The Story of My Father (8 page)

The combined effect of the growth of these amyloid deposits and the transformation of normal brain cells into neurofibrillary tangles is simply to stop brain activity in the damaged areas. Where those blobs and tangles occur, signals fizzle out in the brain, unable to pass through the fibrous thicket, the unresponsive plaque. Events that occur and are seen cannot “get across” to be apprehended, to be recorded in memory. Signals from the body—a full bladder, hunger—are no longer able to trigger the socially appropriate response—or any other response. Things that are seen cannot be recognized or categorized correctly.

The typical age of perceptible onset is sometime in the victim’s seventies, but it can be much earlier; and the fact is that neurofibrillary tangles have been found in brains as young as twenty, long before symptoms are in evidence. It seems possible, then, that Alzheimer’s is a lifelong disease whose expression in dementia is simply the closing episode, a kind of crossing the threshold for the long-failing brain, the last step that finally makes clear what the earlier steps have meant.

A few years ago there was a highly speculative research project done using writing samples collected early in life from nuns whose histories through old age and death were known and whose lives, because they were all in the same convent, were presumably controlled after the age of twenty or so for many variables. The nuns whose writing samples were more elemental—whose thinking, as expressed in the writing, was more reductive—had a very high incidence of later mental impairment or posthumously diagnosed Alzheimer’s disease. But both “high idea density” and greater grammatical complexity were consistently characteristic of the writing samples of nuns at age twenty-two who would still be mentally intact fifty-eight years later.

One of the possible implications of this study seems to be that we may gradually learn to recognize other markers of the disease earlier than the now-familiar dementia; that there will be aspects of the personality or behaviors we think of now as completely normal that we will come to understand as connected to the illness and symptomatic of it.

After I read this article, I spent a few days looking back at my father’s younger self and wondering whether some aspects of his personality that seemed so essentially
who he was
might really have been the disease expressing itself. Or, alternatively, whether the disease was so entwined with who he was, even early on, as to be part of him. Perhaps it could account for his even temperament, I thought, his imperviousness to mayhem, noise. Even some of what gave him sex appeal to my mother might have been connected to it—his abstractedness, his distractedness, which she saw as evidence of his intellectual superiority, his fineness as a person.

I thought too about the dynamics between them, and what their deeper meaning might be if he had the disease much earlier than we thought. Because it was in my mother’s nature to try to absorb other people, to yearn for a kind of merging with those she loved intensely. All her life she threw herself against what she saw as the mystery of my father, the self he was hiding from her. His unavailability to her kept her pursuing him, sometimes desperately, sometimes angrily, sometimes adoringly. Perhaps then it was in part his Alzheimer’s-ness she fell in love with. Perhaps what she was really engaged with in her lifelong struggle was his disease. And perhaps, then, her struggle kept him attached to life, working to resist his illness, to keep certain synapses firing longer than they might have otherwise. There are, in the brain, chemical substances called neurotransmitters that open channels between nerve cells, allowing for the possibilities of what are called “action potentials,” the passing of impulses between the cells—the source of all thought and behavior. One of these neurotransmitters, serotonin, has been made famous by Prozac. Another one, which is notably diminished in the brains of people with Alzheimer’s disease, is acetylcholine. This diminishment is thought to be partly responsible for the diminished brain activity of Alzheimer’s patients. In fact, several of the few therapies used now for Alzheimer’s patients are based in finding ways to increase or replace lost acetylcholine.

It’s funny to me to think of my mother as a chemical force in this sense, laying siege to my father’s brain, insisting, “Fire, damn you! Fire!” And perhaps even having some success: the structures of the brain are changing constantly in response to the use of sensory pathways. We
can
affect the microscopic shape of our brains with what we study, what we learn, what we do. The brain of a musician is different from the brain of a quarterback, in part because they have repeatedly stimulated quite different pathways in quite different ways. When my mother wailed to my father, “I would like you
just once, just once
to try and remember what it was that attracted you to me in the first place!” maybe she was really insisting that he lay down some new neural pathways, just for her. And if he did it, and did it often enough, maybe that added density helped him resist AD a little longer than he might have otherwise.

My mother may have made a kind of invisible dent in my father after all.

There are researchers, though, who believe we are all pre-Alzheimer’s. They point to the occurrence of plaques and tangles in the brains of normal, sane older people as evidence for this. Of course, in the nonsymptomatic brain they are smaller in number and more confined; but if these people lived long enough, the theory goes—and maybe some of them would have to live 120, 130, or 140 years—their brains too would gradually be destroyed by these same processes.
When
you get the disease,
how fast
it progresses: these are a matter of luck—or of certain risk factors. But these researchers believe that the increase in the percentage of people with Alzheimer’s as you look at each decade of old age is just the beginning of a steady line on a chart that would rise inevitably to 100 percent if we prolonged life more or less indefinitely—if we “saved” people from all the other ways of dying.

In this context, what sense can be made of the differences drawn among the nuns’ writing samples? Or of my notion that perhaps I could have been seeing the disease in my father at age forty, or forty-five, or fifty?

There will be answers to some of the questions and conflicts raised by these theories in years to come—and to many others. Nearly every day now there is new information about the disease and about the brain generally. The development of extraordinary new technologies for looking at what goes on in the living brains of normal people as well as in those with organic brain diseases like schizophrenia has already explained a great deal about what the physiological bases are for various behaviors and for various “misunderstandings” of the universe: hallucinations, delusions. Other research will lead to a clearer explanation of what causes illnesses such as Alzheimer’s disease. For now we can say that the specific history of each Alzheimer’s patient—when he or she fails and at what—offers a unique map, if we care to draw it, of what is happening in that patient’s brain, where it is happening, and how fast cells are dying.

Phrenology is a curious theory, curious in some measure because it anticipated crudely the truth that specialized parts of the brain control, in connection with other parts, specific aspects of human thought and behavior. Phrenology erred in seeing each of these areas, or centers, as utterly independent of the others and as reflecting certain isolable human
traits:
intelligence, “amativeness,” wit, conscientiousness, and so on. Proponents of phrenology also believed, erroneously, that the more highly developed a faculty was, the larger the center of that faculty in the head would be—skull included. Thus you could understand something about a person by running your hand over his head, recording with your fingertips those enlarged areas on the skull—the phrenological “bumps.”

Now surely not many people took all of this as factually, literally true. But these ideas, like those of psychiatry, achieved a kind of currency anyway in the culture at large, became part of the general vocabulary, part of the way you could think about what made people as they were. We can see them emerge in nineteenth-century literature, just as ideas based on Freudian psychology have in twentieth-century literature. Here is Poe’s description of the uselessly brilliant, neurasthenic Roderick Usher.

A cadaverousness of complexion; an eye large, liquid, and luminous beyond comparison; lips somewhat thin and very pallid, but of a surpassingly beautiful curve; a nose of a delicate Hebrew model, but with a breadth of nostril unusual in similar formations; a finely moulded chin, speaking, in its want of prominence, of a want of moral energy . . . these features, with an inordinate expansion above the regions of the temple, made up altogether a countenance not easily to be forgotten.

My father, too, had a high forehead and an open intellectual liveliness in his face until AD clouded his eyes and slackened his mouth. If I were a phrenologist, I might have theorized that he was governed by intelligence, specifically
causality, comparison, eventuality, time.
All these occur in the forehead and temples, so pronounced and well shaped in my father.

But new research tells us that even in the beetle-browed it isn’t the size of the skull, much less of the brain or any part of the brain, that matters. Rather it’s the speed, the efficiency, and the density of neural pathways, those developed networks of connections between nerve cells in the brain. It may be for this reason that low education levels are a risk factor for AD— because education increases the density of neural pathways— “works” the brain, as it were. And at least one theory proposes that with equal numbers of tangles and plaques, the educated brain simply has more alternative options left for neuronal firing than the uneducated one—more ways for thought processes still to take place. “Neurocognitive reserve,” it’s called. Take twenty pathways away, and the educated person still has another twenty, carefully developed by reading, by study, by making the brain perform certain tasks.

This may be, too, why smoking has been seen in some studies as a
negative
risk factor: nicotine activates acetylcholine receptors in the brain and thus indirectly facilitates and speeds the passing of impulses between nerve cells.

There are risk factors and negative risk factors. There’s a genetic component to at least some forms of the disease. And the threshold for its appearance symptomatically may vary with different histories, different brains, different lives, different ages. But when enough of the neurons that compose the critical pathways slow down in their activity, shrink, or die, then even the person with the most elegant brow, with the highest level of education, with the most acetylcholine zinging around in his brain experiences changes in his behavior. And in these changes in behavior, the amazing specificity of the parts of the brain reveals itself.

My father never lost the ability to recall the names of those who had been important to him or to remember in some essential way who they were. Well after he’d been diagnosed, I took him to a picnic in the summer town we went to in New Hampshire, and his dear friend Peggy Grant came up to shake his hand, telling him her name as she did so. He commented on it afterward, wondering why she’d done that—because he didn’t need her kind reminder. We’d spoken of Peggy often, and he had mentioned looking forward to seeing her that day. Similarly I could name his nieces and nephews, his colleagues from Princeton or the University of Chicago, his friends, my siblings, his grandchildren—and he knew, he always knew us all.

He had trouble, though, with new names. He called the woman who came in to help him get dressed and shaved and ready to greet the day by a variety of names: Alice, Arlette, or sometimes Jonathan or “that boy”—wrong category, Dad. Her name was Marlene, and he was very fond of her, but there was no way for him to retain this little fact.

Why should this have been?

It happened because the part of his brain whose function was to transfer new information into memory, the hippocampus, was being destroyed by Alzheimer’s disease. New names, new skills—how to open the door on
my
car, for instance, or how to work the remote controls for a television—these couldn’t be retained for more than a few days because they couldn’t get past the hippocampus into permanent “storage” in other parts of the brain.

He began to have trouble, too, with ordinary nouns, and his speech became more and more riddled with substitutions. And of course it turns out there’s a place in the brain specific to nouns, to naming things. Typically, when this region is damaged, the person sounds much the same, his rhythms of speech are intact, but he uses pronouns instead of nouns, and generic words or categories instead of instances. When my brother and his son and his son’s beautiful Latina fiancée visited Dad one day, he remembered the visit to report to me and he remembered them, but he said Bob and Marc had come to call with “a Chinese man.”

Sometimes he’d substitute the name of part of something for the whole. I remember my confusion when he was trying to tell me something was wrong with his rocking chair, because he kept calling it “the cloth” or “the weaving.” When he finally retrieved the color correctly—“the green weaving”—I suddenly recognized that the reference was to his old Victorian rocker with the worn green velvet cover.

Categories and names of relationships flummoxed him. When a polite, mentally intact resident asked, “Oh, is this your daughter?” he answered, “No, I’m his . . . mother.”

Still, he had my name. He could remember my mother by her name. And he could remember her—not always whether she was dead or alive, but
her—
her being, her essence. Stories about her, or about others who had been dear to him, could still light his face and make him laugh. I took pride in this. “He never didn’t know me,” I say now when people say it must have been terrible. And that is almost true. There were seconds or minutes one time when he seemed not to know who I was, but he always greeted me warmly when I first arrived; he always understood, in the first flood of pleasure, our relation to each other. I knew other people whose parent or spouse had lost this part of memory nearer the beginning of the illness. I knew how painful, how isolating that was, and my gratitude that this part of his brain was left to Dad—to all of us—was deep.