Ginger's Gene

A genetic alteration causes premature aging.

By Jeff WheelwrightOct 1, 2004 12:00 AM


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A couple of years ago I flew to Oklahoma City to meet Ginger Weber. She suffers from an extremely rare genetic condition called Werner syndrome. In the landscape of American health, Ginger is one in a million. Although she and I were born within months of each other—two children of the 1940s baby boom—Ginger’s body has aged much faster than mine. Because of her disorder she is now, in effect, more than 20 years older than I am.

I became interested in Werner syndrome, and its gene, WRN, while researching medical genetics and the Human Genome Project. If DNA could be likened to a revealed scripture, the scientists of the genome project were its scribes, scratching out the sequence of the 3 billion chemical letters that define a human being (the mechanical version). In fact two projects, a public effort and a private venture, had competed to capture the sequence. The primary motivation was to speed the hunt for disease genes and for new drugs to counter them.

In 2000 the rival teams agreed to a tie and prepared to publish their readings of the human genome simultaneously. When the two publications appeared the following year, there was much cap flinging and commentary about the coming transformation of medicine. The competition had whetted everyone’s enthusiasm for the age of the gene, along with creating some anxiety about what the knowledge would mean for individual privacy.

So before driving to Ginger’s house, I stopped at the library of Oklahoma City Community College, which carried Science and Nature, the journals containing the results of the two projects. From one I borrowed a pullout illustration of the human genome. It mapped all the genes known to date. My idea was to show Ginger the location of the Werner syndrome gene, the source of all her pain. I was hoping that this would help break the ice between us.

The Werner gene hadn’t been identified through the Human Genome Project, but it had spun out of the same excitement about genomics and pharmaceutical development during the late 1990s. Indeed, Ginger’s gene had already been patented, traded, and cast aside. Long before I sought her out, I had learned that the great majority of the breakthroughs that are reported in biomedicine are not breakthroughs at all but dazzling dead ends. The light is always at the beginning of the tunnel, rarely at the end.

In 1903 Otto Werner, a German medical student, was introduced to four sisters and brothers who shared the signs and symptoms of an unusual ailment. In their thirties, the siblings were old before their time. Werner, according to an account, “noted they had cataracts, premature graying and loss of hair, as well as skin changes he referred to as scleroderma [excess fibrous tissue].” The student wrote up the cases for his medical dissertation.

Thirty years later, two American doctors described a second instance of Werner syndrome, recognizing it to be an inherited condition. Cases were reported sporadically in the following decades around the world, especially in Japan, where inbreeding had allowed the gene to gain a foothold in some extended families.

The Werner gene—then known to be a single gene, although what genes were exactly was not known—produced characteristic features, including short stature and a squeaky voice. After puberty there was a subtle acceleration of signs of aging, but the disease was not usually noticed until early adulthood, when bones broke unaccountably. Then the affected person, sliding into the crippling conditions of old age, would die of heart failure or cancer or diabetes before reaching 50.

By the 1960s the mechanisms of genes were crudely grasped. Made of long strings of DNA (deoxyribonucleic acid), genes cause proteins to be manufactured, and then proteins run the body. Scientists understood that the Werner gene, being faulty, must make a faulty protein or none at all. But the gene itself, hidden among thousands that were themselves hidden, was a mystery. And the path from the gene to all that could go wrong in the body because of that gene was an even greater puzzle, which remains unanswered today.

By the 1960s, when Ginger was a teenager and still feeling healthy, scientists began to study Werner syndrome for another purpose. They thought the gene might shed light on the prospect of normal human aging. If senescence was happening too fast in the cells of Werner patients, it might mean that a biochemical gas pedal was stuck on the floor. Find the bad gene, the stuck pedal of aging, and you might also find a means to slow down the same process in people who weren’t yet old or sick. A rare genetic flaw could become a model, a research tool, to attack the “disease” of aging in humanity. The pharmaceutical industry has long believed that a pill to increase longevity would be the ultimate blockbuster drug. Thus Americans who never knew Ginger Weber might benefit from her disease.

Ginger lived in Choctaw, a woodsy development east of Oklahoma City. She met me at the door wearing a flowered blouse and pants, leaning on her walker. Her husband was off at work. Isolated by her disease, she’d never had a journalist ask her questions before.

The rooms of the house were kept dark because Ginger, who was recovering from a cornea transplant in one eye, was sensitive to light. In the shadowy living room I noticed mainly that she was very small. Right away she told me, in a high, bright voice, that her red hair was a wig. “I have baby-fine hair, and it was starting to fall out in ’92. That’s when I went to Dr. Rubin,” she said.

Craig Rubin was the geriatric care specialist at the University of Texas Southwestern Medical Center in Dallas who had diagnosed her Werner syndrome and put me in touch with her. The most dangerous sign of Werner, in her case, was premature osteoporosis, a grave loss of bone density. In a research paper, Rubin had listed Ginger’s other physical deficits as they occurred from her teenage years until the time he first saw her at age 43: a maximum height of 4 feet 10 inches; graying and thinning of her hair, beginning in high school; two miscarriages in her late twenties; menopause at 31; cataract surgery in both eyes before 40; a broken left femur [thighbone] at 41 (from “playfully wrestling with her husband”); recent heel surgery; and a progressive loss of tissue from the soles of her feet.

Rubin had told me that Ginger had the classic manifestations of Werner syndrome, such as thin extremities and a large waist. “Now I’m down to 4 foot 7,” she said. Her age when we met, almost 53, would have been difficult for me to guess. She looked older, no doubt, yet her skin was smooth and her features were lively.

I asked if we could go into a brighter room so that I could show her my map of the chromosome where the Werner gene resided. Briskly, she led the way to the kitchen. Her four-legged walker had two wheels in front and, for faster action, two tennis balls cupping the rubber stoppers on the back legs. We sat at the kitchen table, where she kept her back to the light from the window.

When I spread out the illustration, the rendering of the chromosome looked like Sanskrit squeezed from a toothpaste tube; it was far too technical. I pointed out the Werner syndrome locus nonetheless. Ginger looked at it blankly.

Another try. In my notebook, I drew something akin to the double helix, the double-stranded spiral of DNA. There are four kinds of chemical letters—A, T, C, and G—dotted along each strand, I said. Then I wrote out a hypothetical row of these letters and put my initials next to it. Below that I copied the same letters, except that I made a change in the middle, putting a G in the place where a T had been. I named that row Ginger’s gene. You see how it’s spelled differently from mine, I said. So the protein that your gene makes is going to be different too.

Ginger followed me politely, her injured eye watering slightly. The scheme I sketched in the notebook was vastly oversimplified, because Ginger had two damaged copies of the gene (genes come in pairs), and the differences between her set and mine entailed more than one letter. But I was trying to point out that disease genes are simply normal genes gone awry. A gene may be hundreds or thousands of letters long, and if a mutation alters some part of the sequence, a disease may ensue.

Ginger got the gist. “That’s interesting. You mean we all have the Werner gene?”

“Yes,” I said, “and its normal purpose is to make the Werner protein.” In my notebook I drew arrows from our two genes to a box labeled “protein,” wondering if she could make them out with her failing eyesight. “This particular protein is involved in the repair of DNA. Without the Werner protein, the cells in the body die sooner, and you age more rapidly.”

Ginger thought for a moment. “Dr. Rubin said, ‘I hate to tell you this, but you have got the bones of someone who’s 80.’ My mother says I don’t look any older, but I can tell I do. I tell my mother it’s the orneriness in me coming out, but in a different way. And she says, ‘No, Ginger, you’re good.’”

In the 1970s scientists cultured skin cells taken from people with Werner syndrome. As the researchers suspected, the Werner cells didn’t divide and replicate as many times as normal cells. Under the microscope the chromosomes of the Werner cells showed more signs of damage than did the healthy counterparts. For the first time it was possible to study the disease without having a patient present. Many labs ordered shipments of Werner cells for experiments. But the master molecule, the Werner gene, remained invisible within the nucleus, as tiny to the cell as the cell was to the body.

Beginning in the 1970s, cloning techniques enabled researchers to create multiple copies of a gene by inserting it into a bacterial colony. Sequencing techniques followed. Given a large enough sample of DNA, the sequencing machines could not only read the lettering of a gene but could also distinguish a healthy gene from one with a harmful mutation—a disease gene. But figuring out where on the chromosomes to look for a specific gene was cumbersome and time-consuming. During the 1980s scientists pulled out fewer than 10 disease genes from the haystack of DNA.

The most celebrated of the early discoveries, in 1989, was the gene for cystic fibrosis. The pace sped up in the 1990s as the technology improved and the map of the human genome came into focus. Genes were found for familial breast cancer, for Huntington’s disease, for fragile X syndrome. Still, the preponderance of genes were for odd and oddly named conditions you would never have heard of because they were so uncommon: Aarskog-Scott syndrome, X-linked agammaglobulinemia, and spinocerebellar ataxia 3, for instance.

The Human Genome Project, which was by then under way, approached disease genes differently: The goal was to sequence every bit of DNA on the chromosomes and to see what disease genes might fall out of the inventory. The amounts of data were immense. Fortunately, DNA is easily digitized because it has only four different letters. When molecular biology was married to computer science, a new specialty was sired, called bioinformatics, and a new term inspired, genomics, standing for the lightning-fast appraisal of multiple genes. Silicon Valley jumped into biotechnology, as did another center of the booming information economy, the Seattle area.

In 1992 a group of scientists with backgrounds in pharmaceutical research founded Darwin Molecular Corporation in a suburb of Seattle. Darwin’s declared strategy was to capture the sequence information streaming from the genome project and apply it to the development of new drugs. With modest funding and a staff of 10, Darwin was indistinguishable from a dozen other biotech firms. The buzz began in 1994, when Bill Gates and Paul Allen, the pioneers of Microsoft, invested $10 million. Gates, taking a seat on the company’s board, had strong ties to the University of Washington. A $12 million gift from Gates to the university had lured Leroy Hood, a coinventor of gene-sequencing technology, to the Seattle campus in 1992. Hood was one of the founders of Darwin.

The company’s top scientist was David Galas, a molecular biologist who had helped launch the Human Genome Project. Galas looked for genes that would lead to new ideas for drugs. Two medical researchers at the university, Gerard Schellenberg and George Martin, happened to be experts on Werner syndrome. In addition, the university’s medical school maintained an international registry of Werner patients. The largest input was from extended families in Japan, but the registry also included scattered individuals like Ginger Weber. Studies of the affected families had previously determined that the Werner gene must lie somewhere on chromosome 8. For several years the University of Washington doctors had been searching patients’ DNA for the flawed gene. Darwin could push the hunt into high gear.

Galas told me, looking back: “Darwin was founded on the idea of pulling out genes and seeing if they’d be useful or therapeutic. Even if it didn’t pan out [for drug discovery], we might profit indirectly. We could show that we did what we said we could do.”

In 1995, at the request of Darwin investigators, Rubin sent a sample of Ginger’s blood to Seattle.

Nobody knows how many people have Werner syndrome. A very rough estimate is that for every million people, between one and 20 have the disorder. When her condition was diagnosed, Ginger was told that there were perhaps 125 patients in the country. She has not met any of them, for there is no support group or Internet site.

Ginger told me that as far as she knew there were no other cases of Werner in her family. When she was a baby in Texas, her parents divorced and couldn’t afford to keep her, so a friend of her mother’s adopted her. “Their genes didn’t click,” she said of her biological parents. “My mother was short, but not as short as I am.”

Actually their genes did click, if not in the way she meant. I remarked to Ginger that her mother and father were most probably carriers of the Werner gene. Although both parents were unaffected, each would have transmitted one bad copy of the gene to Ginger.

The mother in Ginger’s life is her adoptive parent. The two have remained very close, speaking to each other on the phone every day. The bones and tissues of the woman over 80 are in better condition than her daughter’s, an irony they do not discuss.

Ginger grew up in a farming community and was active in sports. Her height wasn’t particularly noticed, but her mother kept remarking that Ginger’s size 4 feet ought to grow bigger. They didn’t. “I always felt like they might grow, even after I got married,” Ginger said.

Ginger met Tom at a dance at the state university they attended in Alva, Oklahoma. Outgoing, she liked to rock and roll, twist, slow dance to “whatever was playing.” Tom was younger than she was and a little shy. They were married in 1969.

On the mantelpiece in the living room of the Webers’ home is a picture of the young couple. Ginger was red-haired and bright-eyed beside Tom, a foot taller.

“We’ve been married almost 32 years. I told my husband I was going to keep him young—I was 21 and he was 19—but that’s no longer going to happen. I did the opposite,” she said, without any emotion.

“I started my period at 10 and quit having my period at 27. I had two miscarriages. I lost a little boy in ’72 and later a girl in ’77, and both times I didn’t know I was pregnant.”

After the first miscarriage she dropped out of college. Tom had good jobs in the computer industry, so Ginger didn’t feel pressure to work. She was a beautician for a while, and a receptionist, but she was experiencing mounting problems with her body. She stopped work in 1992, after Rubin told her how fragile her bones were.

Still, she traveled with Tom on his business trips, and she didn’t hang back. “I said to him not long ago, ‘I’m gonna take you dancing again.’ And I will.”

When I saw Ginger, however, she was confined to the house except when her husband was able to take her out. Other than Tom and her mother, she had no friends to mention, nor did she have helpers in the community. As a treat for her and a favor for me, Ginger and I planned to have lunch in town, and I would drive her to a scheduled medical appointment. If her husband took her to the doctor, he had to rush home during his lunch hour to pick her up, and then she had to sit in the waiting room until he came again at the end of the day.

Here is what Ginger has suffered since her disease was diagnosed: Appendicitis in 1993. A broken femur (the other one) in 1996. Hip replacement in 1997, two months after she fractured her pelvis without realizing it. A broken arm in 1998: “Again, I didn’t fall or anything.” But the bone of the arm pierced the skin, and the external wound would not mend, necessitating plastic surgery a year later. A cornea transplant in her right eye in 1998 and in her left eye in 2001, two weeks before my visit.

The fractures didn’t concern her. She talked primarily about the ordeal of her feet. “I used to have muscles, and I walked a mile a day, but now my feet burn all the time.” Gradually her joints had become fused, so that her brittle legs now rested upon little bony blocks. Recently, Ginger had been plagued with topical ulcers and floating deposits of bone that cropped up in the paper-thin skin of her feet.

“They told me I’d have these formations off and on because . . . because of the way I am,” Ginger said. She avoided using the term Werner syndrome, focusing rather on her “little problems here and there” and attempting to divide and conquer them one at a time. “Due to what I have, they don’t know how to doctor me.”

There is no cure or treatment for Werner. In an effort to strengthen her bones, Rubin gave her a growth factor called IGF-I—donated by a drug company because her insurance would not cover it—but the experiment had almost no measurable benefit. Now she was taking calcium and sodium fluoride. Positive thinking was her credo and her therapy. “I just try to keep more up than down,” she explained. Once she chewed out an orderly for saying “terminally ill” in her presence. “‘Hey—that’s not in my vocabulary!’”

Rubin believed that attentive medical care had enabled Ginger to survive longer than is typical for a Werner patient. When the doctor admitted to Ginger, then 44, that Werner patients generally did not live past 48, she vowed to him, and now to me, “I’m going to outlive that, I’m going to beat that. I’m going to be the exception to the rule. There’s always an exception to the rule,” she said, nodding bravely, pleased by the thought that she might be one.

Tens of thousands of patent applications have been filed on human genes, more applications than there are genes in the genome. To many people, it seems wrong that a piece of nature can be patented, but since 1980 the courts have upheld the principle, not so much on the ownership of the raw DNA as on the ideas for making use of it. The shorthand for genes in the genomics world is IP, for intellectual property.

When a gene is up for grabs, speed is essential because the basic techniques of discovery are open to every laboratory. The University of Washington researchers and Darwin Molecular Corporation, intensifying the hunt in 1995, knew they weren’t alone. If they managed to discover the Werner gene, the first thing they would do was file a patent on it.

Once the gene was pinpointed and spelled out, the team expected to quickly grasp the Werner protein. Ideally, it would be a hormone or an enzyme circulating in the bloodstream, a chemical overlooked to date but one with terrific powers. With the Werner protein in hand, drugs might be fashioned to replace, increase, or otherwise interact with it. The obvious beneficiaries would be the Werner patients themselves, particularly if they received a diagnosis early. Some genetic disorders are treatable by enzyme replacement or by a dietary adjustment to the missing protein, and Werner might belong to that category.

However, Darwin was not in business to make a pill for a couple of hundred people with a rare disease. At the end of the 20th century the biomedical industry was focused on an aging population—millions of Americans who might be well today but who would inevitably experience cancer, cardiovascular disease, arthritis, diabetes, Alzheimer’s, Parkinson’s, and so on. A bizarre ailment such as Werner syndrome was valuable for the leads it might provide to more-traveled pathways of disease.

Gerard Schellenberg, the molecular geneticist at the University of Washington, explained: “Aging is a major component for cancer and heart disease. All these entail aging, at least for the risk. The hope was to understand the aging process at that fundamental level.”

At Darwin’s lab, eight sequencing machines ran around the clock, decoding the DNA samples that had been collected from Ginger and the others, while Schellenberg and George Martin and their colleagues combed through the results for suspect genes. They found one in a matter of months. In April 1996 the journal Science announced the discovery of the “premature aging gene.” In news media accounts, two of the three principals were buoyant. “A kind of Holy Grail of aging research has been to find this gene,” said Schellenberg.

“[It’s] a whole new window into age-related diseases,” said Darwin’s David Galas, adding, “The exciting thing about this is it shows an error in DNA metabolism that actually connects cancer with cardiovascular disease. It’s the first gene that’s ever really made that connection.”

But Martin demurred: “It’s not the gene for aging.” He questioned whether the gene would be any help in understanding longevity.

All along researchers had debated whether Werner syndrome hastened normal aging or only mimicked the aspects of getting old. Yes, the disorder prompted the early onset of cancer and heart disease and osteoporosis, but it did not cause Alzheimer’s disease. The brains of Werner patients didn’t degenerate; their blood pressure remained normal. Women with the Werner form of osteoporosis had weak bones in their legs but not the telltale widow’s hump in their spines. Werner cancers were of a different mix from those commonly experienced by the elderly.

The Werner protein did not resolve the matter. The protein turned out to belong to a class of molecules called helicases, which assist in the repair of the DNA molecule and help unwind the double-stranded DNA when cells divide. Did the absence of the protein cause the bodies of Werner patients to break down? Conversely, did its presence in a healthy person slow the aging process? Could more of it be useful?

The biologists didn’t know. But they did know that the protein’s activity takes place within the cell nucleus—not in the bloodstream, not in the tissues and organs. Locked within each cell, it has no systemwide function. That meant the protein was not suitable as a drug, because it could not be delivered or manipulated directly. At the time, none of the researchers acknowledged this fact. Darwin, the University of Washington, and Schellenberg filed a patent on the WRN gene and its protein.

“We are now working to identify the best initial medical targets related to the Werner gene,” Galas said to the press, which was true. But the company did not put its full weight into landing the fish it had hooked at considerable cost. Internally, the WRN project began to die.

Before Ginger and I left for lunch, she taped a patch over her recovering left eye. She put on a large red windbreaker, a knit hat, and a pair of rakish sunglasses. After escorting her small bowed figure to the car, I folded her walker into the trunk, and we drove off to her favorite Mexican restaurant.

On the sidewalk she kept her chin down and slid the walker forward with a kind of shuffle step, now and then talking softly to herself. She wore white socks and special podiatric sandals that had open toes and Velcro straps.

When we came to the restaurant, she hauled herself up the steps, taking the rail with both hands, as I followed with the walker. At the table she drank a glass of water straight down, exclaiming, “Oooh, that tastes good.”

After the meal we would go to the wound clinic for the biweekly removal of ulcers from her feet. Ginger said she was considering an experimental boot in lieu of having surgery on her right foot. Her recurrent sores were slow to heal. “When I’m walking, I’m walking on skin. That’s why they burn. But they’ve been doing it so long, I’ve just gotten used to it. ‘Don’t quit walking,’ my mother said. And I said, ‘I’ve got to walk on it, regardless if it kills me.’” Then she jerked her mind away from the negative, telling me of the fun trips she had made with Tommy to Hawaii and Orlando, times gone by.

“Several of the doctors said, ‘If I had what you had, I wouldn’t be so cheerful.’ But I say, ‘It’s just little itty-bitty things.’”

“But you know they aren’t itty-bitty.”

“You want me to be moany?” Ginger replied. “‘Oh, that hurts’ all the time? I tell my mother it’s the meanness coming out of me.”

On hearing that peculiar exorcism again, I responded, “Well, if the meanness is coming out, that means that the good in the person is what’s left behind.” Awkwardly, I added a bromide I’d read in a fitness column: “Pain is just weakness leaving your body.”

Ginger said flatly, “I just think of something else.”

Driving to the Deaconess Hospital Wound Care Center, I let Ginger out of the car, and we progressed across the parking lot. “They tell me I shouldn’t be here, because I blow the statistics,” she remarked when we arrived. The rest of the patients were much older.

The pain today was “not too much,” she told the nurse. “About a three.” In the examining room, as the medical technician picked at and pressed upon her tiny ankles and toes, I saw how Ginger dealt with pain. She sucked in a breath and concentrated a sharp stare on her pain.

The podiatric specialist, Robert Sowell, came in to see how the patient was doing. “This is a rare disease in a unique person,” he said, seemingly proud of her. “We’ve had a limited success—”

“No, keep positive,” she interjected.

“—with that left ankle, but not the other,” he said. A spot of fresh blood appeared where he picked off some dead skin. “We’re right on bone here. . . .We’ve got some of her wounds to heal,” Sowell went on. “Chronic foot ulcers like this we see in diabetics, ordinarily. Her tissue is more like an 80-year-old’s.”

After Sowell left the room, the technician took photos of her feet. “Another doctor said he wouldn’t touch me with a 10-foot pole,” Ginger recalled. But Sowell was hanging in with her, proposing plastic surgery, experimental skin grafts, the new boot, whatever Ginger might agree to. On the drive back she insisted: “I don’t want to say I’m handicapped. I don’t feel handicapped. But I told Tommy I wish I’d quit having something go wrong with me.”

Ginger squeezed out a high-pitched cough. She dangled her feet above the floor and chatted about this and that. Scrunched into her seat belt and windbreaker, she could have been my child being driven home from a game or get-together. Wisps of white hair peeked from beneath her pageboy wig.

“My husband asked if when I die I wanted to be buried wearing my wig. ‘Honey, yes!’ I said. ‘That’s how people know me!’”

Having patented the Werner gene, Darwin’s strategy was to understand the biology surrounding the Werner protein. Although it couldn’t serve as a drug itself, the protein might prove useful in other ways.

“We gave ourselves six to nine months and put a half-dozen people on it to see if there were therapeutic targets lurking in there,” recalled Galas. “If there were targets, they’d be proteins that the Werner protein interacted with. Our goals at Darwin were more diffuse than aging research—for example, cancer. We thought it [the protein] might have to do with the control mechanisms of cancer.”

However, Darwin’s study did not make headway, because the biology of the protein was just too complex. No drug targets related to the Werner gene emerged by the end of 1996.

“By the time we did the merger with Chiroscience, I thought, it’s a long shot that it’d have a therapeutic value,” Galas said. “We’d had this exciting discovery, but . . . ” His voice trailed off.

Chiroscience was a pharmaceutical-research company based in the United Kingdom. When Chiroscience acquired Darwin Molecular in December 1996, the Werner syndrome project was put on hold. Nevertheless, the gene performed a final service for its owner:

Chiroscience and Geron Form Joint Research Collaboration Around Gene for Premature Aging

LONDON, UK, and MENLO PARK, CA September 15, 1997—Chiroscience Group pic (CRO-L), through its subsidiary Darwin Molecular Corporation, and Geron Corporation (NASDAQ:GERN) today announce a research collaboration agreement focusing on diseases associated with the process of aging. The collaboration capitalizes on Darwin’s earlier discovery of the Werner syndrome gene, the first discovered human gene which directly affects the aging process.

Geron Corporation was the hot biotech of 1997 on the strength of its own patented “antiaging” gene. The Geron gene made a protein called telomerase. To insiders, telomerase was a much better prospect for drug development than the Werner protein.

Ironically, Geron had been one of the original bidders to corner the Werner gene.

Now Geron picked up the gene as a throw-in to a deal whose purpose was not divulged in the press releases issued by the two companies. Geron’s chief scientist told me that Geron paid Chiroscience “next to nothing” for the option to utilize the Werner gene. In fact, he said, Geron never did exercise its option.

Today Galas says, “It would be crazy to marshal a large research program now to figure out how to cure the disease. She [Ginger] would be long dead. If the biology were understood and it were simple, those patients might be helped. But it’s an extremely orphan disease”—too rare to merit funding.

Galas left Chiroscience soon after the Geron deal. In 1999, before the bubble burst and biotech stocks collapsed, Chiroscience merged with Celltech, another British firm. Then Celltech Chiroscience was bought by an outfit called Minerva. I think of Ginger’s gene as a pea in a shell game, hidden today beneath one company or another. I gave up trying to follow it.

But investments are flowing again into biotechnology; a number of new firms pursue antiaging drugs. The hopefully named start-ups are Elixir, LifeGen, Chronogen, GeroTech, and Juvenon, just to name a few, each having a proprietary target within the matrix of the cell. The buzz about the Werner gene seems a lifetime ago.

Ginger contracted gangrene in her left foot. Her leg had to be amputated between the ankle and knee. Although fitted for a prosthesis, she could not wear it until the wound from her surgery healed. And the wound, naturally, persisted.

A year later the doctors gave up on her right foot, and it, too, was taken off. Her left leg was ready for the artificial foot, but when I spoke with her last, Ginger was still waiting for the right leg to heal. She was in a nursing home. Her husband came to see her every evening.

“I’ll be up and about on my walker,” she promised. “I told Tommy I would.” Her voice sounded strong. “A lot of other people are worse off than I am.”

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