The walking dream is of a dead city.
It comes upon me when I forget where the car is parked, or to pick up milk along with the bread, or that one of the greatest female impersonators of our time is also named Charles Pierce. I can taste the sour rain. I can feel the gritty wind on my face. I can see smoke rising from faceless buildings, flattening itself into bleak, lowering clouds. I can smell fire on damp wood, far away. I am awake, but I am back in the country of my disease, and the walking dream is of a dead city.
When I feel the walking dream coming, I remember. I remember everything. I remember anything. I do not believe in trivia because I do not believe that anything you can remember is trivial—not when you’ve seen memory go cold and dead. Why do you know stuff like that? some people ask me when I dredge up some obscure fact, and I smile, and I do not tell them that I know stuff like that because not to know it is, for me, to begin to die, piecemeal, a fact at a time. So I remember things, and I do not look these things up. Honest. And, sometimes, the walking dream goes away.
I remember that Hubert Humphrey’s middle name was Horatio.
I remember that John Paul Jones’s ship was called the Bon Homme Richard.
I remember that Cerberus was the three-headed dog that guarded the entrance to Hades.
I remember that my grandmother’s maiden name was Lynch.
What if, one day, I can’t remember my son any more than my father could remember me? And what if, one day, my daughter can’t remember her father any more than she can remember her children?
She had four sons and a daughter. One of her sons was my father, John. He died, in 1989, of pneumonia brought on because he had Alzheimer’s disease, and the disease had made him forget how to swallow, so he breathed in his food and it eventually killed him. Since then two of his brothers have developed Alzheimer’s and died. The oldest, Thomas, was a superbly educated priest, a doctor of sacred theology. One day Alzheimer’s made him forget how to stand up. The youngest, James, was a physician who’d worked his way through Georgetown University School of Medicine during World War II, breaking codes for the FBI. One day Alzheimer’s made him forget that he should not try to walk twenty-five miles into Boston, so his family secured the house to keep him from doing that. One brother is still alive. Michael is a Jesuit priest. At his youngest brother’s funeral Mass, Michael lost track of the ritual, turning left once when he should have turned right, nearly colliding with another priest. He is one of 4 million Americans with a disease that costs the country $80 billion a year. He lives mostly in bed now, at a place called the Campion Health Center, in a nursing pavilion they named for him last June.
There were four brothers. All of them developed Alzheimer’s disease. There is one sister, and she is beginning to forget things, and we are worried about her driving. I am 41, the oldest of the next generation. Sometimes, at night, I will walk down the hallway and look at my son as he sleeps. Brendan has the line of his grandfather’s jaw. Sometimes, in the morning, I will hold my daughter. Molly has the round, full face of a farm girl from the Derrynasaggarts, whence a woman once came to America to have five children, four boys and a girl. What if, one day, I can’t remember my son any more than my father could remember me? And what if, one day, my daughter can’t remember her father any more than she can remember her children? The delicate chain of memory crumbles, link by link, until there is nothing left. The family cannot continue if there is no common history, no shared memory. We become lost. We become random. In those moments, in the dark of the hallway while my children sleep, I again see the shattered city.
One night in 1982, drunk as an owl on Jameson’s good product, I called the woman whom I had yet to marry. A dying newspaper in Baltimore had offered to make me its Jimmy Breslin, heady stuff for a 27-year-old working for sweatshop wages in what was still known here and there as the “underground” press. It sounded like a good deal, until I thought about my father, who was 66 then, and how strangely he had been speaking, in roundabout sentences that led him back to exactly where he had begun without proceeding much of anywhere at all. Of course, this was never talked about around the house.
In my family, in personal matters like disease, truth was considered little more than an occasional nuisance. All conversation ran on pretense, and we were very good at it. I learned entirely on my own that it was important to remember the truth about things, and the value of remembering is part of why I do what I do.
“I can’t take the job,” I said. “There is something wrong with my father’s brain.” I was crying, pounding at the wall of my apartment. I was spinning into savage incoherency, careering toward the kind of truth I had been raised to ignore. I hung up the phone and collapsed onto the sofa until winter sunlight woke me like a hammer in the morning.
A week or so later, after I’d turned down the chance to be the Jimmy Breslin of Baltimore, I again called the woman I had not yet married. It wasn’t much of a job, I told her. The money wasn’t great, and the newspaper was dying, and I couldn’t write there the way I could write for the alternative press. And my father was fine. No, really. He was. I had buried it all, the way I’d been raised to bury such things. It was how I lived my life for a very long time. Until now, when men in lab coats have come to chase me right up the one dark, forbidden tree in the Potemkin Eden of my childhood.
Under a microscope, the human gene looks very much like a child’s xylophone, with a tiny, individual chime for each separate note. They are all over it now in laboratories in Washington state and Boston, in Durham, North Carolina, and Worcester, Massachusetts, where my grandmother came to live and raise her five children, four boys and a girl, three of whom have died of the same disease, a single note, ringing in dirge-like carillon from Gregor Mendel’s xylophone to the men and women who have come to listen for it.
I can know how likely I am to develop one form of Alzheimer’s or another. Whether or not I choose to possess that knowledge is a decision I will have to make, a decision between the imperatives of the way I was raised and the imperatives of what I have become.
They are quite a group, these genome cowboys, descended from the mad monk Mendel with his damned peas, now way out on the permissible frontiers of science. They have identified genes linked to Alzheimer’s disease (AD) on four of the twenty-three pairs of human chromosomes. Chromosomes 1, 14 and 21 each carry a gene linked to three varieties of early-onset AD, which manifests symptoms in its victims before the age of 60. On chromosome 19 is a gene involved in the more common late-onset form of the disease. They are making headlong progress now, mapping the genetic structure of the entire human species. Why we are what we are. Why we do what we do. Why we drink or fight or steal. Why some of us get Huntington’s disease and die before we are 50. Why some of us lose ourselves and all around us, folding entire lifetimes into gummy tangles deep within the brain. Why some of us walk around, shipping toward middle age, haunted by lost car keys, set adrift by a neglected phone message, terrified when the right word won’t come.
I can know how likely I am to develop one form of Alzheimer’s or another. Whether or not I choose to possess that knowledge is a decision I will have to make, a decision between the imperatives of the way I was raised and the imperatives of what I have become. The knowledge is there in laboratories and in clinics, in the heedless pursuit of all the scientists. It is out there if I want it, right at my fingertips, Eve’s ancient temptation. It is a decision my father never had. I can walk, eyes open, following new maps, into the ruined city in the country of my disease.
We have a picture of my father when he was very young standing in a sailor suit with a headful of unruly curls. His maiden aunts made him wear his hair like that, and he used to say that he joined the navy and fought in World War II just so he’d never have to wear his hair that way again. My father hated that haircut until the day he couldn’t remember it anymore.
In the picture, he is a dead ringer for his first grandchild. Out of the depths of his disease, he was fiercely protective of Brendan. One day Brendan toddled too close to the cellar stairs. “Danger,” my father called out, over and over again. “Danger, danger.” He shouted it for a very long time, and then he went into himself again, his eyes blank as slate.
Another day he looked at his first grandchild, who looked so much like my father had back when he was tiny and at the mercy of maiden aunts, and my father complimented me on what a nice little dog I had. And I saw the ruined city as if from above, all its history burned away and gone.
It doesn’t look like a place of revolution. The pine trees along Research Drive on the campus of Duke University, in Durham, drip sweetly from an early rain. The Joseph and Kathleen Bryan Alzheimer’s Disease Research Center is tucked away at the end of a long driveway cut between the placid pines. It is not the kind of place where you expect to find more than seventy years of conventional wisdom thrown up in the air.
In 1907 a German doctor named Alois Alzheimer delivered a brief paper concerning the case of a 51-year-old woman afflicted with what he called “presenile dementia.” The woman’s recent memory was severely impaired, and her language skills had deteriorated markedly. Almost five years later, the woman died. Upon examining her brain, Alzheimer discovered it was a mass of plaques and tangles surrounded by clumps of dead or dying brain cells. The plaques and tangles contained a substance unknown to Alzheimer or his colleagues but which, long after Alzheimer’s name had been attached to the disease, ultimately was identified as a protein called beta-amyloid. Much of the subsequent research—including the latest genetic studies—has been focused on the role beta-amyloid plays in causing Alzheimer’s disease. In 1992, however, neurologist Allen Roses, from quiet little Research Drive, kicked over the entire field.
Roses claimed that he had identified a gene on chromosome 19 that predisposed people to late-onset Alzheimer’s, which very likely is the form that killed my father and two of his brothers, and that is killing my uncle today. Moreover, Roses claimed that the importance of beta-amyloid may well have been exaggerated, touching off a debate that rages to this day.
“I delivered a paper, and nobody thought it meant anything,” Roses recalls. “Then I went out into the hallway and started arguing with everyone, and a guy from The Wall Street Journal went around and talked to all the people I was fighting with.”
Roses is an ebullient, combative sort, with a decidedly roguish reputation in the staid Duke academic community. The son of a wholesale candy merchant from Paterson, New Jersey, Roses came to study Alzheimer’s through his work as a genetic researcher. He was aided throughout by his wife, Ann Saunders, a molecular geneticist, whom Roses met when they were both moonlighting as aerobics instructors up the road from Research Drive. “There are hundreds of people that I’ve met who give me the same story that you do,” Roses explains. “They talk about multiple members of their family. Geneticists say that’s an aggregation of a common disease.”
It is Roses’s contention that Alzheimer’s disease is a function of aging and that the only variable is when the disease occurs. “If everybody lived to be 130,” he says, “we’d all get Alzheimer’s.” After spending thirteen years studying hundreds of people from dozens of families in which more than one person was afflicted with AD, Roses and his team concentrated on a gene, APOE, involved with the production of a protein called apolipoprotein E, which carries cholesterol through the bloodstream.
The APOE gene comes in three types. Roses maintains that one of them, called APOE4, binds unusually well with beta-amyloid and forms the deposits on the surface of the brain called plaques. Ultimately, Roses not only minimized the role of beta-amyloid but also dismissed the characteristic plaques as mere markers of where the disease has been.
“If I take you to Japan,” Roses says, “and we go into a Shinto cemetery, and you see these massive things with candles and bamboo and you know you’re in a cemetery, and then I send you to Dublin, and you see these big granite slabs, you still know you’re in a cemetery. The markers are there, but nobody ever blamed the death of the people on those things.
“If you believe that amyloid metabolism is the be-all and the end-all, then you interpret the gene with regard to your preconceived notion. So you write erudite papers saying that APOE4 causes more amyloid to form, which it does, and that’s why you see amyloid and people die, but it doesn’t cause the disease.”
A great roar erupted in the Alzheimer’s-research community—to some, Roses’s assertion seemed tantamount to questioning the role of viruses in the common cold—but now Roses’s findings have been verified in more than one hundred laboratories around the world, and his work is considered to be a significant breakthrough even by many of its severest critics.
A test exists to determine the presence of the APOE4 gene. One company even began marketing such a test in the initial burst of publicity that surrounded Roses’s discovery. The test, however, verifies only that a person could be at a greater risk of developing AD in the future.
“Look,” Roses says, “I know that APOE is the relevant gene in every population in the world that lives long enough to get Alzheimer’s disease. The problem is that, unlike with some other diseases, we can’t predict who or when, even with APOE4. All we can say is that you might be at a higher risk. People hear that and say, ‘What the hell? Am I going to get it or not? And when?’”
It is a mad, blind walk through the conditional voice. Outside Roses’s laboratory, under the sweet and placid pines, I sit in my car and think through the elusive probabilities: If I take the test and find that I have the gene, I’ll know that I’m at a higher risk of developing the disease if I manage to live as long as my father and uncles. And then what? Do I set my affairs in order just because I have a gene that might cause me to get a disease if I get to 65? Keep the old genotype secret so that the bean counters at the insurance companies don’t begin to work the odds in their favor? Live my life on a bet to show? The trees drip on my car as I pull out of Research Drive on the campus of Duke University, which was named for the family that produced Angier Biddle Duke, who was chief of protocol in the Kennedy administration. I remembered that. I didn’t have to look it up.
In 1984, while my father was clearly failing and I was pretending out of long practice not to notice, my wife and I watched the first debate between Walter Mondale and Ronald Reagan. Reagan was a mess, flustered and confused, and my wife and I exchanged horrified glances.
Now Reagan is acknowledged to have Alzheimer’s, and his name is raising great gobs of research money, and some Secret Service men are being trained as caregivers in the way that hundreds of spouses, children and daughters-in-law have had to learn. How to speak slowly and quietly. How to make the house subtly safer. How not to run screaming into the street when you have to change the diaper on your son and your father in the same day. All the things I never learned because I was too stupid and scared, and because I began to hear a distant strain from Mendel’s xylophone that kept me staring at my children in the night.
Then one day last summer, Jesse Helms was fighting to kill the Ryan White bill that helps families deal with AIDS, and he fulminated beyond reason and decency, saying that too much money is spent fighting a disease spread by “disgusting, revolting conduct.” Within days, speaking at the National Press Club, Newt Gingrich sort of disagreed with Helms, in the course of which he cited Alzheimer’s as a disease that has been comparatively lost in the scramble after a way to combat the HIV virus. And I thought about how easy it has been for tinhorn politicians to divide us, class against class, or race against race. And it dawned on me that, with all the knowledge that will soon be at our disposal, there will be yet another way to polarize ourselves: Soon it will be disease against disease, grief against grief, gene against gene.
“Very soon,” says Dr. Rudolph Tanzi, “we’ve got to have a constitutional amendment that says you cannot discriminate against somebody based on their creed or their DNA sequence, period.” Tanzi is the director of the Genetics and Aging Unit at Massachusetts General Hospital, in Boston. He worked on the discovery of the gene for Huntington’s disease and on the search for three of the genes now connected to Alzheimer’s. Already, in a custody case in South Carolina, a court ordered a woman to take the test for Huntington’s disease. Children elsewhere have been denied medical coverage based on the genetic profiles of their parents.
“Race and color don’t cut it anymore,” says Tanzi. “We are born with the DNA sequences that we have. There is no choice. If we say all men are created equal, we have to go the full route. Race and color are not scientific terms.”
But they are political terms, and useful ones at that. And so will diseases be, and genes as well. It’s beginning now, one sickness at a time. They’re already there, hustling on the cheap, organizing in the precincts of the ruined city.
One day we finally got my father examined at the University of Massachusetts Medical Center, in Worcester. His neurologist was a man named Dr. Daniel Pollen, something of a specialist in Alzheimer’s disease, a gentle fellow with a persistent way of asking questions, a soft inquisitor. My wife went in with my father. I stayed outside because Mendel’s xylophone was playing in my head, and I was too selfish to hear anything else. After the examination, we met with Dan Pollen. My father was smiling and happy and utterly vacant. Outside I told my wife that I thought my father had done well.
She rounded on me. “Oh, absolutely,” she said. “He asked your father how many sons he had, and he said he had three: John, James and Henry.” I am an only child. John was my father’s name. James was one of his brothers. To this day, we wonder what fired through the plaques and tangles and produced a Henry. That night I had the walking dream, and I heard glass breaking.
A fatigued hulk on an exhausted street, the Fifth Avenue Building in Moline, Illinois, is dark and cool on a summer’s day. Upstairs Dr. Ben Williamson has tended to the practice of ophthalmology for more than fifty years. He is 84 now, sharp and clear and focused, and he vividly remembers the day in 1938 he brought his mother into the Fifth Avenue Building to see a doctor because Minnie Williamson had tried to pay a $3.50 grocery bill for the second time in a week. “She came home, and she told me, ‘I think I’m getting the family disease,’ ” Williamson says.
The remarkable thing about Hannah’s family is that they confronted the disease. They talked about it among themselves, assuming some sort of hereditary link long before Allen Roses, Rudy Tanzi or anyone else started looking for one.
Williamson’s maternal great-grandmother’s name was Hannah, and she lived in a Jewish community in the Ukraine just before the turn of the century. In middle age, she became something of a burden to the rest of her family. The younger children had to comb her hair because Hannah had forgotten how to do it herself. In the late 1890s, in the middle of the savage pogroms that followed the assassination of Czar Alexander II, Hannah died of respiratory failure. Later her grandchildren came to America and had their own children. One of them was Ben Williamson. Of Hannah’s descendants, twenty-six have developed a devastating form of early-onset Alzheimer’s disease, gradually fading away from their early forties on. Ben Williamson has lost his mother and three of his siblings. He sits in the cool old building, the evening shadows cutting across the floor and up the walls, and he talks about life in the country of his disease.
“It altered my life,” he muses. “By about 30, I’d made the decision not to get married. I almost came close to getting married, and I had to stop it because we might have had a child. That was when I was 45. I did get married when I was 55, when three people in my family had already died of Alzheimer’s. I thought I could take a chance then.
“My sister had three kids, and I love them all. I set up trust funds for them. They’re under the cloud now. One’s 47, one’s 50, and one’s 54. They didn’t ask for this stuff. I have a nephew who has an 8-year-old kid. Now, if you have only one child and the child develops Alzheimer’s, you haven’t increased it much. But if you have a dozen kids, you’re spreading it, and that’s crossing the line of reason.”
The remarkable thing about Hannah’s family is that they confronted the disease. They talked about it among themselves, assuming some sort of hereditary link long before Allen Roses, Rudy Tanzi or anyone else started looking for one. They made decisions, life-and-death decisions, based on true history and unflinching instinct. They recorded how Ben’s sister once insisted that squirrels were eating the wallpaper in her house. They set down in writing how Ben’s brother, a dermatologist, once began working on the feet of a patient who’d come in to have a cyst removed from his face. They wandered, bravely, blind, through the country of their disease, and they helped draw true charts for everyone who would have to follow them there.
Ben Williamson told me all of this, and it was then that he and I talked about the worst weekend of my life. In 1985 my father left the house for the grocery store and disappeared for three days. They had torn up Main Street in my hometown in Massachusetts. My father took the detour, kept heading due north and, finally out of gas, wound up in Montpelier, Vermont. He stood shivering in the rain, so incoherent that the cops who found him at first tossed him in the drunk tank.
We went to pick him up, I and my wife, who was pregnant at the time. He had been moved to a local mental-health facility and was happy to see us, although he had no clue who we were. We stayed in a motel that night, and he kept seeing his dead mother in the hallway. She was calling to him, and I thought I might eventually have to tackle him. I told Ben Williamson all of this, and I told him how, even after this episode, the family denial was so strong that nobody except my wife mentioned Alzheimer’s disease until Dan Pollen heard my father talk about his son Henry. We spoke about knowing and not knowing, and about the difference between not knowing and not wanting to know, and about the importance of remembering anyway the squirrels in the wallpaper and an old man shivering in the rain, so very far from home.
“I don’t think I’d have been tested,” says Ben Williamson. “If there was a treatment, well, that’d have been different. I mean, I figured at one point I was pretty safe. You keep busy. You don’t pay any attention to it. You concentrate on your work. That’s the only way to handle it. My sister was 28 when she told me one day, ‘I’m going to develop it,’ and she started crying. She had the feeling that she was going to get it, and she did.”
Outside, the sun falls behind the Mississippi River, sluggish and gummy in the midsummer heat. Down Fifth Avenue in Moline, the buildings are shuttered with plywood and there are only the shadows of letters left on the bricks from the signs of the old department stores. Bob Cousy almost played basketball here once, for the Tri-Cities Blackhawks, but the team folded and the Boston Celtics ultimately picked his name out of a hat owned by a man named Danny Biasone, who also invented the twenty-four-second clock. The Tri-Cities are Davenport, Rock Island and Moline. I remembered this, and I did not have to look it up.
My father died in yellow light, well after midnight.
He died in June of 1989, in a special Alzheimer’s unit, where he’d lived since the previous January, after he’d sat down in the middle of his front hallway and refused to stand up. I finally pried him out of the house where he’d lived since 1951, the house in which I had grown up, the house I had learned to hate because it was sour and malignant with disease and denial, and I was sick to my soul of them both.
During his final two weeks, I spent more time with him than I’d spent with him throughout most of his illness, because I’d been scared and selfish, and because the walking dream had come upon me too often. Now, though, as he died, we talked. I talked, and I think he listened. We talked about Sugar Ray Robinson, his favorite fighter, who’d died of an Alzheimer’s that probably had more to do with Gene Fullmer than Gregor Mendel. While I talked about Sugar Ray, my father squeezed my hand.
On the morning of the day before he died, his brother Michael came to give him the last rites of the Roman Catholic Church. Michael said them in the old Latin of what used to be called extreme unction in the days before the banjo Mass.
“Benedicat vos,” said my uncle Michael.
My father raised both hands and, torturously, as though reaching for something beyond his grasp, he put his palms together.
“Pattis, et Filii, et Spintus Sancti,” said my uncle Michael.
My father dropped his hands. He died very early the next morning.
There was a single yellow bulb above his head, the only light in the room. I was sleeping in a chair next to the bed, and the bustling of nurses woke me. I kissed him, once, on the forehead. And they brought the sheet up over his face. I waited for the undertaker, and I thought about how he’d brought his hands together on that final morning. I closed my eyes and saw the ruined city, bathed in gypsy moonlight.
Introibo ad altare Dei.
To God, who gives joy to my youth.
What is left of my father is in a small black case in Dan Pollen’s lab in Worcester. The case folds in the middle, and it looks a little like a backgammon set. It contains slides of material from my father’s brain taken at autopsy. I sit with Carol Lippa, a neuropathologist, and she puts the slides into a microscope that sends the images to a television screen in front of me. The matter on the slides is tinted orange so that the progress of the disease can be more readily seen.
Pollen’s laboratory has become central to genetic research into Alzheimer’s. In 1985 one of Ben Williamson’s relatives was diagnosed by Pollen, and the new patient brought with him the family’s detailed records, a collective pedigree of the disease as compiled through the years by Hannah’s descendants. A precise map of a suspect population is a genetic researcher’s fondest wish. At the time, Pollen was working with Peter St. George-Hyslop, a neurologist and geneticist, who, based on the data supplied to him by Pollen, announced last June that a rare mutation on a gene on chromosome 14 accounted for most of the early-onset cases, including those in Ben Williamson’s family. Each child born to a parent with the mutant gene stands a fifty-fifty chance of carrying the mutation. Two months later, Rudy Tanzi and molecular geneticist Gerard Schellenberg, as well as Hyslop, announced that a gene on chromosome 1 is linked to the rest of the early-onset cases. As it turns out, when it comes to Mendel’s xylophone, the reclusive Peter St. George-Hyslop is Lionel Hampton.
The data all came from little black cases like the one in which is contained what is left of my father. Dr. Lippa and I are looking at slides taken from my father’s frontal lobes, the area concerned with thinking and judgment and personality. (Usually, AD strikes most severely in the hippocampus, the region of the brain that deals with new memory.) The plaques show up as amorphous blotches; the tangles look almost like dark tadpoles. “Around there,” Lippa says, “you can see the dying neurons.” With its orange tint broken up by patches of black, the image looks like, of all things, an aerial view of a burning city—Dresden, perhaps, or Tokyo—a firestorm with wild swirls of dark smoke. It is the city of my walking dream, caught in its own death.
I think, Which of these blotches stole World War II from him? And where did his wedding day disappear? And in which of these dark areas did my entire life go to ashes for him until he had three sons, and their names were John, James and Henry? In the last three years of his life, I never felt real around him. I could feel myself fading within his mind. Where does existence go when memory fails? Like few other diseases, Alzheimer’s disappears its victims. If you have no memory, if the tendrils that bind you to yourself and your life curl up in the fire, you are not who you were, and neither is anyone else.
It’s possible that this is happening in my brain right now. If there is a familial link to the Alzheimer’s that killed my father and his brothers, it’s likely a late-onset form of the disease, which means that the most likely culprit is the APOE4 gene identified by Allen Roses. Perhaps it’s at work right now, toting along its load of beta-amyloid and taking away where I left the car keys and whether or not I was supposed to pick up milk with the bread. Or maybe I’ve just forgotten all that because it’s a hot day and I’m distracted.
I could find out. There are tests for all of them now, the genes on chromosomes 1, 14, 19 and 21. I choose not to be tested. In part this is because my genotype is nobody else’s damned business. I do not intend to hand over the fundaments of my being to the same insurance company that can’t keep my wife and daughter straight. However, I choose not to know for another reason: I have no idea what I’d do with the knowledge once I had it. The only thing a test can tell me is the odds that I might one day develop this disease. For example, if I have two copies of the APOE4 gene, I am eight times more likely than the average person is to develop late-onset Alzheimer’s by the time I’m 75, which is thirty-four years from now. Ben Williamson chose to be childless based on careful observation of his family’s unfolding tragedy. It was a good decision for him. I have a son with the line of his grandfather’s jaw and a daughter with the face of a Kerry woman, and I look at them in the night, and I decide that I don’t really need definite confirmation of a probability. As Dan Pollen once told me, quite merrily, as I was leaving his house: “The best thing you’ve got going for you is that you’re 41. Likely, you can give science twenty years to come up with something.” The genome cowboys seem to have the thing surrounded. I’ll leave it to them, for a while anyway, and I’ll live with the walking dream.
I say good-bye to Dr. Lippa, and I head up the hill to the parking garage. This is where I parked when I first brought my father to Pollen’s clinic, when I was still pretending that going to the grocery store and winding up in Vermont was perfectly appropriate behavior for the elderly. It is where I took my first steps into the country of my disease. I reach the second level of the parking garage.
I can’t find the car.
It is not there, and I know I left it there. I can taste the sour rain now, and I can feel the gritty wind. I go up one level, and I find the car. I sit there behind the wheel, lost in a fever of memory.
I remember that Gerald Ford’s real name was Leslie King.
I remember that Muddy Waters’s real name was McKinley Morganfield.
I remember that Alzheimer’s first name was Alois.
I remember all of this, and I do not have to look it up.