When a friend handed her the book “Still Alice,” Emily Greene knew the subject was Alzheimer’s disease. But much of the book, the first novel by Harvard-trained neuroscientist Lisa Genova, came as a surprise to Greene.
“Like many others, I thought Alzheimer’s was a disease of old age,’’ said Greene, a nutritional counselor and mother of two in Milton. “It was shocking to discover that Genova’s focus was on a brilliant, capable, physically active wife and mother, who is at the height of her career, and peak of physical health.”
In the story, Dr. Alice Howland is 50-year-old psycholinguist and professor of psychology at Harvard University. She has a successful husband and three grown children, and loves her busy academic life.
When Alice begins to notice she’s experiencing small frequent episodes of forgetfulness, she chalks it up to stress, sleep deprivation, and menopause. However, when she finds herself completely lost just two blocks from home, she knows that something is terribly wrong.
After Alice is diagnosed with early-onset Alzheimers, she quickly begins losing her short-term memory, cognition, and language ability. Now, she must completely reevaluate her relationship with her biologist husband, her expectations of her children, and her ideas about herself. She ponders whether she has worth in this world — whether she is “still Alice” — and if so, whether her new life is worth living.
According to Greene, “The early chapters of the book may be very unnerving for readers over 40,” who may worry that their small memory lapses from time to time are symptoms of something more serious.”
In that sense, Genova’s expertise in neuroscience provides reassurance about differences between normal and clinically signifcant short- term memory problems.
But Greene adds that the novel is in no way a medical textbook, but rather a personal narrative over two years — albeit increasingly disjointed — as the illness progresses from Alice’s first attempts to hide her failing memory to the final scene, in which she can’t recognize her daughter and grandchild.
While Greene feared the novel would be too depressing, she found “The book is moving, but not overly sentimental. It opens dialogue on serious issues such as to the value of pushing for genetic testing of the next generation.”
An equally important question, she added, is the quality of life for terminally ill patients. “Even when lives narrow and become so horribly constricted by Alzheimer’s disease, Genova presents the idea that the lives of patients like Alice still have value and meaning,” Greene said.
At one point in the book, Alice considers suicide when she realizes how serious her condition is.
“Although I was shocked, this made sense for a woman like Alice, whose disease strikes mid-career, and for whom so much of her identity is wrapped up in her intellectual gifts and superior memory,” Greene said.
But Genova challenges our culturally preconceived notions of “quality of life” and shows us that such patients can still fully experience the love of family even when they have deteriorated beyond what many would see as a happy and worthwhile life.
“For me, the climax of the novel comes 14 months after Alice’s diagnosis, when she manages to deliver a speech at an Annual Dementia Care Conference and says, ‘Being diagnosed with Alzheimer’s is like being branded with a Scarlet A . . . but I am not what I say, or what I do, or what I remember . . . I am more than that, so don’t write us off.’ ”
As a psychologist, I see that trying to maintain hope is one of the most difficult things for Alzheimer’s patients and their families struggling with this relentless disease.
However, new research coming out of the lab of D. Martin Watterson at Northwestern University’s Feinberg School of Medicine provides hope. Watterson has identified a new class of experimental drug that shows great promise in targeting a brain enzyme to prevent early memory loss. Called MW108, the drug reduces the activity of the enzyme that is overactivated during Alzheimer’s and is considered a contributor to brain inflammation and neuron malfunction.
Changes in the brain actually start occurring 10 to 15 years before memory problems become apparent.
MW108 halted memory loss and fixed damaged communication among brain cells in a mouse with Alzheimer’s disease. Watterson wrote: “It’s possible this class of drugs could be given to humans early on to arrest beginning memory failure.”
With such remedies still distant, Greene said, “It may seem trite; however, until there is a cure, living each day to its fullest is really the best medicine.”