What Is Parkinson’s Disease?
Illustration of the Parkinson disease
by Sir William Richard Gowers
from A Manual of Diseases of the
Nervous System in 1886 (WikiMedia Commons)
Parkinson’s disease, also known as Parkinson disease, PD, paralysis agitans, and shaking palsy is
a gradually progressive, degenerative neurologic disorder which typically impairs the patient’s motor
skills, speech, writing, as well as some other functions. Sufferers often have a fixed, inexpressive face,
tremor at rest, slowing of voluntary movements (bradykinesia), an unusual posture, and muscle
weakness. In extreme cases there is a loss of physical movement (akinesia).
Parkinson’s disease is both chronic and progressive. Chronic means long-term, while progressive means
it gradually gets worse.
Parkinsonism is a neurological syndrome characterized by tremor, rigidity, postural instability, and
hypokinesia (decreased bodily movement). A syndrome is the association of several clinically
recognizable features, signs, symptoms, phenomena or characteristics that often occur together.
Parkinson's disease is the most common cause of Parkinsonism. Put simply - Parkinsonism includes the
signs and symptoms that resemble Parkinson’s disease.
While about 5% of individuals with Parkinson’s disease are under the age of 40 years, the majority are
over 50. When signs and symptoms develop in an individual aged between 21 and 40 years, it is known
as Young-onset Parkinson’s disease. Approximately 1 in every 20 patients diagnosed with PD is under 40
years of age. When signs and symptoms appear in people under 18 years of age, it is known as Juvenile
Parkinson’s disease. It affects both sexes; males slightly more than females.
According to the National Institutes of Health (NIH), USA, approximately 500,000 Americans are affected
by Parkinson’s disease; about 50,000 new diagnoses are made each year. The National Health Service
(NHS), UK, estimates that about 120,000 people in the United Kingdom are affected.
As a significant number of elderly patient with early Parkinson’s disease symptoms assume that their
symptoms may form part of normal aging and do not seek medical help, obtaining accurate statistics is
probably impossible. There are also a several different conditions which sometimes have comparable
signs and symptoms to PD.
PD is named after James Parkinson (1755-1824), an English apothecary surgeon, paleontologist,
geologist and political activist. In his most famous work An Essay on the Shaking Palsy (1817), he was
the first person to describe paralysis agitans, which eventually was named after him.
Parkinson’s disease belongs to a group of conditions called movement disorders. Movement disorders
describe a variety of abnormal body movements that have a neurological basis, and include such
conditions as cerebral palsy, ataxia, and Tourette syndrome. Parkinson’s disease results from decreased
stimulation of the motor cortex by the basal ganglia, typically caused by insufficient formation and action
There is no current cure for Parkinson’s disease (April, 2010). Treatment focuses on alleviating
symptoms. Sometimes treatment may include surgery.
What Are The Causes of Parkinson’s Disease?
The symptoms of Parkinson’s disease are caused by a loss of nerve cells (dopaminergic cells) in a part of
the brain called the substantia nigra (literally means “black substance”). The dopaminergic cells are
responsible for producing dopamine. Dopamine is a neurotransmitter; it helps transmit messages from the
brain that control and coordinate body movements - dopamine allows the substantia nigra and another
area of the brain, the corpus striatum to communicate; this communication coordinates proper muscle
If the Dopaminergic cells in the brain are damage or perish, dopamine production goes down and the
messages from the substantia nigra and the corpus striatum do not work properly. Parkinson’s disease
signs and symptoms appear when four-fifths of these nerve cells are lost. As dopamine levels continue to
drop, the signs and symptoms of Parkinson’s disease get worse.
Parkinson’s disease is caused by the degeneration or destruction of
dopamine-producing nerve cells (dopaminergic cells), which in turn
makes it harder for the brain to control and coordinate muscle
Experts are not sure why the nerve cells that cause Parkinson’s disease become damaged or die.
What is Multiple Sclerosis?
An unpredictable disease of the central nervous system, multiple sclerosis (MS) can range from relatively
benign to somewhat disabling to devastating, as communication between the brain and other parts of the
body is disrupted. Many investigators believe MS to be an autoimmune disease -- one in which the body,
through its immune system, launches a defensive attack against its own tissues. In the case of MS, it is the
nerve-insulating myelin that comes under assault. Such assaults may be linked to an unknown
environmental trigger, perhaps a virus.
Most people experience their first symptoms of MS between the ages of 20 and 40; the initial symptom of
MS is often blurred or double vision, red-green color distortion, or even blindness in one eye. Most MS
patients experience muscle weakness in their extremities and difficulty with coordination and balance.
These symptoms may be severe enough to impair walking or even standing. In the worst cases, MS can
produce partial or complete paralysis. Most people with MS also exhibit paresthesias, transitory
abnormal sensory feelings such as numbness, prickling, or "pins and needles" sensations. Some may also
experience pain. Speech impediments, tremors, and dizziness are other frequent complaints.
Occasionally, people with MS have hearing loss. Approximately half of all people with MS experience
cognitive impairments such as difficulties with concentration, attention, memory, and poor judgment, but
such symptoms are usually mild and are frequently overlooked. Depression is another common feature of
Is there any treatment?
There is as yet no cure for MS. Many patients do well with no therapy at all, especially since many
medications have serious side effects and some carry significant risks. However, three forms of beta
interferon (Avonex, Betaseron, and Rebif) have now been approved by the Food and Drug Administration
for treatment of relapsing-remitting MS. Beta interferon has been shown to reduce the number of
exacerbations and may slow the progression of physical disability. When attacks do occur, they tend to be
shorter and less severe. The FDA also has approved a synthetic form of myelin basic protein, called
copolymer I (Copaxone), for the treatment of relapsing-remitting MS. Copolymer I has few side effects,
and studies indicate that the agent can reduce the relapse rate by almost one third. An immunosuppressant
treatment, Novantrone (mitoxantrone), is approved by the FDA for the treatment of advanced or chronic
MS. The FDA has also approved dalfampridine (Ampyra) to improve walking in individuals with MS.
One monoclonal antibody, natalizumab (Tysabri), was shown in clinical trials to significantly reduce the
frequency of attacks in people with relapsing forms of MS and was approved for marketing by the U.S.
Food and Drug Administration (FDA) in 2004. However, in 2005 the drug’s manufacturer voluntarily
suspended marketing of the drug after several reports of significant adverse events. In 2006, the FDA
again approved sale of the drug for MS but under strict treatment guidelines involving infusion centers
where patients can be monitored by specially trained physicians.
While steroids do not affect the course of MS over time, they can reduce the duration and severity of
attacks in some patients. Spasticity, which can occur either as a sustained stiffness caused by increased
muscle tone or as spasms that come and go, is usually treated with muscle relaxants and tranquilizers such
as baclofen, tizanidine, diazepam, clonazepam, and dantrolene. Physical therapy and exercise can help
preserve remaining function, and patients may find that various aids -- such as foot braces, canes, and
walkers -- can help them remain independent and mobile. Avoiding excessive activity and avoiding heat
are probably the most important measures patients can take to counter physiological fatigue. If
psychological symptoms of fatigue such as depression or apathy are evident, antidepressant medications
may help. Other drugs that may reduce fatigue in some, but not all, patients include amantadine
(Symmetrel), pemoline (Cylert), and the still-experimental drug aminopyridine. Although improvement of
optic symptoms usually occurs even without treatment, a short course of treatment with intravenous
methylprednisolone (Solu-Medrol) followed by treatment with oral steroids is sometimes used.
What is the prognosis?
A physician may diagnose MS in some patients soon after the onset of the illness. In others, however,
doctors may not be able to readily identify the cause of the symptoms, leading to years of uncertainty and
multiple diagnoses punctuated by baffling symptoms that mysteriously wax and wane. The vast majority
of patients are mildly affected, but in the worst cases, MS can render a person unable to write, speak, or
walk. MS is a disease with a natural tendency to remit spontaneously, for which there is no universally
What research is being done?
The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National
Institutes of Health (NIH) conduct research in laboratories at the NIH and also support additional research
through grants to major medical institutions across the country. Scientists continue their extensive efforts
to create new and better therapies for MS. One of the most promising MS research areas involves
naturally occurring antiviral proteins known as interferons. Beta interferon has been shown to reduce the
number of exacerbations and may slow the progression of physical disability. When attacks do occur,
they tend to be shorter and less severe. In addition, there are a number of treatments under investigation
that may curtail attacks or improve function. Over a dozen clinical trials testing potential therapies are
underway, and additional new treatments are being devised and tested in animal models.
What are Stem Cells?
Stem cells are a class of undifferentiated cells that are able to differentiate into specialized cell types.
Commonly, stem cells come from two main sources:
1. Embryos formed during the blastocyst phase of embryological development (embryonic stem
2. Adult tissue (adult stem cells).
Both types are generally characterized by their potency, or potential to differentiate into different cell types
(such as skin, muscle, bone, etc.).
Adult stem cells
Adult or somatic stem cells exist throughout the body after embryonic development and are found inside
of different types of tissue. These stem cells have been found in tissues such as the brain, bone marrow,
blood, blood vessels, skeletal muscles, skin, and the liver. They remain in a quiescent or non-dividing
state for years until activated by disease or tissue injury.
Adult stem cells can divide or self-renew indefinitely, enabling them to generate a range of cell types from
the originating organ or even regenerate the entire original organ. It is generally thought that adult stem
cells are limited in their ability to differentiate based on their tissue of origin, but there is some evidence to
suggest that they can differentiate to become other cell types.
Embryonic stem cells
Embryonic stem cells are derived from a four- or five-day-old human embryo that is in the blastocyst
phase of development. The embryos are usually extras that have been created in IVF (in vitro fertilization)
clinics where several eggs are fertilized in a test tube, but only one is implanted into a woman.
Sexual reproduction begins when a male's sperm fertilizes a female's ovum (egg) to form a single cell
called a zygote. The single zygote cell then begins a series of divisions, forming 2, 4, 8, 16 cells, etc. After
four to six days - before implantation in the uterus - this mass of cells is called a blastocyst. The
blastocyst consists of an inner cell mass (embryoblast) and an outer cell mass (trophoblast). The outer
cell mass becomes part of the placenta, and the inner cell mass is the group of cells that will differentiate
to become all the structures of an adult organism. This latter mass is the source of embryonic stem cells -
totipotent cells (cells with total potential to develop into any cell in the body).
In a normal pregnancy, the blastocyst stage continues until implantation of the embryo in the uterus, at
which point the embryo is referred to as a fetus. This usually occurs by the end of the 10th week of
gestation after all major organs of the body have been created.
However, when extracting embryonic stem cells, the blastocyst stage signals when to isolate stem cells
by placing the "inner cell mass" of the blastocyst into a culture dish containing a nutrient-rich broth.
Lacking the necessary stimulation to differentiate, they begin to divide and replicate while maintaining
their ability to become any cell type in the human body. Eventually, these undifferentiated cells can be
stimulated to create specialized cells.
Research with stem cells
Scientists and researchers are interested in stem cells for several reasons. Although stem cells do not
serve any one function, many have the capacity to serve any function after they are instructed to
specialize. Every cell in the body, for example, is derived from first few stem cells formed in the early
stages of embryological development. Therefore, stem cells extracted from embryos can be induced to
become any desired cell type. This property makes stem cells powerful enough to regenerate damaged
tissue under the right conditions.
Organ and tissue regeneration
Tissue regeneration is probably the most important possible application of stem cell research. Currently,
organs must be donated and transplanted, but the demand for organs far exceeds supply. Stem cells
could potentially be used to grow a particular type of tissue or organ if directed to differentiate in a certain
way. Stem cells that lie just beneath the skin, for example, have been used to engineer new skin tissue
that can be grafted on to burn victims.
Brain disease treatment
Additionally, replacement cells and tissues may be used to treat brain disease such as Parkinson's and
Alzheimer's by replenishing damaged tissue, bringing back the specialized brain cells that keep unneeded
muscles from moving. Embryonic stem cells have recently been directed to differentiate into these types
of cells, and so treatments are promising.
Cell deficiency therapy
Healthy heart cells developed in a laboratory may one day be transplanted into patients with heart
disease, repopulating the heart with healthy tissue. Similarly, people with type I diabetes may receive
pancreatic cells to replace the insulin-producing cells that have been lost or destroyed by the patient's
own immune system. The only current therapy is a pancreatic transplant, and it is unlikely to occur due to
a small supply of pancreases available for transplant.
Blood disease treatments
Adult hematopoietic stem cells found in blood and bone marrow have been used for years to treat
diseases such as leukemia, sickle cell anemia, and other immunodeficiencies. These cells are capable of
producing all blood cell types, such as red blood cells that carry oxygen to white blood cells that fight
disease. Difficulties arise in the extraction of these cells through the use of invasive bone marrow
transplants. However hematopoietic stem cells have also been found in the umbilical cord and placenta.
This has led some scientists to call for an umbilical cord blood bank to make these powerful cells more
easily obtainable and to decrease the chances of a body's rejecting therapy.
General scientific discovery
Stem cell research is also useful for learning about human development. Undifferentiated stem cells
eventually differentiate partly because a particular gene is turned on or off. Stem cell researchers may
help to clarify the role that genes play in determining what genetic traits or mutations we receive. Cancer
and other birth defects are also affected by abnormal cell division and differentiation. New therapies for
diseases may be developed if we better understand how these agents attack the human body.
Another reason why stem cell research is being pursued is to develop new drugs. Scientists could
measure a drug's effect on healthy, normal tissue by testing the drug on tissue grown from stem cells
rather than testing the drug on human volunteers.
Stem cell controversy
The debates surrounding stem cell research primarily are driven by methods concerning embryonic stem
cell research. It was only in 1998 that researchers from the University of Wisconsin-Madison extracted the
first human embryonic stem cells that were able to be kept alive in the laboratory. The main critique of this
research is that it required the destruction of a human blastocyst. That is, a fertilized egg was not given
the chance to develop into a fully-developed human.
When does life begin?
The core of this debate - similar to debates about abortion, for example - centers on the question, "When
does life begin?" Many assert that life begins at conception, when the egg is fertilized. It is often argued
that the embryo deserves the same status as any other full grown human. Therefore, destroying it
(removing the blastocyst to extract stem cells) is akin to murder. Others, in contrast, have identified
different points in gestational development that mark the beginning of life - after the development of
certain organs or after a certain time period.
People also take issue with the creation of chimeras. A chimera is an organism that has both human and
animal cells or tissues. Often in stem cell research, human cells are inserted into animals (like mice or
rats) and allowed to develop. This creates the opportunity for researchers to see what happens when
stem cells are implanted. Many people, however, object to the creation of an organism that is "part
The stem cell debate has risen to the highest level of courts in several countries. Production of embryonic
stem cell lines is illegal in Austria, Denmark, France, Germany, and Ireland, but permitted in Finland,
Greece, the Netherlands, Sweden, and the UK. In the United States, it is not illegal to work with or create
embryonic stem cell lines. However, the debate in the US is about funding, and it is in fact illegal for
federal funds to be used to research stem cell lines that were created after August 2001.
What is Alzheimer's Disease?
Alzheimer's disease (AD) is an age-related, non-reversible brain disorder that develops over a period of
years. Initially, people experience memory loss and confusion, which may be mistaken for the kinds of
memory changes that are sometimes associated with normal aging. However, the symptoms of AD
gradually lead to behavior and personality changes, a decline in cognitive abilities such as decision-
making and language skills, and problems recognizing family and friends. AD ultimately leads to a severe
loss of mental function. These losses are related to the worsening breakdown of the connections between
certain neurons in the brain and their eventual death. AD is one of a group of disorders called dementias
that are characterized by cognitive and behavioral problems. It is the most common cause of dementia
among people age 65 and older.
There are three major hallmarks in the brain that are associated with the disease processes of AD.
Amyloid plaques, which are made up of fragments of a protein called beta-amyloid peptide
mixed with a collection of additional proteins, remnants of neurons, and bits and pieces of other
Neurofibrillary tangles (NFTs), found inside neurons, are abnormal collections of a protein
called tau. Normal tau is required for healthy neurons. However, in AD, tau clumps together. As a
result, neurons fail to function normally and eventually die.
Loss of connections between neurons responsible for memory and learning. Neurons can't
survive when they lose their connections to other neurons. As neurons die throughout the brain,
the affected regions begin to atrophy, or shrink. By the final stage of AD, damage is widespread
and brain tissue has shrunk significantly.
Is there any treatment?
Currently there are no medicines that can slow the progression of AD. However, four FDA-approved
medications are used to treat AD symptoms. These drugs help individuals carry out the activities of daily
living by maintaining thinking, memory, or speaking skills. They can also help with some of the
behavioral and personality changes associated with AD. However, they will not stop or reverse AD and
appear to help individuals for only a few months to a few years. Donepezil (Aricept), rivastigmine
(Exelon), and galantamine (Reminyl) are prescribed to treat mild to moderate AD symptoms. Donepezil
was recently approved to treat severe AD as well. The newest AD medication is memantine (Namenda),
which is prescribed to treat moderate to severe AD symptoms.
What is the prognosis?
In very few families, people develop AD in their 30s, 40s, and 50s. This is known as "early onset" AD.
These individuals have a mutation in one of three different inherited genes that causes the disease to begin
at an earlier age. More than 90 percent of AD develops in people older than 65. This form of AD is called
"late-onset" AD, and its development and pattern of damage in the brain is similar to that of early-onset
AD. The course of this disease varies from person to person, as does the rate of decline. In most people
with AD, symptoms first appear after age 65.
We don't yet completely understand the causes of late-onset AD, but they probably include genetic,
environmental, and lifestyle factors. Although the risk of developing AD increases with age, AD and
dementia symptoms are not a part of normal aging. There are also some forms of dementia that aren't
related to brain diseases such as AD, but are caused by systemic abnormalities such as metabolic
syndrome, in which the combination of high blood pressure, high cholesterol, and diabetes causes
confusion and memory loss.
What research is being done?
The National Institute of Neurological Disorders and Stroke (NINDS) supports basic and translational
research related to AD through grants to major medical institutions across the country. Current studies are
investigating how the development of beta amyloid plaques damages neurons, and how abnormalities in
tau proteins create the characteristic neurofibrillary tangles of AD. Other research is exploring the impact
of risk factors associated with the development of AD, such as pre-existing problems with blood flow in
the blood vessels of the brain. Most importantly, the NINDS supports a number of studies that are
developing and testing new and novel therapies that can relieve the symptoms of AD and potentially lead
to a cure.
Alzheimer's Disease Fact Sheet
Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory
and thinking skills, and eventually even the ability to carry out the simplest tasks. In most
people with Alzheimer’s, symptoms first appear after age 60.
Alzheimer’s disease is the most common cause of dementia among older people. Dementia is the
loss of cognitive functioning—thinking, remembering, and reasoning—to such an extent that it
interferes with a person’s daily life and activities. Estimates vary, but experts suggest that as
many as 5.1 million Americans may have Alzheimer’s.
Alzheimer’s disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes
in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms
included memory loss, language problems, and unpredictable behavior. After she died, he
examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled
bundles of fibers (now called neurofibrillary tangles). Plaques and tangles in the brain are two of
the main features of Alzheimer’s disease. The third is the loss of connections between nerve cells
(neurons) in the brain.
Changes in the Brain in Alzheimer’s Disease
Although we still don’t know what starts the Alzheimer’s disease process, we do know that
damage to the brain begins as many as 10 to 20 years before any problems are evident. Tangles
begin to develop deep in the brain, in an area called the entorhinal cortex, and plaques form in
other areas. As more and more plaques and tangles form in particular brain areas, healthy
neurons begin to work less efficiently. Then, they lose their ability to function and communicate
with each other, and eventually they die. This damaging process spreads to a nearby structure,
called the hippocampus, which is essential in forming memories. As the death of neurons
increases, affected brain regions begin to shrink. By the final stage of Alzheimer’s, damage is
widespread and brain tissue has shrunk significantly.
Very Early Signs and Symptoms
Memory problems are one of the first signs of Alzheimer’s disease. Some people with memory
problems have a condition called amnestic mild cognitive impairment (MCI). People with this
condition have more memory problems than normal for people their age, but their symptoms are
not as severe as those with Alzheimer’s. More people with MCI, compared with those without
MCI, go on to develop Alzheimer’s.
Other changes may also signal the very early stages of Alzheimer’s disease. For example, brain
imaging and biomarker studies of people with MCI and those with a family history of
Alzheimer’s are beginning to detect early changes in the brain like those seen in Alzheimer’s.
These findings will need to be confirmed by other studies but appear promising. Other recent
research has found links between some movement difficulties and MCI. Researchers also have
seen links between some problems with the sense of smell and cognitive problems. Such findings
offer hope that some day we may have tools that could help detect Alzheimer’s early, track the
course of the disease, and monitor response to treatments.
Mild Alzheimer’s Disease
As Alzheimer’s disease progresses, memory loss continues
and changes in other cognitive abilities appear. Problems can
include getting lost, trouble handling money and paying bills,
repeating questions, taking longer to complete normal daily
tasks, poor judgment, and small mood and personality
changes. People often are diagnosed in this stage.
Moderate Alzheimer’s Disease
In this stage, damage occurs in areas of the brain that control
language, reasoning, sensory processing, and conscious
thought. Memory loss and confusion increase, and people
begin to have problems recognizing family and friends. They
may be unable to learn new things, carry out tasks that involve
multiple steps (such as getting dressed), or cope with new
situations. They may have hallucinations, delusions, and Click to view a larger image
paranoia, and may behave impulsively.
Severe Alzheimer’s Disease
By the final stage, plaques and tangles have spread throughout the brain and brain tissue has
shrunk significantly. People with severe Alzheimer’s cannot communicate and are completely
dependent on others for their care. Near the end, the person may be in bed most or all of the time
as the body shuts down.
What Causes Alzheimer’s
Scientists don’t yet fully understand what causes Alzheimer’s disease, but it is clear that it
develops because of a complex series of events that take place in the brain over a long period of
time. It is likely that the causes include genetic, environmental, and lifestyle factors. Because
people differ in their genetic make-up and lifestyle, the importance of these factors for
preventing or delaying Alzheimer’s differs from person to person.
The Basics of Alzheimer’s
Scientists are conducting studies to learn more about plaques, tangles, and other features of
Alzheimer’s disease. They can now visualize plaques by imaging the brains of living individuals.
They are also exploring the very earliest steps in the disease process. Findings from these studies
will help them understand the causes of Alzheimer’s.
One of the great mysteries of Alzheimer’s disease is why it largely strikes older adults. Research
on how the brain changes normally with age is shedding light on this question. For example,
scientists are learning how age-related changes in the brain may harm neurons and contribute to
Alzheimer’s damage. These age-related changes include atrophy (shrinking) of certain parts of
the brain, inflammation, and the production of unstable molecules called free radicals.
In a very few families, people develop Alzheimer’s disease in their 30s, 40s, and 50s. Many of
these people have a mutation, or permanent change, in one of three genes that they inherited
from a parent. We know that these gene mutations cause Alzheimer’s in these “early-onset”
familial cases. Not all early-onset cases are caused by such mutations.
Most people with Alzheimer’s disease have “late-onset” Alzheimer’s, which usually develops
after age 60. Many studies have linked a gene called APOE to late-onset Alzheimer’s. This gene
has several forms. One of them, APOE ε4, increases a person’s risk of getting the disease. About
40 percent of all people who develop late-onset Alzheimer’s carry this gene. However, carrying
the APOE ε4 form of the gene does not necessarily mean that a person will develop Alzheimer’s
disease, and people carrying no APOE ε4 forms can also develop the disease.
Most experts believe that additional genes may influence the development of late-onset
Alzheimer’s in some way. Scientists around the world are searching for these genes. Researchers
have identified variants of the SORL1, CLU, PICALM, and CR1 genes that may play a role in
risk of late-onset Alzheimer’s. For more about this area of research, see the Alzheimer’s Disease
Genetics Fact Sheet, available at www.nia.nih.gov/Alzheimers/Publications/geneticsfs.htm.
A nutritious diet, physical activity, social engagement, and mentally stimulating pursuits can all
help people stay healthy. New research suggests the possibility that these factors also might help
to reduce the risk of cognitive decline and Alzheimer’s disease. Scientists are investigating
associations between cognitive decline and vascular and metabolic conditions such as heart
disease, stroke, high blood pressure, diabetes, and obesity. Understanding these relationships and
testing them in clinical trials will help us understand whether reducing risk factors for these
diseases may help with Alzheimer’s as well.
How Alzheimer’s Disease Is Diagnosed
Alzheimer’s disease can be definitively diagnosed only after death by linking clinical course
with an examination of brain tissue and pathology in an autopsy. But doctors now have several
methods and tools to help them determine fairly accurately whether a person who is having
memory problems has “possible Alzheimer’s disease” (dementia may be due to another cause) or
“probable Alzheimer’s disease” (no other cause for dementia can be found). To diagnose
ask questions about the person’s overall health, past medical problems,
ability to carry out daily activities, and changes in behavior and
conduct tests of memory, problem solving, attention, counting, and
carry out medical tests, such as tests of blood, urine, or spinal fluid
perform brain scans, such as computerized tomography (CT) or
magnetic resonance imaging (MRI)
These tests may be repeated to give doctors information about how the person’s memory is
changing over time.
Early diagnosis is beneficial for several reasons. Having an early diagnosis and starting treatment
in the early stages of the disease can help preserve function for months to years, even though the
underlying disease process cannot be changed. Having an early diagnosis also helps families plan
for the future, make living arrangements, take care of financial and legal matters, and develop
In addition, an early diagnosis can provide greater opportunities for people to get involved in
clinical trials. In a clinical trial, scientists test drugs or treatments to see which are most effective
and for whom they work best. (See the box, below, for more information.)
How Alzheimer’s Is Treated
Alzheimer’s disease is a complex disease, and no single “magic bullet” is likely to prevent or
cure it. That’s why current treatments focus on several different aspects, including helping
people maintain mental function; managing behavioral symptoms; and slowing, delaying, or
preventing the disease.
Helping People with Alzheimer’s Maintain Mental Function
Four medications are approved by the U.S. Food and Drug Administration to treat Alzheimer’s.
Donepezil (Aricept®), rivastigmine (Exelon®), and galantamine (Razadyne®) are used to treat
mild to moderate Alzheimer’s (donepezil can be used for severe Alzheimer’s as well).
Memantine (Namenda®) is used to treat moderate to severe Alzheimer’s. These drugs work by
regulating neurotransmitters (the chemicals that transmit messages between neurons). They may
help maintain thinking, memory, and speaking skills, and help with certain behavioral problems.
However, these drugs don’t change the underlying disease process and may help only for a few
months to a few years.
Managing Behavioral Symptoms
Common behavioral symptoms of Alzheimer’s include sleeplessness, agitation, wandering,
anxiety, anger, and depression. Scientists are learning why these symptoms occur and are
studying new treatments—drug and non-drug—to manage them. Treating behavioral symptoms
often makes people with Alzheimer’s more comfortable and makes their care easier for
Slowing, Delaying, or Preventing Alzheimer’s Disease
Alzheimer’s disease research has developed to a point where scientists can look beyond treating
symptoms to think about addressing the underlying disease process. In ongoing clinical trials,
scientists are looking at many possible interventions, such as cardiovascular and diabetes
treatments, antioxidants, immunization therapy, cognitive training, and physical activity.