as well. It’s possible that after all the time and money invested, Lilly could still be beat to a drug by one of its many competitors.

“We want to make a dent in this horrible disease,” says incoming Lilly CEO Dave Ricks. “I was doing the math recently, and we’ve had 10,000 patients take part in our Alzheimer’s trials. Part of the success we’ll hopefully have is to honor them as well. Is there pressure? Of course.”

Patrick May saw his career at Lilly end before learning whether his life’s work would bear fruit. Now 66, he retired in 2014 and moved to Fort Wayne. He still talks to former Lilly colleagues at scientific conferences, but there is only so much they can share with him about their ongoing Alzheimer’s research. Like many who have worked on the project, May compares the enterprise to that of NASA scientists. “It’s like the moonshot, but the difference is NASA could plot exactly where the moon was,” May explains. “They had a target that they knew. But we don’t have that target. That’s what makes it so hard.”

Meanwhile, every 66 seconds in the United States, the disease takes its first steps in what can be a decades-long march to hollow out another mind, laying wasting to neurons—plundering memories, taking identities, burning it all down.

One summer evening, as the last rays of sunlight filtered through the trees around his home in the Meridian-Kessler neighborhood, Patient 12765 sat inside his living room, nursing a beer. “I sincerely believe that this Lilly drug that’s being pumped into me is working. I think it’s probably going away,” he said of his disease.

His wife tilted her head, narrowed her eyes. “Hmm mmm,” she corrected him. “It’s not going away.”

“Hmm,” he said, pulling his bottom lip under his teeth. “I’m sure the Lilly people are getting feedback.”

The couple talked about what their lives used to be like, about how he learned to work with wood during shop class while he was in high school. They talked about how they quickly put an estate plan together, before the bad days came. They talked about the family meeting in which they told their children that their father had the disease. Did he have three grandchildren or four? He couldn’t remember. Four, his wife told him.

On a table in the corner of the room sat a huge potted plant, a night-blooming cereus, stretching out its branches and leaves. Most of its life, it wouldn’t bloom, but the times it did were just amazing. Sometimes, the aroma would wake them up in the middle of the night. “The bloom is there, and then it’s gone,” his wife said.

A few moments passed.

“Like thoughts,” she continued, looking at her husband of more than five decades. “Like memories.”