The Story of My Father by Sue Miller Page B

plaques—senile plaques, or SPs—are extracellular deposits of aggregated proteins, an abnormal and complex material, waxy and translucent, primarily composed of beta-amyloid. Normally the protein is benign and soluble. In the course of Alzheimer’s disease there is an increase in its amount and also a change in its form, so that it becomes fibrous and toxic to neurons.
    When you look at microscopic pictures of these plaques and tangles, stained, there’s a Jackson Pollock quality to their appearance. The tangles appear the darker of the two, like small distinct blobs of paint thrown hard at the canvas—so hard that often a thin tail is left streaking out behind. The plaques are bigger, more amorphous blobs than the tangles, with less-well-defined edges.
    There are smaller dark squiggles visible under the microscope too, called, in this world, “curly fibers.” They are threads made of swollen synaptic nerve fibers—nerve endings normally involved in the passage of electrical impulses—which have now become fibrillar: fibrous. In the house I grew up in there was a linoleum on the kitchen floor that, though more riotous in color than any of the available stains used to reveal these structures, bore some resemblance in its splattered pattern to this picture of disease.
    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