Free Essay on Alzheimer's Disease
Alzheimer's Disease
Alzheimer's Disease, progressive brain disorder
that causes a gradual and irreversible decline in memory, language skills,
perception of time and space, and, eventually, the ability to care for oneself.
First described by German psychiatrist Alois Alzheimer in 1906, Alzheimer's
disease was initially thought to be a rare condition affecting only young
people, and was referred to as presenile dementia. Today late-onset Alzheimer's
disease is recognised as the most common cause of the loss of mental function in
those aged 65 and over. Alzheimer's in people in their 30s, 40s, and 50s, called
early-onset Alzheimer's disease, occurs much less frequently, accounting for
less than 10 percent of the estimated 4 million Alzheimer's cases in the United
States.
Although Alzheimer's disease is not a normal part of the aging
process, the risk of developing the disease increases, as people grow older.
About 10 percent of the United States population over the age of 65 is affected
by Alzheimer's disease, and nearly 50 percent of those over age 85 may have the
disease.
Alzheimer's disease takes a devastating toll, not only on the
patients, but also on those who love and care for them. Some patients experience
immense fear and frustration as they struggle with once commonplace tasks and
slowly lose their independence. Family, friends, and especially those who
provide daily care suffer immeasurable pain and stress as they witness
Alzheimer's disease slowly take their loved one from them.
The onset of
Alzheimer's disease is usually very gradual. In the early stages, Alzheimer's
patients have relatively mild problems learning new information and remembering
where they have left common objects, such as keys or a wallet. In time, they
begin to have trouble recollecting recent events and finding the right words to
express themselves. As the disease progresses, patients may have difficulty
remembering what day or month it is, or finding their way around familiar
surroundings. They may develop a tendency to wander off and then be unable to
find their way back. Patients often become irritable or withdrawn as they
struggle with fear and frustration when once commonplace tasks become unfamiliar
and intimidating. Behavioural changes may become more pronounced as patients
become paranoid or delusional and unable to engage in normal conversation.
Eventually Alzheimer's patients become completely incapacitated and
unable to take care of their most basic life functions, such as eating and using
the bathroom. Alzheimer's patients may live many years with the disease, usually
dying from other disorders that may develop, such as pneumonia. Typically the
time from initial diagnosis until death is seven to ten years, but this is quite
variable and can range from three to twenty years, depending on the age of
onset, other medical conditions present, and the care patients receive.
The brains of patients with Alzheimer's have distinctive
formations—abnormally shaped proteins called tangles and plaques—that are
recognised as the hallmark of the disease. Not all brain regions show these
characteristic formations. The areas most prominently affected are those related
to memory.
Tangles are long, slender tendrils found inside nerve cells,
or neurons. Scientists have learned that when a protein called tau becomes
altered, it may cause the characteristic tangles in the brain of an Alzheimer's
patient. In healthy brains, tau provides structural support for neurons, but in
Alzheimer's patients this structural support collapses.
Plaques, or
clumps of fibres, form outside the neurons in the adjacent brain tissue.
Scientists found that a type of protein, called amyloid precursor protein, forms
toxic plaques when it is cut in two places. Researchers have isolated the enzyme
beta-secretase, which is believed to make one of the cuts in the amyloid
precursor protein. Researchers also identified another enzyme, called gamma
secretase that makes the second cut in the amyloid precursor protein. These two
enzymes snip the amyloid precursor protein into fragments that then accumulate
to form plaques that are toxic to neurons.
Scientists have found that
tangles and plaques cause neurons in the brains of Alzheimer's patients to
shrink and eventually die, first in the memory and language centers and finally
throughout the brain. This widespread neuron degeneration leaves gaps in the
brain's massaging network that may interfere with communication between cells,
causing some of the symptoms of Alzheimer's disease.
Alzheimer's
patients have lower levels of neurotransmitters, chemicals that carry complex
messages back and forth between the nerve cells. For instance, Alzheimer's
disease seems to decrease the level of the neurotransmitter acetylcholine, which
is known to influence memory. A deficiency in other neurotransmitters, including
somatostatin and corticotropin-releasing factor, and, particularly in younger
patients, serotonin and norepinephrine, also interferes with normal
communication between brain cells.
The causes of Alzheimer's disease
remain a mystery, but researchers have found that particular groups of people
have risk factors that make them more likely to develop the disease than the
general population. For example, people with a family history of Alzheimer's are
more likely to develop Alzheimer's disease.
Some of the most promising
Alzheimer's research is being conducted in the field of genetics to learn the
role a family history of the disease has in its development. Scientists have
learned that people who are carriers of a specific version of the apolipoprotein
E gene (apoE gene), found on chromosome 19, are several times more likely to
develop Alzheimer's than carriers of other versions of the apoE gene. The most
common version of this gene in the general population is apoE3. Nearly half of
all late-onset Alzheimer's patients have the less common apoE4 version, however,
and research has shown that this gene plays a role in Alzheimer's disease.
Scientists have also found evidence that variations in one or more genes located
on chromosomes 1, 10, and 14 may increase a person's risk for Alzheimer's
disease. Scientists have identified the gene variations on chromosomes 1 and 14
and learned that these genes produce mutations in proteins called presenilins.
These mutated proteins apparently trigger the activity of the enzyme gamma
secretase, which splices the amyloid precursor protein.
Researchers have
made similar strides in the investigation of early-onset Alzheimer's disease. A
series of genetic mutations in patients with early-onset Alzheimer's has been
linked to the production of amyloid precursor protein, the protein in plaques
that may be implicated in the destruction of neurons. One mutation is
particularly interesting to geneticists because it occurs on a gene involved in
the genetic disorder Down syndrome. People with Down syndrome usually develop
plaques and tangles in their brains as they get older, and researchers believe
that learning more about the similarities between Down syndrome and Alzheimer's
may further our understanding of the genetic elements of the disease.
Some studies suggest that one or more factors other than heredity may
determine whether people develop the disease. One study published in February
2001 compared residents of Ibadan, Nigeria, who eat a mostly low-fat vegetarian
diet, with African Americans living in Indianapolis, Indiana, whose diet
included a variety of high-fat foods. The Nigerians were less likely to develop
Alzheimer's disease compared to their U.S. counterparts. Some researchers
suspect that health problems such as high blood pressure, atherosclerosis
(arteries clogged by fatty deposits), high cholesterol levels, or other
cardiovascular problems may play a role in the development of the disease.
Other studies have suggested that environmental agents may be a possible
cause of Alzheimer's disease; for example, one study suggested that high levels
of aluminium in the brain may be a risk factor. Several scientists initiated
research projects to further investigate this connection, but no conclusive
evidence has been found linking aluminium with Alzheimer's disease. Similarly,
investigations into other potential environmental causes, such as zinc exposure,
viral agents, and food-borne poisons, while initially promising, have generally
turned up inconclusive results.
Some studies indicate that brain trauma
can trigger a degenerative process that results in Alzheimer's disease. In one
study, an analysis of the medical records of veterans of World War II
(1939-1945) linked serious head injury in early adulthood with Alzheimer's
disease in later life. The study also looked at other factors that could
possibly influence the development of the disease among the veterans, such as
the presence of the apoE gene, but no other factors were identified.
Alzheimer's disease is only positively diagnosed by examining brain
tissue under a microscope to see the hallmark plaques and tangles, and this is
only possible after a patient dies. As a result, physicians rely on a series of
other techniques to diagnose probable Alzheimer's disease in living patients.
Diagnosis begins by ruling out other problems that cause memory loss, such as
stroke, depression, alcoholism, and the use of certain prescription drugs. The
patient undergoes a thorough examination, including specialised brain scans, to
eliminate other disorders. The patient may be given a detailed evaluation called
a neuropsychological examination, which is designed to evaluate a patient's
ability to perform specific mental tasks. This helps the physician determine
whether the patient is showing the characteristic symptoms of Alzheimer's
disease—progressively worsening memory problems, language difficulties, and
trouble with spatial direction and time. The physician also asks about the
patient's family medical history to learn about any past serious illnesses,
which may give a hint about the patient's current symptoms.
There is no
known cure for Alzheimer's disease, and treatment focuses on lessening symptoms
and attempting to slow the course of the disease. Drugs that increase or improve
the function of brain acetylcholine, the neurotransmitter that affects memory,
have been approved by the United States Food and Drug Administration (FDA) for
the treatment of Alzheimer's disease. Called acetylcholinesterase inhibitors,
these drugs have had modest but clearly positive effects on the symptoms of the
disease. These drugs can benefit patients at all stages of illness, but they are
particularly effective in the middle stage. This finding corresponds with new
evidence that low acetylcholine levels in patients with Alzheimer's disease may
not be present in the earliest stage of the illness.
Evidence shows that
there is inflammation in the brains of Alzheimer's patients, which may be
associated with the production of amyloid precursor protein. Studies are under
way to find drugs that prevent this inflammation, to possibly slow or even halt
the progress of the disease. Other promising approaches center on mechanisms
that manipulate amyloid precursor protein production or accumulation. Drugs are
in development that may block the activity of the enzymes that cut the amyloid
precursor protein, halting amyloid production. Other studies in mice suggest
that vaccinating animals with amyloid precursor protein can produce a reaction
that clears amyloid precursor protein from the brain. Physicians have started
vaccination studies in humans to determine if the same potentially beneficial
effects can be obtained. There is still much to be learned, but as scientists
better understand the genetic components of Alzheimer's, the roles of the
amyloid precursor protein and the tau protein in the disease, and the mechanisms
of nerve cell degeneration, the possibility that a treatment will be developed
is more likely.
The responsibility for caring for Alzheimer's patients
generally falls on their spouses and children. Care givers must constantly be on
guard for the possibility of an Alzheimer's patient wandering away or becoming
agitated or confused in a manner that jeopardises the patient or others. Coping
with a loved one's decline and inability to recognise familiar faces causes
enormous pain.
The increased burden faced by families is intense, and
the life of the Alzheimer's care giver is often called a 36-hour day. Not
surprisingly, care givers often develop health and psychological problems of
their own as a result of this stress. The Alzheimer's Association, a national
organisation with local chapters throughout the United States, was formed in
1980 in large measure to provide support for Alzheimer's care givers. Today,
national and local chapters are a valuable source for information, referral, and
advice.