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The Changing Brain in AD
No one knows exactly what starts the AD process or why some of the normal
changes associated with aging become so much more extreme and destructive in
people with the disease. We know a lot, however, about what happens in the brain
once AD takes hold and about the physical and mental changes that occur over
time. The time from diagnosis to death varies—as little as 3 or 4 years if the
person is older than 80 when diagnosed to as long as 10 or more years if the
person is younger. Several other factors besides age also affect how long a
person will live with AD. These factors include the person’s sex, the presence
of other health problems, and the severity of cognitive problems at diagnosis.
Although the course of the disease is not the same in every person with AD,
symptoms seem to develop over the same general stages.
Preclinical AD
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PRECLINICAL AD
AD begins deep in the brain, in the entorhinal
cortex, a brain region that is near the hippocampus and has direct
connections to it. Healthy neurons in this region begin to work less
efficiently, lose their ability to communicate, and ultimately die. This process
gradually spreads to the hippocampus, the brain region that plays a major role
in learning and is involved in converting short-term memories to long-term
memories. Affected regions begin to atrophy. Ventricles,
the fluid-filled spaces inside the brain, begin to enlarge as the process
continues.
Scientists believe that these brain changes begin 10 to 20 years before any
clinically detectable signs or symptoms of forgetfulness appear. That’s why
they are increasingly interested in the very early stages of the disease
process. They hope to learn more about what happens in the brain that sets a
person on the path to developing AD. By knowing more about the early stages,
they also hope to be able to develop drugs or other treatments that will slow or
stop the disease process before significant impairment occurs (see "The
Search for New Treatments" for more information).
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PiB and PET
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Imagine being able to see deep inside the brain tissue of a
living person. If you could do that, you could find out whether
the AD process was happening many years before symptoms were
evident. This knowledge could have a profound impact on
improving early diagnosis, monitoring disease progression, and
tracking response to treatment.
Scientists have stepped closer to this possibility with the
development of a radiolabeled compound called Pittsburgh
Compound B (PiB). PiB binds to beta-amyloid plaques in the brain
and it can be imaged using PET scans. Initial studies showed
that people with AD take up more PiB in their brains than do
cognitively healthy older people. Since then, scientists have
found high levels of PiB in some cognitively healthy people,
suggesting that the damage from beta-amyloid may already be
underway. The next step will be to follow these cognitively
healthy people who have high PiB levels to see whether they do,
in fact, develop AD over time.
In this PET scan, the red and yellow colors indicate that PiB
uptake is higher in the brain of the person with AD than in the
cognitively healthy person.
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VERY EARLY SIGNS
AND SYMPTOMS
At some point, the damage occurring in the brain begins to show itself in very
early clinical signs and symptoms. Much research is being done to identify these
early changes, which may be useful in predicting dementia or AD. An important
part of this research effort is the development of increasingly sophisticated
neuroimaging techniques (see "Exciting
New Developments in AD Diagnosis" for more on neuroimaging) and the use
of biomarkers. Biomarkers are indicators, such as changes in sensory abilities,
or substances that appear in body fluids, such as blood, cerebrospinal
fluid, or urine. Biomarkers can indicate exposure to a substance,
the presence of a disease, or the progression over time of a disease. For
example, high blood cholesterol is a biomarker for risk of heart disease. Such
tools are critical to helping scientists detect and understand the very early
signs and symptoms of AD.
Mild Cognitive Impairment
As some people grow older, they develop memory problems greater than those
expected for their age. But they do not experience the personality changes or
other problems that are characteristic of AD. These people may have a condition
called mild
cognitive impairment (MCI). MCI has several subtypes. The type most
associated with memory loss is called amnestic MCI. People with MCI are a
critically important group for research because a much higher percentage of them
go on to develop AD than do people without these memory problems. About 8 of
every 10 people who fit the definition of amnestic MCI go on to develop AD
within 7 years. In contrast, 1 to 3 percent of people older than 65 who have
normal cognition will develop AD in any one year.
However, researchers are not yet able to say definitively why some people
with amnestic MCI do not progress to AD, nor can they say who will or will not
go on to develop AD. This raises pressing questions, such as: In cases when MCI
progresses to AD, what was happening in the brain that made that transition
possible? Can MCI be prevented or its progress to AD delayed?
Scientists also have found that genetic factors may play a role in MCI, as
they do in AD (see "Genetic
Factors at Work in AD" for more information). And, they have found that
different brain regions appear to be activated during certain mental activities
in cognitively healthy people and those with MCI. These changes appear to be
related to the early stages of cognitive impairment.
| Charting the
Course from Healthy Aging to AD |
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This chart shows current thinking about the evolution from healthy aging
to AD. Researchers view it as a series of events that occur in the brain
over many years. This gradual process, which results from the
combination of biological, genetic, environmental, and lifestyle
factors, eventually sets some people on a course to MCI and possibly AD.
Other people, whose genetic makeup may be the same or different and who
experience a different combination of factors over a lifetime, continue
on a course of healthy cognitive aging.
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Other Signs of Early AD Development
As scientists have sharpened their focus on the early stages of AD, they have
begun to see hints of other changes that may signal a developing disease
process. For example, in the Religious Orders Study, a large AD research effort
that involves older nuns, priests, and religious brothers, investigators have
explored whether changes in older adults’ ability to move about and use their
bodies might be a sign of early AD. The researchers found that participants with
MCI had more movement difficulties than the cognitively healthy participants but
less than those with AD. Moreover, those with MCI who had lots of trouble moving
their legs and feet were more than twice as likely to develop AD as those with
good lower body function.
It is not yet clear why people with MCI might have these motor function
problems, but the scientists who conducted the study speculate that they may be
a sign that damage to blood vessels in the brain or damage from AD is
accumulating in areas of the brain responsible for motor function. If further
research shows that some people with MCI do have motor function problems in
addition to memory problems, the degree of difficulty, especially with walking,
may help identify those at risk of progressing to AD.
Other scientists have focused on changes in sensory abilities as possible
indicators of early cognitive problems. For example, in one study they found
associations between a decline in the ability to detect odors and cognitive
problems or dementia.
These findings are tentative, but they are promising because they suggest
that, some day, it may be possible to develop ways to improve early detection of
MCI or AD. These tools also will help scientists answer questions about causes
and very early development of AD, track changes in brain and cognitive function
over time, and ultimately track a person’s response to treatment for AD.
Mild to Moderate AD
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MILD AD
As AD spreads through the brain, the number of plaques and tangles grows,
shrinkage progresses, and more and more of the cerebral cortex is affected.
Memory loss continues and changes in other cognitive abilities begin to emerge.
The clinical diagnosis of AD is usually made during this stage. Signs of mild AD
can include:
 | Memory loss
| Confusion about the location of familiar places (getting lost begins to
occur)
| Taking longer than before to accomplish normal daily tasks
| Trouble handling money and paying bills
| Poor judgment leading to bad decisions
| Loss of spontaneity and sense of initiative
| Mood and personality changes, increased anxiety and/or aggression |
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In mild AD, a person may seem to be healthy but is actually having more and
more trouble making sense of the world around him or her. The realization that
something is wrong often comes gradually to the person and his or her family.
Accepting these signs as something other than normal and deciding to go for
diagnostic tests can be a big hurdle for people and families. Once this hurdle
is overcome, many families are relieved to know what is causing the problems.
They also can take comfort in the fact that despite a diagnosis of MCI or early
AD, a person can still make meaningful contributions to his or her family and to
society for a time.
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AD Spreads Through the Brain
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MODERATE AD
By this stage, AD damage has spread to the areas of the cerebral cortex that
control language, reasoning, sensory processing, and conscious thought. Affected
regions continue to shrink, ventricles enlarge, and signs and symptoms of the
disease become more pronounced and widespread. Behavioral problems, such as
wandering and agitation, can occur. More intensive supervision and care become
necessary, which can be difficult for many spouses and families. The symptoms of
this stage can include:
| Increasing memory loss and confusion
| Shortened attention span
| Inappropriate outbursts of anger
| Problems recognizing friends and family members
| Difficulty with language and problems with reading, writing, and working
with numbers
| Difficulty organizing thoughts and thinking logically
| Inability to learn new things or to cope with new or unexpected situations
| Restlessness, agitation, anxiety, tearfulness, wandering—especially in
the late afternoon or at night
| Repetitive statements or movement, occasional muscle twitches
| Hallucinations, delusions, suspiciousness or paranoia, irritability
| Loss of impulse control (shown through undressing at inappropriate times
or places or vulgar language)
| An inability to carry out activities that involve multiple steps in
sequence, such as dressing, making a pot of coffee, or setting the table |
| | | | | | | | | | |
Behavior is the result of complex brain processes, all of which take place in
a fraction of a second in the healthy brain. In AD, many of those processes are
disturbed, and these disrupted communications between neurons are the basis for
many distressing or inappropriate behaviors. For example, a person may angrily
refuse to take a bath or get dressed because he does not understand what his
caregiver has asked him to do. If he does understand, he may not remember how to
do it. The anger can be a mask for his confusion and anxiety. Or, a person with
AD may constantly follow her husband or caregiver and fret when the person is
out of sight. To a person who cannot remember the past or anticipate the future,
the world can be strange and frightening. Sticking close to a trusted and
familiar caregiver may be the only thing that makes sense and provides security.
Severe AD
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SEVERE AD
In the last stage of AD, plaques and tangles are widespread throughout the
brain, most areas of the brain have shrunk further, and ventricles have enlarged
even more. People with AD cannot recognize family and loved ones or communicate
in any way. They are completely dependent on others for care. Other symptoms can
include:
| Weight loss
| Seizures
| Skin infections
| Difficulty swallowing
| Groaning, moaning, or grunting
| Increased sleeping
| Lack of bladder and bowel control |
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Near the end, the person may be in bed much or all of the time. The most
frequent cause of death for people with AD is aspiration pneumonia. This type of
pneumonia develops when a person is not able to swallow properly and takes food
or liquids into the lungs instead of air.
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The Buddy Program at Northwestern
University
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 The
medical school curriculum demands that students spend enormous amounts
of time in the classroom and clinic learning the information and skills
necessary for a career in medicine. However, little or no time is set
aside for students to be with patients outside the hospital or clinic
setting. As a result, it is hard for medical students to get to know the
human side of the diseases they are learning about.
A program at Northwestern University’s Cognitive Neurology and
Alzheimer’s Disease Center is adding just that element to its medical
education. The Buddy Program, begun in 1998, matches first-year medical
students with people diagnosed with AD or another form of dementia.
About 10 to 15 medical students participate every year. They first take
a 3-hour orientation course on AD, family issues, and communication
skills. Then, for the next year, they spend at least 4 hours a month
with a person with dementia in addition to monthly meetings with the
program coordinators. Together with the person’s caregiver and the
program’s professional staff, students and their “buddies” choose
activities for their visits together. Activities can include shopping,
visiting museums, exercising together, or even just sharing a coffee or
a meal. The students also are able to observe their buddies’ clinical
evaluations at the Center. Other medical schools have started similar
programs.
The people with AD and their families are selected from
Northwestern’s Alzheimer’s Disease Center and other related programs
at the university. Families are contacted about participating, and the
people with AD are selected based on their ability to understand the
nature of the program and their willingness to spend time every month
with the student buddy.
The program has clear benefits for both the medical student and the
person with AD. For the medical student, it provides a hands-on way to
learn about AD and related dementias, and it helps him or her understand
the daily realities and issues involved in caring for and supporting
people with AD and their families. It also introduces them to the career
path of research and clinical practice in AD and related dementias. For
the person with AD, participation in the program provides an opportunity
for friendship and socializing and an outlet for sharing their
experiences with a sympathetic listener.
For many of the students, the program is a transformative experience.
They become very close to their buddies and family caregivers during
their year together, and continue the friendship even after the year is
over.
The Buddy Program pairs medical students with people with AD to spend
time with—and learn from—each other.
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