by:
Michael
Sang
Alzheimer's
Disease
Introduction to
Alzheimer's
Alzheimer's disease is a progressive
degenerative disease of
the brain. It is
first described by the German neuropathologist Alois
Alzheimer (1864-1915)
in 1905. This disease worsens with
advancing age,
although there is
no evidence that it is cause by the aging process.
The average life expectancy of a person with
the disease is between
five and ten
years, but some patients today can live up to 15 years due to
improvements in
care and medical treatments. The cause of Alzheimer's
has not been
discovered yet and it cannot be possible to confirm a person
has Alzheimer's
until their autopsy following death.
How does
Alzheimer's develop
What causes Alzheimer's? Well no one know
exactly the
development
of this
debilitating disease. But recent advances has produced several clues
as to how it is
born. Initially when we study the brain of a Alzheimer's
victim, we focus
on two specific areas. One is the cortex of the frontal and
cerebral lobes1.
The second is the hippocampus (meaning seahorses in
Greek which it
resembles2) which is located below the cerebral cortex and
responsible for
short-term memory. If we study samples of these two
section, we would
find three irregularities which are not found in normal
brain matter.
These three are called neurofibrillary tangles, neuritic plagues
and
granulovacuolar degeneration3.
A nerve cell has numerous axons and dendrites
coming out of it. A
neurofibrillary
tangle is when the neuron changes. A number of dendrites
are missing and
the nucleus is filled with protein filaments resembling steel
wool4.
Although all
elderly people has a few of these helix shaped bundles in their
brain for they are
normal indicators of aging, Alzheimer's patients has more
than usual. Their
presence usually in the frontal and temporal lobes is a
indication of AD.
Senile neuritic plagues are small round
objects. They are masses of
amyloid protein
material composed of residue left over from healthy nerve
endings that were
broken off and decayed. Their presence near the cell
further indicates
something gone wrong. Neuritic plaques is the best
evidence for
diagnostics to make the determination of AD.
A third sign of neuron deterioration is
granulovacuolar degeneration.
This is when
fluid-filled vacuoles are seen crowding inside the nerve cell,
specifically in
the triangular shaped cells of the hippocampus. This
condition can
only be observed in carefully sliced, stain and analyzed brain
tissue.
The cell having lost all it's dendrites and
nucleus soon disintegrates
entirely,
vanishing into the body's waste disposal system. With the
depletion of
enough nerve material the brain actually shrinks, sometimes by
as much as ten
percent5. The more cells the AD sufferer loses, the more
mental functions
he loses. Soon the person will have limited motor skills.
People who were
once witty and quick on their feet were reduced to the
mental status of
small children.
Diagnosis of
Alzheimer's
How would you now if a person you knew has
Alzheimer's? There
are certain
telltale signs that point to it. There was one patient6 that was
convinced she was
suffering from AD. As proof of her condition, she
bought the a meeting
several recent newspaper clippings, which she began
to quote from
memory. Obviously this person did not have the disease,
she wouldn't have
memorized complex and lengthy information. But
forgetting on a
regular basis doesn't indicate Alzheimer's either.
Stages of AD
In the initial stage, there is no clear
evidence of memory trouble and
deterioration in
brain functions. The individual performs well on exams that
test mental
abilities (psychometric tests7) similar to those given to measure
IQ.
In the second stage, the patient shows very
mild memory problems
with difficulty
in remembering names of friends. The changes at this point
is still very
small. Occasionally, the patient might make a surprising
statement such as
inquiring about the health of a friend who everyone
knows, died years
ago. Only extensive psychometric testing can determine
if the person's
mental ability changed. A close family member like a
husband or wife
might suspect something is wrong.
By the third stage, there is definite evidence
of memory loss, which
might interfere
with job performance, The person might have difficulty
competing a job
that use to be routine. The person may avoid social
situations
because he or she realizes there's a problem
In stage four there is clinical evidence of
memory impairment when
the mental status
is tested by doctors. The disease has now become
obvious to the
family. A sign of this stage is when the patient keeps asking
the same question
which has already been answered, this make daily
companionship
difficult because his friends and family are frustrated.
By stage 5, the patient show problems with both
recent and past
memories, they
even forget events that are important like Christmas,
birthdays,
friendships and interests. Judgment is failing, the individual is no
longer able to
select clothes for a particular weather of season and cannot
match items by
color. Eventually, the victim of AD may leave the water
running, the
stove on, or the front door open. At this point wandering
becomes a major
problem.
In stage six, understanding of languages
diminishes and simple
commands aren't
understood. Victims may go back to their first language
if they have one.
Eventually languages disappear entirely.
In stage seven or the terminal stage, the
victim becomes bedridden
and totally
dependent for all functions. He cannot speak coherently and
can't eat
unassisted. Death usually occurs at this stage form aspiration
pneumonia8, pneumonia caused by breathing in food or
other objects
because the
victim doesn't remember how to swallow food safely, or from
urinary
infections.
Recent Research
on Alzheimer's
Some progress has been made in understanding
the nature of the
Alzheimer's
disease. Scientists has recently found medicine that can slow
down the progress
of AD. The average survival period from the time of
diagnosis to
death in 1985 is 10 years. Today the rate has increase a third
to 15 years9.
A recent media release stated the discovery of
a mutant gene called
"triplet
repeat" disease genes10. These genes produce proteins that may
block from
properly functioning key enzymes that are important to the
production of
energy in the brain. This gene was found in several diseases
like AD,
Huntingtons, and Haw River Syndrome as well as three other rare
neurological
disorders.
Another press release from the Alzheimer's
Association is one
concerning the
new study of an important advance toward early detection
of AD11.
"Through investigations such as these, in addition to those
involving
apolipoprotien E (APOE), positron emission tomography (PET),
and other
approaches, we will improve our ability for accurate detection of
individual at
risks for the disease"12 said Zaven Khachaturian Ph.D.,
director of the
Alzheimer's Association's Ronald and Nancy Reagan
Research
Institute.
Among the drugs being tested to treat AD are
-Cholinergic
agents: choline, lecithin, and the agonist (RS 86, arecholine,
and bethanechol)
-Peptides:
vasopressin, ACTH 4-10, naloxone
-Nootropic
agents: pramiracetem, CI 911, Praxilene, Oxiratem
-other general
drugs: chelating agents, Nimodipine, Vinpocetine13
most of these are
still in experimental stages. Some has proved to work
slightly but is
generally unsafe, others has tested safe but not beneficial, but
none has been
both. People who offer "cures" to Alzheimer's are either
frauds or
ignorant14.
When people realizes that AD is a serious
disease, perhaps as much
as HIV, then
maybe they will pay attention. The reason why there hasn't
been a cure is
because scientists tries to attract grants by working on a
problem that
people think is serious and controversial. If there was as
much attention
that was paid to AIDS as there was in AD, then maybe
there will be an
answer.
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