The Obama administration has announced a bold research program to test whether a
drug can prevent the onset of Alzheimer’s disease well before any symptoms
appear. It is a long shot, but the payoff could be huge.
Currently, there is no cure for Alzheimer’s, which steadily robs patients of
their memory, followed by full-blown dementia. There is also no diagnostic test
to identify who has it, and no treatment to slow patients’ deterioration for
more than a few months.
While work continues on those fronts, the new clinical trial will test whether
the drug, Crenezumab, made by Genentech, can prevent the disease in a group of
people whose genetic heritage guarantees that they will develop it. If the drug
successfully prevents the loss of mental capacities as measured by a sensitive
new cognitive test there is hope — but no guarantee — that it could do the same
for members of the general public. As Pam Belluck described in The Times last
week, the trial will focus on members of an extended family in Colombia who
carry a rare genetic mutation that causes them to develop Alzheimer’s early in
life. They typically experience cognitive impairment at about age 45 and
dementia by 51. The trial will also include a smaller number of individuals in
the United States with the same genetic mutation.
Instead of recruiting thousands of volunteers and following them for an extended
period as in a customary prevention trial, the researchers in Colombia will give
the drug to only 100 people with the early-onset genetic mutation. They will
give placebos to another 100 people with the mutation and to 100 family members
who do not carry the deadly gene.
The study will cost more than $100 million and is being financed mostly by
Genentech, buttressed by $16 million from the National Institutes of Health and
$15 million raised by the Banner Alzheimer’s Institute in Phoenix, which is
leading the study.
The prevailing, but not universally accepted, hypothesis is that amyloid plaques
in the brain play a major role in causing Alzheimer’s. Crenezumab attacks the
formation of such plaques, apparently by binding to amyloid proteins and
clearing them from the brain. If the drug fails to work, the trial will probably
demolish the amyloid hypothesis and set researchers scrambling to find other
targets to attack.
A prevention trial of a different drug that was also intended to slow formation
of amyloid plaques actually made patients’ symptoms worse, possibly because it
interfered with various other proteins needed by the brain. Researchers believe
that Crenezumab will be safer and more effective, but again there are no
guarantees. The risk is justified given that without the treatment the
recipients will inevitably get Alzheimer’s in the prime of their lives. The
truly big payoff will come if the drug succeeds in this group and lays the
groundwork for preventing or slowing the progress of Alzheimer’s that appears
late in life. The researchers will be gathering data on a variety of biomarkers
— glucose activity in the brain, shrinkage of the brain, certain proteins in
cerebral spinal fluid, for example — to see which if any are related to
preventing amyloid plaques and the loss of mental abilities.
If the drug prevents the deterioration of particular biomarkers and ultimately
sustains mental capacity, then the same markers might be useful in identifying
and treating older people likely to develop the disease. And federal regulators
might be willing to approve other prevention drugs based on their short-term
effects on biomarkers, speeding the conduct of clinical trials.
More than five million Americans currently have Alzheimer’s. Without an
effective preventive, the number will rise steadily as the population ages.
He threw away tax documents, got a ticket for trying to pass an ambulance and
bought stock in companies that were obviously in trouble. Once a good cook, he
burned every pot in the house. He became withdrawn and silent, and no longer
spoke to his wife over dinner. That same failure to communicate got him fired
from his job at a consulting firm.
By 2006, Michael French — a smart, good-natured, hardworking man — had become
someone his wife, Ruth, felt she hardly knew. Infuriated, she considered
divorce.
But in 2007, she found out what was wrong.
“I cried,” Mrs. French said. “I can’t tell you how much I cried, and how much I
apologized to him for every perceived wrong or misunderstanding.”
Mr. French, now 71, has frontotemporal dementia — a little-known, poorly
understood and frequently misdiagnosed group of brain diseases that eat away at
personality and language. Although it was first recognized more than 100 years
ago, there is still no cure or treatment, and patients survive an average of
only eight years after the diagnosis.
But recently, researchers have been making important discoveries about the
biochemical and genetic defects that cause some forms of the disease. And for
the first time, they have identified drugs that may be able to treat one of
those defects, the buildup of abnormal proteins in the brain. Tests in people,
the first ever such drug trials in this disease, could begin as soon as early
next year at the University of California, San Francisco.
“There’s really been an explosion related to the biology,” said Dr. Bruce L.
Miller, a professor of neurology and psychiatry there. “I think at least some
subtypes of frontotemporal dementia will be the first neurodegenerative diseases
we find a cure for.”
This disease is different from Alzheimer’s, the most common form of dementia.
But it is perhaps even more devastating, because it strikes younger people,
progresses faster and, unlike Alzheimer’s, does not attack memory at first but
begins with silence, apathy or bizarre personality changes. It is thought to
afflict at least 50,000 to 60,000 people in the United States.
The scientific findings in frontotemporal dementia may also reshape thinking
about the fundamental flaws involved in Alzheimer’s disease.
“I think the way dementia is going in general now is to realize there are many
different subtypes,” Dr. Miller said, adding that what is now labeled
Alzheimer’s disease may actually turn out to include hundreds of different
illnesses.
Dementia is a formidable adversary, and the history of efforts to treat
Alzheimer’s has to temper any excitement about potential medicines for
frontotemporal disease. The drugs for Alzheimer’s have been a disappointment,
with just temporary effects on symptoms at best.
But even if treatments or cures for frontotemporal dementia do emerge, they will
almost certainly come too late for people with advanced cases, like Mr. French
or Richard Rainwater, a billionaire investor who learned in 2009 that he had
progressive supranuclear palsy, which some consider a form of frontotemporal
dementia. Mr. Rainwater and his family have donated more than $20 million to a
research consortium, but given that he has a rapidly progressive form, any
advances from the consortium may be more likely to help others than to save him.
Looking for Answers
Looking back, Mrs. French, who is 66 and lives in Manhattan, recalled episodes
of odd behavior over the years and realized that her husband’s mind had probably
begun to slip while he was in his 50s, at least a decade before the disease was
diagnosed. He had always changed jobs a lot. At the time she took it as a sign
of a stubborn personality, not of illness — and it is still not clear which it
was. He always wanted to do things his own way, and that did not sit well with
some bosses.
“I thought it was just Michael being Michael,” she said.
A friend described Mr. French as being unable to read the tea leaves, oblivious
of corporate politics. At one point Mrs. French even bought him a self-help
book. But he never changed.
And he always found another job, better than the one before. But things went
downhill in 2006.
“His immediate boss was so frustrated by him that she called up, and we were at
the dinner table, and I could hear her screaming,” Mrs. French said.
He was fired, and this time he did not find another job. At 66, he retired.
Soon after, because he had trouble speaking, he consulted a neurologist. When
they got the diagnosis, Mrs. French asked the doctor, “How do we treat it?”
“It’s brain atrophy,” he replied.
Her thoughts of divorce evaporated. Instead, she told her husband: “Whatever
happens, we will go through this together. I will be there.”
From then on, the silence at the dinner table no longer troubled her. It did not
seem personal anymore. He was not refusing to talk; he simply could not. Her
anger melted into sadness.
But sometimes she still blew her top. Once, she came home and found him at the
stove, seemingly unaware that his oven mitt was smoldering.
“I actually hit him a couple times out of frustration,” she said. What made her
lose control, she said, was a toxic mix of frustration and fear — fear of what
was happening to him, and fear that she would not know what to do, how to help.
No amount of information from his doctors could put her at ease.
“They can tell you everything that’s ever happened to anyone, but they can’t
tell you what’s going to happen to you,” she said.
The last five years have been wrenching and often lonely. Michael was the love
of her life. When she married him, her sister asked, “How does it feel to hit
the jackpot?” In more than 30 years of marriage, she never heard him say an
unkind word about anyone. He was an engineer, lectured at conventions, did
volunteer work, belonged to a history book club, ran marathons. Now he can no
longer speak, read, write or walk.
If there is comfort anywhere for Mrs. French, it is in knowing one thing: she
has kept her promise to be there.
The Science
Frontotemporal dementia, also called frontotemporal degeneration or Pick’s
disease, refers to a group of diseases that destroy nerve centers in the frontal
and temporal lobes — the home of decision-making, emotion, judgment, behavior
and language. Some forms of the disease also cause movement disorders.
Most cases occur sporadically, in people with no family history of the illness —
like Michael French — but a small percentage are inherited.
Patients generally receive from one to four misdiagnoses, and it may take years
to finally get the right answer. Mistaken diagnoses can include Alzheimer’s
disease, stroke, midlife crisis or psychiatric illnesses like depression,
bipolar disorder, post-traumatic stress or anxiety. Many relatives of patients
say doctors dismiss their reports of personality change. But it is real.
“They totally break down in their ability to connect with other people and care
about them,” Dr. Miller said.
There are eight subtypes of frontotemporal degeneration, sorted by the symptoms
they cause. Some affect behavior. Others, grouped under the heading primary
progressive aphasia, affect language. Still others affect movement, leading to
disorders that resemble Parkinson’s or Lou Gehrig’s disease (also called
amyotrophic lateral sclerosis or A.L.S.).
But patients may match more than one category, and the subtype may change as the
disease progresses.
“I see a lot who don’t present like the textbook,” said Dr. Edward Huey, an
assistant professor of psychiatry and neurology at Columbia University Medical
Center.
In most patients, MRI and other scans reveal shrinkage in the frontal and
temporal lobes, sometimes to a shocking degree.
“If I showed you more extreme cases, you could read it from across the room,”
Dr. Huey said.
He said researchers were using imaging to find out if specific symptoms could be
mapped to atrophy in certain spots.
“The frontal lobes are sort of the last frontier in the brain,” Dr. Huey said,
adding that the losses these patients suffer are helping researchers understand
more about what the frontal lobes do. As the brain atrophy progresses, Dr. Huey
said, patients “have pieces of psychiatric syndromes, but not the whole
syndrome.” For instance, they have compulsions, but not the usual accompaniment,
obsessions. So they may wash their hands over and over again, but not in a
worried or anxious way. Some lose their inhibitions and moral judgment.
Shoplifting is not uncommon. Many have the apathy and social disconnection that
usually go with depression, but they do not feel depressed.
“They’re not down, but they just don’t enjoy things as much as they used to,”
Dr. Huey said. “There appears to be a dysfunction in the reward circuit, where
activities that were rewarding and pleasurable no longer seem to be. These
patients lose themselves.”
Many seem to go on endless eating binges and gain weight. It is not clear why —
whether they are actually hungry or whether the eating is just another
compulsion. Some people with the illness shower repeatedly or check the mail 100
times a day. One possible reason, Dr. Huey said, is that “the part of the brain
that tells you, ‘No, that task is done,’ is gone.” Some patients collect things
— by the hundreds. A few have had bursts of creativity in music or painting,
possibly because other brain regions come to the fore as the frontal lobes
wither.
A Way of Life Cut Short
Long before her husband became ill, Mrs. French had a successful career in sales
and marketing for textile companies and ultimately became a vice president at
Liberty of London. But she gave it up in 1991 to do something she loved:
teaching English as a second language to adults. She was doing that work when
his condition was diagnosed.
One day, in a moment of inspiration, she asked her students if they knew the
traditional wedding vows in English. She began to recite them. At “for better,
for worse,” she choked up. Struggling to keep her composure, she quickly
finished and moved on to another subject.
After teaching, she would walk home through Central Park, and in the early days
of his illness Mr. French would often meet her halfway. She would see him
heading toward her, smiling and strikingly handsome. “When I look at Michael,
that’s what I see, that’s who he will always be to me.”
In 2007, Mrs. French joined a support group for caregivers of people with
frontotemporal dementia. Jill Goldman, a genetic counselor at Columbia
University Medical Center, said she started the group because patients’
relatives felt that they did not fit in at Alzheimer’s groups; their loved ones
were younger and often had bizarre behaviors that were nothing like Alzheimer’s.
“One of the things that goes first is insight,” Ms. Goldman said. “ ‘There’s
nothing wrong with me. Why can’t I do what I want to do?’ ”
Members of the group tell of loved ones who hug strangers, who fly into
terrifying rages and hit family members and health aides, or who pass their days
in silence cutting up newspapers or watching television. Patients are easily
taken in by financial scams that can cost families thousands of dollars. Often,
apathy sets in, and people once devoted to their families lose interest in
everyone, even their own children.
“My son and I look out the window and see my wife out there, stepping on leaves,
and we start to cry,” one member said.
Some have struggled with uncertain diagnoses because patients have symptoms of
both Alzheimer’s and frontotemporal disease. One wife described trips to
multiple doctors and inconclusive reports on PET scans and spinal taps. Should
she have taken her husband to the Mayo Clinic? She agonized over the idea that
he might have some illness other than frontotemporal dementia or Alzheimer’s,
something treatable, and that there might be some way to rescue him, to bring
him back.
Another said her husband, a judge who had always been mild-mannered and modest,
turned boastful and began talking to strangers in the street, making jokes at
the wrong time and falling for scams.
“He salutes every flag, closes every gate, kisses every hand,” she said.
Riding the bus in Manhattan, he will loudly announce, “I haven’t killed anybody
lately.” Not infrequently it gets him a seat. He can turn violent and has struck
a health aide with his cane.
“He’s just mean and nasty,” his wife said. “He was such a wonderful man. He’s
not a person anymore.”
Ms. Goldman provides stacks of business-size cards that spouses can hand out to
strangers in awkward situations.
“My husband has a terminal brain disease called frontotemporal dementia,” the
cards read. “Thank you for your understanding.”
Many find that friends and family pull away. Nearly all grapple with whether and
when to take away car keys, give drugs to blunt aggression, hire a health aide
or put the patient in a nursing home. One group member said, “The doctor told
me, ‘You’re taking good care of him, he’ll live a long time,’ and I said, ‘Why
is that a good thing?’ ”
Patients are hard to care for at home, and those who are young, strong and
aggressive are sometimes kicked out of nursing homes because they are seen as
posing a physical threat. But employers do not necessarily sympathize with
relatives called out of work in the middle of the day because a patient has
punched or shoved someone at the nursing home.
“My boss says, ‘You just have to deal with this better,’ ” one group member
said.
Another group member, a professor of psychotherapy and mental health counseling,
said she quit her job at the height of her career to take care of her partner
and after a few years became suicidal.
“Being a caregiver in this disease is a grieving process,” she said, “while the
person is still alive.”
Easing the Burden
Ruth and Michael French managed on their own until May 2009, when he fell down a
flight of stairs in their apartment building while she was at work. He fractured
his skull and came home in a wheelchair, so weak and frail that she hired an
aide to help take care of him.
Mrs. French is fine-boned and thin, and as her husband grew weaker, the physical
demands on her became daunting. Streets she had thought flat revealed themselves
to be hills once she found herself trying to push a 140-pound man in a
wheelchair. Potholes yawned like chasms. One night at home, after helping him
clean his teeth, she turned to put the toothbrush away, and in that moment he
fell into the bathtub. She was barely able to pull him up.
“I said, ‘Michael, now we’re at the point where we’re both at risk,’ ” she
recalled.
She injured her wrist, developed a stomach ulcer and lost so much weight that
people worried about her. Mr. French became incontinent, and she would sometimes
wake up in a pool of his urine. The health aide hurt her back lifting him.
“I heard myself say one day, ‘I would never want anybody to do for me what I’m
doing for Michael,’ ” Mrs. French said.
She had hoped to keep him at home until the end but knew it might not be
possible. “This thing is going to kill both of us, and I don’t know who’s going
first,” she told him.
In one way, she had an easier time than many other caregivers. Her husband never
turned hostile. He retained a sweetness, and an acceptance of his illness that
she found inspiring.
At one point, worried about finances, she considered laying off the aide and
taking care of Michael alone. When members of her support group worried that the
stress would kill her, she told them, “That might not be so bad.”
At Ms. Goldman’s urging, she saw a psychotherapist. He recommended medications
to calm her. She filled the prescription but threw the pills away.
“I kind of feel that having gone through the anxiety and the worry is what let
me get to the other side,” Mrs. French said.
While Mr. French was still well enough, they had discussed the possibility of a
nursing home. So when the time came, it was not really a surprise.
“He knew it was something I didn’t want to do, because every time we spoke about
it I would cry,” Mrs. French said. “When I told him that I had made
arrangements, he said — and this is a man who can’t speak, so he had to muster
every bit of energy he could — he said, ‘You did the best you could.’ ”
In April last year, Mrs. French placed her husband in a nursing home in
Manhattan. Along with her sadness came feelings of relief and freedom. Soon
after he was settled, she went out to dinner with friends for the first time in
two years.
“At times, I ache for him to be back in the apartment,” she said. “But I ache
for him to be back as him.”
She said that long after he ceased speaking, he continues to understand what she
says.
“I remember asking his neurologist, ‘Will he know me?’ ” Mrs. French said. “And
he said, ‘Oh, he’ll always know you. He might not be able to express it in a way
that will be familiar to you or that you’ll like, but he’ll always know you.’ ”
She wondered what longings might drive her husband’s dreams:
“I asked him, ‘Do you talk in your dreams?’ and he said, ‘Yes.’ And I asked him,
‘Do you dream about me?’ And he said, ‘Yes.’ ”
She has had time to think about mortality, his and her own.
“Death to me has always been a wake-up call to live,” she said. “This is the
endgame. Sometimes I get upset because I don’t think I have enough money, and
sometimes I get upset because I think I do. You don’t necessarily want to live
too long, but neither do you want to die.”
On most days, she spends several hours at the nursing home with her husband. She
shaves him and sometimes climbs into bed with him to hold him and to nap
together.
“Where do you carry my heart?” she asks him, referring to a poem they love by E.
E. Cummings.
He smiles and pats his chest.
i carry your heart with me(i carry it in
my heart)i am never without it(anywhere
i go you go,my dear;and whatever is done
by only me is your doing,my darling)
i fear no fate(for you are my fate,my sweet)i want
March 30, 2012
The New York Times
By MATT FLEGENHEIMER
His was a love story, Charles D. Snelling wrote — a tale of a shiftless dreamer
and the woman who saved him, of the life they built over six decades and the
disease that stood no chance of erasing it. By the end, he said, their time
together had become a case study in reciprocity.
“She took care of me in every possible way she could for 55 years,” Mr. Snelling
wrote of his wife, Adrienne, months before the two were to celebrate their 61st
wedding anniversary. “The last six years have been my turn, and certainly I have
had the best of the bargain.”
On Thursday, months after contributing a poignant essay to The New York Times
about navigating a six-decade marriage upended by his spouse’s Alzheimer’s
disease, Mr. Snelling killed his wife and himself, the Snelling family said in a
statement released to The Morning Call of Allentown, Pa.. They were found
Thursday in their home in Lehigh County in eastern Pennsylvania, the police
said. Mr. Snelling shot himself, the coroner said. The ruling on Ms. Snelling’s
death was pending. Both were 81.
In the statement, the Snelling family said Mr. Snelling had acted “out of deep
devotion and profound love.”
Last December, in response to an Op-Ed column by David Brooks, Mr. Snelling
contributed a 5,000-word “Life Report” essay to nytimes.com, devoting the final
section to his wife’s disease and his role in managing it.
“It’s not noble, it’s not sacrificial and it’s not painful,” he wrote of his
caretaking duties. “It’s just right in the scheme of things. After all, this
lady rescued me from a fate worse than death, and for a long, long time.”
Mr. Snelling met the woman who would become his wife at a sophomore dance at
Cedar Crest College in Allentown, Pa. She was spoken for then, “on the arm of
the Yalie” who was her date, Mr. Snelling wrote. It would not last.
“That Adrienne was the girl that I wanted, the girl that I needed to bring into
my life, and the girl that I had to marry became very clear to me quite soon,”
Mr. Snelling wrote.
But it soon became apparent that Adrienne Angeletti was studious, he continued,
and so he would have to be, too. When she took her books and a blanket outside
to study, Mr. Snelling tagged along “to pester her,” he wrote.
“You’re not studying,” she would say, according to Mr. Snelling, to which he
would reply, “I’m studying you.”
On March 21, 1951, the two were married. They honeymooned in Bermuda. Soon came
children — five of them, over 10 years — and a series of career ventures ranging
from artificial insemination of dairy cattle to real estate development to the
presidency of the Allentown City Council.
In the 1970s, Mr. Snelling became finance chairman of the Republican Party in
Pennsylvania. At 70, he was named to the Board of Directors of the Metropolitan
Washington Airports Authority.
After decades of her support in these endeavors, the illness was a sort of
“redemption” for him, Mr. Snelling wrote.
“I have dug in with the will,” he said. “Adrienne likes to be with me so,
everywhere I go Adrienne goes as well.”
He went on, “We continue to make a life together, living together in the full
sense of the word; going about our life, hand in hand, with everyone lending a
hand, as though nothing was wrong at all.”
Earlier in the essay, Mr. Snelling had assured readers he did not intend to
sound “boastful” in retelling a life blessed with “more ups than downs.” Mr.
Snelling’s readers required no disclaimer. Some were moved to thank him.
“What a privilege it is to experience the ‘charmed’ life of another and as a
result to appreciate what is valuable in our own,” one reader from London
commented on the article.
“We should all be so lucky to have unconditional love,” wrote another, from
Honolulu.
At the end of his essay, Mr. Snelling described the seal at Phillips Academy in
Andover, Mass., his prep school: a hive abuzz with bees, with the Latin ‘Non
Sibi’: “Not for self alone.”
Then he recalled another school creed. “The motto, also in Latin, is ‘Finis
Origine Pendet,’ ” he wrote. “The Beginning Foretells the End.”
February 1, 2012
The New York Times
By GINA KOLATA
Alzheimer’s disease seems to spread like an infection from brain cell to brain
cell, two new studies in mice have found. But instead of viruses or bacteria,
what is being spread is a distorted protein known as tau.
The surprising finding answers a longstanding question and has immediate
implications for developing treatments, researchers said. And they suspect that
other degenerative brain diseases like Parkinson’s may spread in a similar way.
Alzheimer’s researchers have long known that dying, tau-filled cells first
emerge in a small area of the brain where memories are made and stored. The
disease then slowly moves outward to larger areas that involve remembering and
reasoning.
But for more than a quarter-century, researchers have been unable to decide
between two explanations. One is that the spread may mean that the disease is
transmitted from neuron to neuron, perhaps along the paths that nerve cells use
to communicate with one another. Or it could simply mean that some brain areas
are more resilient than others and resist the disease longer.
The new studies provide an answer. And they indicate it may be possible to bring
Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell
transmission, perhaps with an antibody that blocks tau.
The studies, done independently by researchers at Columbia and Harvard, involved
genetically engineered mice that could make abnormal human tau proteins,
predominantly in the entorhinal (pronounced en-toh-RYE-nal) cortex, a sliver of
tissue behind the ears, toward the middle of the brain, where cells first start
dying in Alzheimer’s disease. As expected, tau showed up there. And, as also
expected, entorhinal cortex cells in the mice started dying, filled with
tangled, spaghettilike strands of tau.
Over the next two years, the cell death and destruction spread outward to other
cells along the same network. Since those other cells could not make human tau,
the only way they could get the protein was by transmission from nerve cell to
nerve cell.
And that, said Dr. Samuel E. Gandy, associate director of the Alzheimer’s
Disease Research Center at Mount Sinai School of Medicine in New York, was “very
unexpected, very intriguing.”
Although the studies were in mice, researchers say they expect that the same
phenomenon occurs in humans because the mice had a human tau gene and the
progressive wave of cell death matched what they see in people with Alzheimer’s
disease.
One study, by Karen Duff and Dr. Scott A. Small and their colleagues at the Taub
Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia
University Medical Center, was published on Wednesday in the journal PLoS One.
The other, by Dr. Bradley T. Hyman, director of the Alzheimer’s Disease Research
Center at Massachusetts General Hospital, and his colleagues, is to be published
in the journal Neuron.
Both groups of researchers were inspired by the many observations over the years
that Alzheimer’s starts in the entorhinal cortex and spreads.
But, said Dr. Small, “what do we mean by ‘spreads?’ ”
Researchers knew that something set off Alzheimer’s disease. The most likely
candidate is a protein known as beta amyloid, which accumulates in the brain of
Alzheimer’s patients, forming hard, barnaclelike plaques. But beta amyloid is
very different from tau. It is secreted and clumps outside cells. Although
researchers have looked, they have never seen evidence that amyloid spreads from
cell to cell in a network.
Still, amyloid creates what amounts to a bad neighborhood in memory regions of
the brain. Then tau comes in — some researchers call it “the executioner” —
piling up inside cells and killing them. If some cells take longer than others
to succumb to the bad neighborhood, that would explain the spread of the disease
in the brain, and there would be no need to blame something odd, like the spread
of tau from cell to cell.
Studies in humans, though, could not determine whether that hypothesis was
correct. They involved autopsy and brain imaging studies and were “indirect and
inconclusive,” Dr. Small said.
Looking at the brains of people who have died of the disease, Dr. Duff said, is
like looking at a wrecked car and trying to figure out the accident’s cause.
Faulty brakes? Broken struts?
The question of which hypothesis was correct — tau spreading cell to cell, or a
bad neighborhood in the brain and cells with different vulnerabilities to it —
remained unanswerable. Dr. Hyman said he tried for 25 years to find a good way
to address it. One of his ideas was to find a patient or two who had had a
stroke or other injury that severed the entorhinal cortex from the rest of the
brain. If the patient developed Alzheimer’s in the entorhinal cortex — and it
remained contained there — he would have evidence that the disease spread like
an infection. But he never found such patients.
The solution came when researchers were able to develop genetically engineered
mice that expressed abnormal human tau, but only in their entorhinal cortexes.
Those mice offered the cleanest way to get an answer, said John Hardy, an
Alzheimer’s researcher at University College London who was not involved in
either of the new studies.
There is another advantage, too, Dr. Hyman said. The mice give him a tool to
test ways to block tau’s spread — and that, he added, “is one of the things
we’re excited about.”
But if tau spreads from neuron to neuron, Dr. Hardy said, it may be necessary to
block both beta amyloid production, which seems to get the disease going, and
the spread of tau, which continues it, to bring Alzheimer’s to a halt.
He and others are also asking if other degenerative diseases spread through the
brain because proteins pass from nerve cell to nerve cell.
Dr. Hardy thought he saw provocative human evidence that it might be happening
in Parkinson’s disease. Two Parkinson’s patients being treated by a colleague
had fetal brain cells implanted to replace dead and dying neurons. When the
patients died, years later, autopsies showed they still had the fetal cells, but
they had balls of a Parkinson’s disease protein, synuclein, inside. The most
obvious way that could happen, the researchers reasoned, was if the toxic
protein had spread from the patient’s diseased cells to the healthy fetal cells.
But they could not rule out the bad-neighborhood hypothesis.
Now, Dr. Hardy said, with the mouse studies, the issue of a bad neighborhood is
settled. The answer in Alzheimer’s disease, he said, “is that isn’t possible.”
“That is what is different between these papers and all the others,” Dr. Hardy
said. “It isn’t a bad neighborhood. It is contagion from one neuron to another.”
September 16, 2011
The New York Times
By ERIK ECKHOLM
The televangelist Pat Robertson’s suggestion that a man whose wife was far
“gone” with Alzheimer’s should divorce her if he felt a need for new
companionship has provoked a storm of condemnation from other Christian leaders
but a more mixed or even understanding response from some doctors and patient
advocates.
On his television show, “The 700 Club,” on Tuesday, Mr. Robertson, a prominent
evangelical who once ran for president, took a call from a man who asking how he
should advise a friend whose wife was deep into dementia and no longer
recognized him.
“His wife as he knows her is gone,” the caller said, and the friend is “bitter
at God for allowing his wife to be in that condition, and now he’s started
seeing another woman.”
“This is a terribly hard thing,” Mr. Robertson said, clearly struggling to think
his way through a wrenching situation. “I hate Alzheimer’s. It is one of the
most awful things, because here’s the loved one — this is the woman or man that
you have loved for 20, 30, 40 years, and suddenly that person is gone “
“I know it sounds cruel,” he continued, “but if he’s going to do something, he
should divorce her and start all over again, but to make sure she has custodial
care, somebody looking after her.”
When Mr. Robertson’s co-anchor on the show wondered if that was consistent with
marriage vows, Mr. Robertson noted the pledge of “’til death do us part,” but
added, “This is a kind of death.”
He said the question presented an ethical dilemma beyond his ability to answer.
“I certainly wouldn’t put a guilt trip on you if you decided that you had to
have companionship, you’re lonely, you have to have companionship,” Mr.
Robertson said.
The reaction from many evangelical leaders, who see lifelong, traditional
marriage as the cornerstone of morality and society, was harsh and disbelieving.
“This is more than an embarrassment,” Russell D. Moore, dean of the School of
Theology at the Southern Baptist Theological Seminary in Louisville, Ky., wrote
in a blog post on Thursday. “This is more than cruelty. This is a repudiation of
the gospel of Jesus Christ.”
But Beth Kallmyer, senior director of constituent services at the Alzheimer’s
Association in Chicago, declined to question Mr. Robertson’s remarks.
“This is a challenging, devastating and eventually fatal illness, and it affects
everybody differently,” she said. “The most important thing is that families get
help.”
In the association’s experience, she said, it is rare for people to get divorced
because of Alzheimer’s. But Alzheimer’s can go on for years or decades,
progressively worsening.
“The decisions people make are personal,” Ms. Kallmyer said.
Dr. Amanda G. Smith, medical director of the University of South Florida
Health’s Alzheimer’s Institute, in Tampa, said of Mr. Robertson’s remarks: “I
think he was trying to give someone the freedom to move on, but he only took
account of the caregiver without taking account of the patient.”
“Even if someone doesn’t recognize a spouse as specifically their spouse, there
is often a familiarity with that person and a feeling of comfort, especially if
they have been married for decades,” Dr. Smith said.
At the same time, Dr. Smith said, when the disease is advanced, she sees nothing
wrong with caregivers developing other relationships “that bring joy and fill a
void.” By the same token, she said, “it’s O.K. if a patient in a facility finds
a girlfriend to sit with at dinner every night.”
Dr. James E. Galvin, a neurologist who runs a dementia clinic at New York
University’s Langone Medical Center, said it was wrong to say that people with
Alzheimer’s were “gone,” or to call its late stages “a kind of death.”
“While it’s true that in terminal phases, patients may not be fully aware of
what’s going on, they tend to recognize the people who are closest to them,” Dr.
Galvin said.
With good care, people may live 15 to 20 years with the disease, most of that
time at home, Dr. Galvin said. If they eventually move to a nursing home and
seem unaware of what is going on around them, he said, then spouses face “an
individualized decision” about when and how to develop new relationships, ones
based on religion and ethics, not science.
Mr. Robertson helped make the Christian Coalition into a formidable political
force in the 1990s and is still popular on television. But over the years, he
has also stirred anger among some conservative Christians with statements
considered unorthodox by one group or another, including a defense of China’s
one-child population policy and assertions that dire events like the Sept. 11,
2001, terrorist attacks and the Haiti earthquake were punishments from God.
“Few Christians take Robertson all that seriously anymore,” wrote Mr. Moore, of
the Southern Baptist seminary. “Most roll their eyes and shake their heads when
he makes another outlandish comment.”
Through a spokesman, Mr. Robertson on Friday declined to elaborate on his
televised remarks.
May 21, 2011
The New York Times
By MARGARET MORGANROTH GULLETTE
Waltham, Mass.
IN our hypercognitive society, fear of forgetfulness has made deep inroads into
the psyche. Misplacing car keys, once considered mere absent-mindedness, is now
a clinical symptom. Technological ineptitude in the prime of adulthood is
ascribed to memory failure.
The mere whiff of perceived memory loss can have terrible consequences in an
insecure economy in which midlife workers are regularly (and illegally) laid off
on account of their age. This epidemic of anxiety around memory loss is so
strong that many older adults seek help for the kind of day-to-day forgetfulness
that once was considered normal.
Greater public awareness of Alzheimer’s, far from reducing the ignorance and
stigma around the disease, has increased it. People over 55 dread getting
Alzheimer’s more than any other disease, according to a 2010 survey by the
MetLife Foundation. The fact that only 1 in 8 Americans older than 65 has
Alzheimer’s fails to register.
Is the prospect of the disease so horrifying that it should prompt someone to
consider suicide? A writer I know whose mother had Alzheimer’s told me she is
stockpiling pills. An academic told me he has found someone who will help him
die “before I lose my mind.”
Advocacy groups, manufacturers of so-called anti-aging products and the news
media have, for varying reasons, tended to inflate the number of sufferers and
the horrors of the condition. Doctors, too, have been complicit: some use
“cognitive impairment” as an argument for ending dialysis or other
life-sustaining treatments.
And some voices in our culture amplify these alarming sentiments. Tony Kushner
links Alzheimer’s to suicide in his new Off Broadway play, “The Intelligent
Homosexual’s Guide to Capitalism and Socialism With a Key to the Scriptures.”
His 72-year-old hero, Gus Marcantonio, a retired union organizer, tells his
assembled family that he has guessed he has Alzheimer’s, and wants to sell the
family house and kill himself over the weekend. Gus has no symptoms that the
audience can see except once losing his place in a voluble, earnest and moving
speech.
In the Korean director Lee Chang-dong’s film “Poetry,” which won the award for
best screenplay at Cannes last year, the graceful and empathetic heroine, who is
66, is given a diagnosis of Alzheimer’s. She too has no symptoms other than once
forgetting the word for “bus station.” Yet in the film she jumps off a bridge.
The characters have other motives besides fear to end their lives — guilt,
mainly. So why is Alzheimer’s brought into these plots so conspicuously? Perhaps
because no other motivation seems as plausible to an audience as a reason to
kill oneself.
Despite the prevalence of Alzheimer’s in our national conversation, diagnosing
the disease is actually difficult. There is no test that can predict whether
forgetting names or words like “bus station” is an indicator of the onset of a
degenerative disease. Many older people lose the ability to remember proper
nouns but then never progress to losing any other part of speech.
Most forgetfulness is not Alzheimer’s, or dementia, or even necessarily a sign
of cognitive impairment. And yet any prophecy about impaired cognition — whether
it is fulfilled or not — harms people’s sense of self. They begin to be treated
like children, patronized with baby talk or avoided. At the assisted living
facility where my mother lived until she died last year at age 96, the nursing
director told me that some people think Alzheimer’s is contagious. Victims of
misdiagnosis — or, just as devastating, self-diagnosis — dread being shunned,
rejected by their offspring, going into debt, becoming a “burden,” losing
selfhood.
It needn’t be this way. People with cognitive impairments can live happily with
their families for a long time. My mother was troubled by her loss of memories,
but she discovered an upside to forgetting. She had forgotten old rancors as
well as President George W. Bush’s name. We sang together. She recited her
favorite poems and surprised me with new material. We had rich and loving times.
Suicide didn’t cross her mind.
The mind is capacious. Much mental and emotional ability can survive mere memory
loss, as do other qualities that make us human.
In fact, a revolution in care-giving might be slowly taking root, at least among
those aware of alternative narratives of memory loss.
Thomas Kitwood, a British psychologist who was a pioneer in the field of
dementia care, died in 1998, but his books, which emphasize personhood instead
of debilitation, remain influential. “Making an Exit,” a memoir by Elinor Fuchs,
a drama professor at Yale, explored the conversational patterns of her mother
when she was in an advanced stage of Alzheimer’s. Anne Basting, director of the
Center on Age and Community at the University of Wisconsin, Milwaukee, who wrote
a play from poems created by people with Alzheimer’s, has a slogan: “Forget
Memory. Try Imagination.”
What a difference it would make if everyone began to share these attitudes. We
could make cognition-related fear-mongering shameful and rare, make debates
about end-of-life care less searing, improve treatment protocols, reaffirm our
collective compact with older people, ease our relationships with people of any
age who are cognitively impaired, and enable adults to look forward to getting
older with hope instead of despair.
For the first time in 27 years, the definition of Alzheimer’s disease is being
recast in new medical guidelines that reflect fast-mounting evidence that it
begins ravaging the brain years before the symptoms of dementia.
The guidelines, to be issued Tuesday by the National Institute on Aging and the
Alzheimer’s Association, divide the disease into three stages: a phase when
dementia has developed, a middle phase in which mild problems emerge but daily
functions can still be performed, and the most recently discovered phase, in
which no symptoms are evident but changes are brewing in the brain.
“We’re redefining Alzheimer’s disease and looking at this in a different way
than had ever been done,” said Creighton Phelps, director of the National
Institute on Aging’s Alzheimer’s Disease Centers Program. “I think we’re going
to start to identify it earlier and earlier.”
The drive to diagnose Alzheimer’s before it has progressed into profound
dementia is also reflected in a bill introduced in Congress this month, which
would create specific Medicare cost codes for Alzheimer’s diagnosis, including
steps involving discussions between the patient’s doctor and caregivers, a
recognition that keeping family members well-informed can result in better
planning and care.
“Early diagnosis is really the key to this,” said Representative Edward J.
Markey, Democrat of Massachusetts and a sponsor of the bill. “Oftentimes family
members notice the symptoms in their loved ones, but it’s only years later that
they get diagnosed or understand what resources are available.”
The most striking addition to the guidelines concerns methods that assess brain
changes involved in Alzheimer’s, including brain scans and tests of cerebral
spinal fluid. Such methods measure what are called biomarkers, physiological
indicators that someone is likely to develop dementia eventually, just as
cholesterol and blood pressure are biomarkers of impending heart disease.
For now, the guidelines specify that Alzheimer’s biomarkers — including abnormal
levels of the proteins amyloid and tau, and shrinkage of certain brain areas —
should not yet be put into widespread use, but used only with patients enrolled
in clinical trials.
That is because scientists cannot yet standardize the results of the tests, or
know “what measure is truly abnormal and what measure is not,” said Marilyn
Albert, director of the Johns Hopkins Alzheimer’s Disease Research Center, and a
leader of one working group that developed the new guidelines.
As many as a third of people with amyloid plaques in their brains, for example,
have not developed Alzheimer’s symptoms by the time they die. The guidelines
also urge caution because there is currently no drug known to halt or
significantly delay the onset of symptoms, so people told they are likely to get
Alzheimer’s have no effective medication to take.
“We don’t have enough information about what to tell people,” said Dr. Steven
DeKosky, dean of the University of Virginia medical school, who participated in
one of the working groups. “Until you can tell a clinician, ‘If you do this test
you have X amount of reliability and to do that will make a difference in the
life of your patient’ — until then, it remains in the lab.”
But the guidelines reflect a sense in the medical community that the moment when
science will have more specific knowledge about biomarkers is not that far off.
They are intended to encourage more research so that drugs can be developed to
attack early brain changes and to identify people who might benefit from such
drugs when they become available.
The goal, said William Thies, chief medical and scientific officer for the
Alzheimer’s Association, is “extending the range of our ability to investigate
this disease and eventually find the treatment that is going to be so necessary
to avoid the epidemic of Alzheimer’s disease that we see facing us over the next
40 years.”
In the short term, the biggest impact is likely to be seen with people who fall
into the middle phase, those with mild cognitive impairment linked to
Alzheimer’s. Experts say there are at least as many people experiencing this
phase as the 5.4 million people estimated to have Alzheimer’s dementia. And they
expect others to now ask their doctors if they are showing signs of mild
impairment, which include experiencing some difficulty or inefficiency with
memory, attention or other mental faculties, while still being able to function
independently.
Dr. Albert said that if patients with symptoms of mild cognitive impairment
wanted to “increase the certainty” of the diagnosis by getting a brain scan or
spinal fluid test, they should obtain such tests in a research trial so they
have a better chance of getting accurate results.
The guidelines also clarify diagnosis criteria for people with dementia
symptoms, distinguishing Alzheimer’s from other dementias, including vascular,
fronto-temporal and Lewy body. And they note that the earliest symptom of
Alzheimer’s dementia is not always memory loss, but could be mood changes or
problems with language, spatial perception or reasoning.
Dr. Pierre Tariot, director of the Banner Alzheimer’s Institute in Phoenix, who
was not involved in drafting the guidelines, called them “a step in the right
direction” that he hoped would not be “misconstrued” as a sign that biomarker
tests are further along than they are. He added, “The notion that Alzheimer’s
disease is a continuum that has an extensive pre-symptomatic phase is a very
important message to get out.”
Dr. Phelps said it would hardly be the last word from the medical community on
Alzheimer’s.
“We’re not drawing a line and saying this is it,” Dr. Phelps said. “What we’re
saying is this is the best of our knowledge and we’re not going to wait 27 years
to revisit these again.”
October 27, 2010
The New York Times
By SANDRA DAY O’CONNOR,
STANLEY PRUSINER
and KEN DYCHTWALD
OUR government is ignoring what is likely to become the single greatest threat
to the health of Americans: Alzheimer’s disease, an illness that is 100 percent
incurable and 100 percent fatal. It attacks rich and poor, white-collar and
blue, and women and men, without regard to party. A degenerative disease, it
steadily robs its victims of memory, judgment and dignity, leaves them unable to
care for themselves and destroys their brain and their identity — often
depleting their caregivers and families both emotionally and financially.
Starting on Jan. 1, our 79-million-strong baby boom generation will be turning
65 at the rate of one every eight seconds. That means more than 10,000 people
per day, or more than four million per year, for the next 19 years facing an
increased risk of Alzheimer’s. Although the symptoms of this disease and other
forms of dementia seldom appear before middle age, the likelihood of their
appearance doubles every five years after age 65. Among people over 85 (the
fastest-growing segment of the American population), dementia afflicts one in
two. It is estimated that 13.5 million Americans will be stricken with
Alzheimer’s by 2050 — up from five million today.
Just as President John F. Kennedy, in 1961, dedicated the United States to
landing a man on the moon by the end of the decade, we must now set a goal of
stopping Alzheimer’s by 2020. We must deploy sufficient resources, scientific
talent and problem-solving technologies to save our collective future.
As things stand today, for each penny the National Institutes of Health spends
on Alzheimer’s research, we spend more than $3.50 on caring for people with the
condition. This explains why the financial cost of not conducting adequate
research is so high. The United States spends $172 billion a year to care for
people with Alzheimer’s. By 2020 the cumulative price tag, in current dollars,
will be $2 trillion, and by 2050, $20 trillion.
If we could simply postpone the onset of Alzheimer’s disease by five years, a
large share of nursing home beds in the United States would empty. And if we
could eliminate it, as Jonas Salk wiped out polio with his vaccine, we would
greatly expand the potential of all Americans to live long, healthy and
productive lives — and save trillions of dollars doing it.
Experience has taught us that we cannot avoid Alzheimer’s disease by having
regular medical checkups, by being involved in nourishing relationships or by
going to the gym or filling in crossword puzzles. Ronald Reagan suffered the
ravages of this disease for a decade despite the support of his loving family,
the extraordinary stimulation of his work, his access to the best medical care
and his high level of physical fitness. What’s needed are new medicines that
attack the causes of the disease directly.
So far, only a handful of medications have been approved by the Food and Drug
Administration to treat Alzheimer’s, and these can only slightly and temporarily
modify symptoms like forgetfulness, disorientation and confusion. None actually
slows the underlying neurodegeneration.
In the mid-1980s, when our country finally made a commitment to fight AIDS, it
took roughly 10 years of sustained investment (and about $10 billion) to create
the antiretroviral therapies that made AIDS a manageable disease. These
medicines also added $1.4 trillion to the American economy. The National
Institutes of Health still spend about $3 billion a year on AIDS research, while
Alzheimer’s, with five times as many victims, receives a mere $469 million.
Most of the medical researchers who study Alzheimer’s agree on what they have to
understand in order to create effective drugs: They must find out how the
aberrant proteins associated with the disease develop in the brain. They need to
model the progression of the illness so they can pinpoint drug targets. And
ultimately they must learn how to get drugs to move safely from the blood into
the brain.
A breakthrough is possible by 2020, leading Alzheimer’s scientists agree, with a
well-designed and adequately financed national strategic plan. Congress has
before it legislation that would raise the annual federal investment in
Alzheimer’s research to $2 billion, and require that the president designate an
official whose sole job would be to develop and execute a strategy against
Alzheimer’s. If lawmakers could pass this legislation in their coming lame-duck
session, they would take a serious first step toward meeting the 2020 goal.
Medical science has the capacity to relegate Alzheimer’s to the list of former
diseases like typhoid, polio and many childhood cancers. But unless we get to
work now, any breakthrough will come too late to benefit the baby boomers.
Whether the aging of America turns out to be a triumph or a tragedy will depend
on our ability to fight this horrific disease and beat it before it beats us.
Sandra Day O’Connor is a retired associate justice
of the Supreme Court.
Stanley Prusiner, who received the 1997 Nobel Prize
in Medicine, is the director of the Institute for
Neurodegenerative Diseases at the University of California,
WASHINGTON (Reuters) - More than 5 million people in the United States have
Alzheimer's disease and an aging population is likely to fuel a steady rise in
new cases, a report released by the Alzheimer's Association said on Tuesday.
The association's figure of 5 million is up about 10 percent from its previous
estimate in 2000, and it said there are about 400,000 new cases a year.
The group predicts that the number of Alzheimer's cases will rise to 7.7 million
people by 2030 as the U.S. baby boom population ages, unless a cure or a way to
prevent the disease is found.
Alzheimer's is the seventh leading cause of death in the United States, and it
is the leading cause of dementia. It is marked by a steady loss of memory that
soon takes away a person's ability to cope and care from himself or herself, and
there is no cure.
Drugs can help slow its progression but they eventually stop working. Patients
die of pneumonia or other causes as their bodily functions deteriorate.
"In 2005, Medicare spent $91 billion on beneficiaries with Alzheimer's and other
dementias and that number is projected to more than double to $189 billion by
2015," the association said in its report.
"However there is hope. There are currently nine drugs in Phase III clinical
trials for Alzheimer's, several of which show great promise to slow or stop the
progression of the disease," Harry Johns, president and chief executive officer
of the Alzheimer's Association, said in a statement.
"This, combined with advancements in diagnostic tools, has the potential to
change the landscape of Alzheimer's."
I LOVE reading history, and the shelves in my living room are lined with fat,
fact-filled books. There’s “The Hemingses of Monticello,” about the family of
Thomas Jefferson’s slave mistress; there’s “House of Cards,” about the fall of
Bear Stearns; there’s “Titan,” about John D. Rockefeller Sr.
The problem is, as much as I’ve enjoyed these books, I don’t really remember
reading any of them. Certainly I know the main points. But didn’t I, after
underlining all those interesting parts, retain anything else? It’s maddening
and, sorry to say, not all that unusual for a brain at middle age: I don’t just
forget whole books, but movies I just saw, breakfasts I just ate, and the names,
oh, the names are awful. Who are you?
Brains in middle age, which, with increased life spans, now stretches from the
40s to late 60s, also get more easily distracted. Start boiling water for pasta,
go answer the doorbell and — whoosh — all thoughts of boiling water disappear.
Indeed, aging brains, even in the middle years, fall into what’s called the
default mode, during which the mind wanders off and begin daydreaming.
Given all this, the question arises, can an old brain learn, and then remember
what it learns? Put another way, is this a brain that should be in school?
As it happens, yes. While it’s tempting to focus on the flaws in older brains,
that inducement overlooks how capable they’ve become. Over the past several
years, scientists have looked deeper into how brains age and confirmed that they
continue to develop through and beyond middle age.
Many longheld views, including the one that 40 percent of brain cells are lost,
have been overturned. What is stuffed into your head may not have vanished but
has simply been squirreled away in the folds of your neurons.
One explanation for how this occurs comes from Deborah M. Burke, a professor of
psychology at Pomona College in California. Dr. Burke has done research on
“tots,” those tip-of-the-tongue times when you know something but can’t quite
call it to mind. Dr. Burke’s research shows that such incidents increase in part
because neural connections, which receive, process and transmit information, can
weaken with disuse or age.
But she also finds that if you are primed with sounds that are close to those
you’re trying to remember — say someone talks about cherry pits as you try to
recall Brad Pitt’s name — suddenly the lost name will pop into mind. The
similarity in sounds can jump-start a limp brain connection. (It also sometimes
works to silently run through the alphabet until landing on the first letter of
the wayward word.)
This association often happens automatically, and goes unnoticed. Not long ago I
started reading “The Prize,” a history of the oil business. When I got to the
part about Rockefeller’s early days as an oil refinery owner, I realized, hey, I
already know this from having read “Titan.” The material was still in my head;
it just needed a little prodding to emerge.
Recently, researchers have found even more positive news. The brain, as it
traverses middle age, gets better at recognizing the central idea, the big
picture. If kept in good shape, the brain can continue to build pathways that
help its owner recognize patterns and, as a consequence, see significance and
even solutions much faster than a young person can.
The trick is finding ways to keep brain connections in good condition and to
grow more of them.
“The brain is plastic and continues to change, not in getting bigger but
allowing for greater complexity and deeper understanding,” says Kathleen Taylor,
a professor at St. Mary’s College of California, who has studied ways to teach
adults effectively. “As adults we may not always learn quite as fast, but we are
set up for this next developmental step.”
Educators say that, for adults, one way to nudge neurons in the right direction
is to challenge the very assumptions they have worked so hard to accumulate
while young. With a brain already full of well-connected pathways, adult
learners should “jiggle their synapses a bit” by confronting thoughts that are
contrary to their own, says Dr. Taylor, who is 66.
Teaching new facts should not be the focus of adult education, she says.
Instead, continued brain development and a richer form of learning may require
that you “bump up against people and ideas” that are different. In a history
class, that might mean reading multiple viewpoints, and then prying open brain
networks by reflecting on how what was learned has changed your view of the
world.
“There’s a place for information,” Dr. Taylor says. “We need to know stuff. But
we need to move beyond that and challenge our perception of the world. If you
always hang around with those you agree with and read things that agree with
what you already know, you’re not going to wrestle with your established brain
connections.”
Such stretching is exactly what scientists say best keeps a brain in tune: get
out of the comfort zone to push and nourish your brain. Do anything from
learning a foreign language to taking a different route to work.
“As adults we have these well-trodden paths in our synapses,” Dr. Taylor says.
“We have to crack the cognitive egg and scramble it up. And if you learn
something this way, when you think of it again you’ll have an overlay of
complexity you didn’t have before — and help your brain keep developing as
well.”
Jack Mezirow, a professor emeritus at Columbia Teachers College, has proposed
that adults learn best if presented with what he calls a “disorienting dilemma,”
or something that “helps you critically reflect on the assumptions you’ve
acquired.”
Dr. Mezirow developed this concept 30 years ago after he studied women who had
gone back to school. The women took this bold step only after having many
conversations that helped them “challenge their own ingrained perceptions of
that time when women could not do what men could do.”
Such new discovery, Dr. Mezirow says, is the “essential thing in adult
learning.”
“As adults we have all those brain pathways built up, and we need to look at our
insights critically,” he says. “This is the best way for adults to learn. And if
we do it, we can remain sharp.”
And so I wonder, was my cognitive egg scrambled by reading that book on Thomas
Jefferson? Did I, by exploring the flaws in a man I admire, create a suitably
disorienting dilemma? Have I, as a result, shaken up and fed a brain cell or
two?
And perhaps it doesn’t matter that I can’t, at times, recall the given name of
the slave with whom Jefferson had all those children. After all, I can Google a
simple name.
