Caring For Alzheimer's Disease

Patients And Families

Beyond the patient, AD takes a considerable
toll on families, caregivers, and friends.
The memory loss and altered emotions and
behaviors associated with the disease are an
almost impossible burden, posing an
enormous physical and emotional challenge
for caregivers. One recent survey indicates
that caring for someone with dementia,
compared with attending to someone with
other types of illnesses, involves significantly
more time spent on care-giving tasks, greater
employment complications, caregiver strain,
mental and physical health problems (including lowered
resistance to disease) and family conflict, as well as less time for
leisure and other family members.
Caring For Alzheimer's Disease
Patients And Families
Research on care-giving and long-term care
examines ways to alleviate or prevent some
of these problems. The effectiveness of
support groups, behavioral skills training
programs, family-based interventions,
computer-based information and
communications services is now being tested.
Data are now being reviewed from a number
of sites in the NIA and NINR-supported
REACH (Resources to Enhance Family
Caregiver Health) initiative, which should provide important clues about
what works-and what doesn't-to support families of patients with AD.
Studies so far suggest that information and problem solving needs of
caregivers change with time as the disease progresses and issues change.
"The study of care-giving, with its mix of physical, emotional, and social
and cultural factors, is an especially challenging one for research," notes
Dr. Morrison-Bogorad. The Institute works closely with the Alzheimer's
Association and other groups to share research findings on care-giving
and other aspects of AD and aging.
Alzheimer's
Self-management
Program
Nutrient Associations
Vitamins:
Vitamin B12
Vitamin B12 deficiency is one of the most common vitamin
deficiencies among the elderly. Vitamin B12 deficiency causes motor
skill disturbances, confusion, delusion, fatigue, memory loss,
numbness, and ringing in the ears.

Vitamin B6
Deficiency can cause depression and mental difficulties. Produces
neurotransmitters.

Vitamin B5
Plays a role in converting choline into acetylcholine, needed for
memory.

Nutrient Associations
Vitamins:

Vitamin C
Powerful antioxidant and immune system enhancer that reduces
allergies, protects the brain and spinal cord, keeps white blood cells
healthy, fights fatigue, and increases energy.

Vitamin E
An antioxidant that helps transport oxygen to the brain cells and
protects them from free radical damage. Click for more about vitamin
E and Alzheimer's Disease

Acetylcholine
Deficiency has been implicated as possibly causing dementia.
Maintains brain function and memory.
Nutrient Associations
Amino Acids:
Acetyl L-carnitine
Proven in double blind studies to enhance brain function and slows
the deterioration of memory. Proven through extensive research to
improve mental function.
Nutrient Cofactors :
Ginkgo Biloba
Improves circulation and delivery of oxygen to the brain, heart. Proven
through research to improving mental function.
Melatonin
Improves brain function and aids sleep.
Coenzyme Q10
Increases oxygenation of cells and is involved in the generation of
cellular energy.


Nutrient Associations
THINK ANTIOXIDANTS: Free radicals damage
the brain, and this damage may be partially
responsible for the development of
Alzheimer's disease. Antioxidants combat
free radical damage, and studies with
antioxidants, especially with the antioxidant
Vitamin E, have shown memory improvement in Alzheimer's patients.
So make sure that you're getting the antioxidants that your body needs.

EAT A HEALTHY DIET: Eat a well-balanced diet. Better nutritional
status means better memory and mental function.

BE SURE TO GET ENOUGH FIBER: Include plenty of fiber in your
diet. Oat and rice bran are good sources
Lifestyle Changes
EXERCISE: Regular exercise will keep your body strong
and able to fight off disease.
DON'T SMOKE OR DRINK: Avoid alcohol, cigarette
smoke, processed foods, and environmental toxins,
especially metals like aluminum and mercury.
AVOID ALUMINUM: Autopsies of people who have died
of Alzheimer's disease have revealed higher than normal
amounts of aluminum in the brain, especially in the parts
of the brain concerned with memory. Aluminum can be
found in things such as aluminum cookware, antacids,
antidiarrheal preparations, buffered aspirin, aluminum
coated containers such as those used to store acidic
juices, deodorants, douches, food additives, and
shampoos. Extra aluminum is also sometimes added to
the naturally occurring aluminum in our drinking water.
Medical Options and Precautions
DRUGS:
Cognex(Tacrine): This drug is used to treat mild to
moderate Alzheimer's disease with some benefits for the
treatment of advanced Alzheimer's disease. Cognex is
only effective for 20-40% of those who take it and may of
cause liver damage. Because of this risk, using Cognex
requires regular liver function tests which may be
difficult to constantly administer to someone suffering from Alzheimer's.

Aricept(Donepezil): This drug prevents the breakdown of acetylcholine in the
brain and, unlike Cognex, does not cause liver enzyme abnormalities. It does
however, come with an extensive list of side effects, some of them severe.

Exelon(Rivastigmine): Like Aricept this drug does not cause liver
abnormalities but it does have many unpleasant side effects. One of these side
effects if nausea and vomiting serious enough to cause weight loss. For a more
extensive list of side effects.
Overview

Alzheimers disease is one of the
most common causes of dementia
(deterioration of intellectual and
mental abilities), a medical condition
that inhibits the way the brain works.

Scientists know that Alzheimer disease is caused by damage to brain
nerve cells, as well as a loss of certain chemicals that facilitate
communication between nerve cells. What is still not clearly
understood is why this damage occurs.

Several disorders that are similar to Alzheimer disease can cause
dementia; therefore a proper diagnosis by your doctor is needed.
Loss of normal sleep patterns
Problems with reasoning or judgment
Decline in the ability to perform routine tasks
Gradual loss of memory
Disorientation
Difficulty in learning
Loss of language skills

Overview
Overview
The disease usually begins after age 65 and manifests itself
slowly and subtly. At first there may be mild
forgetfulness. Over time, the forgetfulness becomes more
severe as the person has trouble remembering recent events,
activities or the names of familiar people or things. People with
Alzheimers disease may forget how to do simple things like
writing with a pen or pencil, brushing their teeth or taking a
shower. Later on, they may become anxious; show personality
changes like aggressiveness or hostility; and they may begin to
wander away from home. Over time, these changes may
become so severe that the patient cannot function or
communicate.

Eventually the individual dies, sometimes as the result of the
disease, often from other causes. The length of the disease
can vary from 3 to 20 years.
Through research, scientists continue to learn more about
Alzheimers disease, but at present the cause remains
unknown. This disease was first described in 1906 by Dr.
Alois Alzheimer. He examined the brain tissue of a woman
who had died of an unusual mental illness and he found odd
clumps (now called senile or neuritic plaques) and
tangled bundles of fibers (now called neurofibrillary
tangles). These plaques and tangles are still considered
hallmarks of Alzheimers disease. Scientists have also found
other changes in the brain, including a loss of nerve cells
and lower levels of chemicals. These changes disrupt
normal thinking and memory by blocking messages between
nerve cells.
Brain autopsies of Alzheimer patients always
show two characteristic brain abnormalities:
neurofibrillary tangles (twisted nerve cell fibers)
- found inside nerve cells in the hippocampus and
temporal and frontal lobes of the brain A type of protein called
tau is found within these tangles.
neuritic plaques
- located outside the nerve cells. The plaques are
surrounded by dying neurons (nerve cells), and contain a sticky
protein called beta amyloid. It is believed that beta amyloid may
cause narrowing of blood vessels in the brain, which in turn cuts
off the blood supply and kills nerve cells. The presence of the
neuritic plaques seems to be linked to reduction of an important
chemical called acetylcholine. Acetylcholine helps neurons relay
messages in the brain and is essential for memory and learning.

Current research can be summarized
into the following areas:

Genetic Factors

Toxic Exposure

Nutritional Disorders

Free Radical Damage
GENETIC FACTORS
Several genetic factors have been identified that play a role with
genes that are associated with Alzheimer's Disease (AD).
Amyloid precursor protein on chromosome 21. This is a
genetic factor also associated with Down's syndrome; and
explains the association between Down's syndrome and
Alzheimer's Disease.
Presenilin genes on chromosomes 14 and 1. Although rare,
these are associated with AD symptoms occurring before the
age of 50.
Apolipoprotein E (ApoE) gene on chromosome 19. This is most
interesting because it is both negative and positive. The e4-
type is linked to significantly higher risk for AD, the e2-type is
linked to significant protection from AD symptoms.

Although it is evident that genetics does play a role in
susceptibility, someone with questionable genetics should not
consider AD an inevitable event. Powerful environmental factors
(which are obviously more controllable) can play a great role to
protect against genetic weakness. By minimizing exposure to
toxins like aluminum, silicon, neurotoxins (drugs that affect the
brain and nervous system), and by maintaining high levels of
antioxidants, genetic weakness could be nullified.
TOXIC EXPOSURE
One of the main toxic elements associated with
Alzheimer's Disease is aluminum. Brain cells
get tangled and die off; a study has shown that
aluminum is a cofactor in the formation of these
neurofibrillary tangles. As people get older, their
body's ability to detoxify harmful toxins like aluminum
decreases, and so concentrations of toxins remain
and build up to unhealthy levels. This logically
explains why Alzheimer's Disease usually occurs in
relation to age increases. Also explained is the fact that those with Alzheimer's
Disease show higher levels of aluminum.

In a study of dialysis patients, they took 13 patients with a positive level of aluminum in
their body and compared them to 13 patients with low amounts of aluminum. The whole
group was subjected to two memory tests and the results were conclusive. Those with
higher levels of aluminum had a moderate to considerable disturbance of mental
function. With the association of aluminum to Alzheimer's Disease, the main concern is
where this toxic aluminum is coming from. Many of the elderly have digestive
difficulties and use antacids. While antacids may seem to help with their digestive
condition, antacids are loaded with unhealthy "aluminum." A much better digestive aid
would be to take a digestive enzyme supplement like Enzyme Plus.
TOXIC EXPOSURE
Aluminum exposure also comes from deodorants; pots, pans, and
silverware; food wrapped with aluminum foil; and non-dairy
creamer, baking powder, and many brands of table salt. Minimal
exposure to these items is crucial in keeping aluminum levels low.

The most alarming aluminum-containing substance is drinking
water! Yes, horrifying but true. It is well documented that
aluminum is added in the treatment process of over 50 percent of
the water supplies in the United States.

Daniel Perl, M.D., director of the neuropathology division at Mount
Sinai School of Medicine in New York City says that if the water is
purified properly no problems should occur. "But the question is,
how much of it is done properly? I'm reluctant to guess," he says.
Obviously, those who want to control their health process should
not leave water purification a matter of "guesswork."
NUTRITIONAL DISORDERS
Vitamin E is believed to be a vitamin breakthrough in the treatment of
Alzheimer's disease. Although the actual research we present here
was done regarding the effect Vitamin E has on Stroke Victims (where
a stroke has caused damage to brain cells); this stroke research
crosses over and has application in Alzheimer's Disease (AD).
During a stroke, damaged brain cells release a neurotransmitter called
glutamic acid. This glutamic acid causes a chain reaction that
destroys more brain cells, releasing even more dangerous glutamic
acid. David Schubert, Ph.D., professor of neurobiology at the Salk
Institute for Biological Studies in San Diego indicates that in their
studies exposing brain cells to vitamin E in a laboratory seems to
shield the cells from the effects of a stroke. He states that "Vitamin E
actually has a protective effect on brain cells, limiting the number
killed by glutamic acid."
In another study, Dr. Schubert's laboratory showed that bathing brain
cells in vitamin E protects them from a toxic protein found in amyloid
plaques. Just as soaking a peeled apple in lemon juice prevents
oxidation from turning it brown, antioxidants such as vitamin E protect
brain cells by neutralizing free radicals.
NUTRITIONAL DISORDERS
Vitamin B12 is also a key link to Alzheimer's Disease. Impaired mental
function, which sometimes mimics Alzheimer's Disease in elderly
people, is caused by a vitamin B12 deficiency. Vitamin B12 deficiency
exists in up to 42% of persons aged 65 and over. In fact, as people
age, levels of vitamin B12 decrease. It is important to detect B12
deficiency early because it is easy to resolve; but if left untreated it
can lead to impaired neurological and cognitive function that may not
ever be reversed.

Vitamin B12 supplementation was shown to reverse impaired mental
function in a study where 61% of cases with low levels of vitamin B12
had a complete recovery. It was thought that the 39% that did not
respond had probably had long-term low levels of vitamin B12.

This correlation is also true of people with Alzheimer's disease. If
Alzheimer's Disease patients supplement with vitamin B12 there could
be a complete reversal, but people who have had this disease for
longer than 6 months will probably only have minimal improvement.
NUTRITIONAL DISORDERS
Thiamin takes on a different role in the treatment of Alzheimer's disease.
While Vitamin E helps protect the brain from various acids and plaques,
thiamin concentrates on improving the memory. Thiamin has a RDA of
1.5 mg and most people fail to consume this daily allowance, especially
the elderly who need it the most. Thiamin is by no means a miracle pill,
but it is a step in the right direction, and in research has been shown to
slow or even stop the memory decline process. The following will tell you
how!

Acetylcholine is an important neurotransmitter that helps the nerve
impulses that carry thoughts to leap across the gaps between brain
nerve cells. This acetylcholine is made more available with thiamin
supplementation.
NUTRITIONAL DISORDERS
Numerous studies have shown the positive effects of Thiamin in
Alzheimer's patients. In one study, 18 Alzheimer's patients were treated
for five months with megadoses of thiamin ranging from 3,000 to 8,000
mgs a day. The results were not overwhelmingly impressive, but a little
improvement in an Alzheimer's patient means a lot. Most of the patients
just maintained the same level of memory, but this is incredible
considering the disease gets worse every six months. According to Dr.
Meador, head of the Section of Behavioral Neurology at the Medical
College of Georgia, "In particular, on the bedside exam you can expect a
three-point drop almost every four to six months. We didn't see that in
these people."
NUTRITIONAL DISORDERS
Zinc is important for maintaining high mental capacity and a key factor in
the enzymes used for DNA replication, repair, and transcription. It is
believed that dementia could be the result of long-term effects of
malfunctioning DNA-handling enzymes. This makes zinc deficiency a
serious problem, and since zinc deficiency is one of the most common
nutrient deficiencies in the elderly the problem is even more serious.

To test the benefits of zinc supplementation in Alzheimer's patients, 10
patients were given 27 mg of zinc per day. An amazing 80% showed
improvement and one patient was labeled "unbelievable" by both medical
staff and family.

NUTRITIONAL DISORDERS
Acetyl L-carnitine (ALC) has been shown to benefit Alzheimer's disease
patients by acting similar to acetylcholine and as a powerful antioxidant
within the brain cells to stabilize cell membranes and improve energy
production. The results of studies using ALC are outstanding, and the
studies have been well controlled and extremely thorough, which gives a
high level of confidence for accross-the-board successful results using
ALC.[J.W. Pettegrew et al. Clinical and neurochemical effects of acetyl-L-
carnitine in Alzheimer's Disease.

One study with 130 patients measured fourteen different areas
(assessment scales, cognitive function tests, memory tests, physician
evaluations) over a 12-month period. The group taking ALC ranked better
in all fourteen areas in comparison to the placebo group.
NUTRITIONAL DISORDERS
In another group study, 1,500 mg of ALC daily resulted in significant
improvement in mental function, particularly in memory and in
constructional thinking.

The only drawback to ALC supplementation is the cost. Out of all the
potential nutrient options for Alzheimer's alternative nutrition therapy;
ALC is the most expensive item that can be incorporated
FREE RADICAL DAMAGE
Chemically unstable molecules known
as free radicals are produced
simultaneously when the body burns
oxygen to produce energy. Free radicals
cause damage to brain cells by taking
electrons from the body's healthy
molecules to balance themselves. The
body can usually handle a small amount
of free radicals, but when the number of
free radicals becomes excessive, then
the danger sets in. A large amount of
free radicals leads to even more free
radicals, and this excessive free radical
formation damages cells and tissues.
When this oxidative damage affects
your brain the effect sneaks up slowly,
and ever so quietly steals away a
person's memory and personality,
eventually eroding his ability to even
take care of himself.
FREE RADICAL DAMAGE
Numerous studies have been conducted to test the role antioxidants
have in the development of heart disease, cancer, Parkinson's
disease, and other diseases linked to excessive oxidation. In one
study, Parkinson's disease patients were given doses of vitamin A
and C for seven years. Eventually all the patients needed some drug
treatment, but the antioxidant nutrients slowed the progression of
the disease considerably.

Because of these results, scientists decided to try antioxidant
nutrients on Alzheimer's disease patients, but there has been only
one trial study published so far. In this study, patients with
moderately severe Alzheimer's disease were given either the
monoamine oxidase inhibitor selegiline, vitamin E, a combination of
selegiline and vitamin E, or a placebo. Of the four groups, those who
were given vitamin E clearly showed the most positive results.
Compared to the 39 percent placebo patients who had to be
institutionalized, the vitamin E group only had 26 percent.
How the Brain and Nerve Cells Change During
Alzheimer's Disease
One of the hallmarks of
Alzheimer's disease is the
accumulation of amyloid
plaques between nerve
cells (neurons) in the
brain. Amyloid is a general
term for protein fragments
that the body produces
normally. Beta-amyloid is a
fragment of a protein that
is snipped from another
protein called amyloid
precursor protein (APP). In
a healthy brain, these
protein fragments would
be broken down and
eliminated. In Alzheimer's
disease, the fragments
accumulate to form hard,
insoluble plaques.
How the Brain and Nerve Cells Change During
Alzheimer's Disease
Neurofibrillary tangles
consist of insoluble
twisted fibers that are
found inside of the brain's
cells. They primarily
consist of a protein called
tau, which forms part of a
structure called a
microtubule. The
microtubule helps
transport nutrients and
other important
substances from one part
of the nerve cell to another
(the axon is the long
threadlike extension that
conducts nerve impulses
away from the body of a
nerve cell, and dendrites
are any of the short
branched threadlike
extensions that conduct
nerve impulses towards
the nerve cell body. In
Alzheimer's disease the
tau protein is abnormal
and the microtubule
structures collapse.
How the Brain and Nerve Cells Change During
Alzheimer's Disease
There is an overall
shrinkage of brain tissue
as Alzheimer's disease
progresses. In addition,
the ventricles, or
chambers within the
brain that contain
cerebrospinal fluid, are
noticeably enlarged. In
the early stages of
Alzheimer's disease,
short-term memory
begins to decline when
the cells in the
hippocampus, which is
part of the limbic system,
degenerate. The ability to
perform routine tasks
also declines. As
Alzheimer's disease
spreads through the
cerebral cortex (the outer
layer of the brain),
judgment declines,
emotional outbursts may
occur and language is
impaired.
How the Brain and Nerve Cells Change During
Alzheimer's Disease
Progression of the
disease leads to the
death of more nerve
cells and subsequent
behavior changes, such
as wandering and
agitation. The ability to
recognize faces and to
communicate is
completely lost in the
final stages. Patients
lose bowel and bladder
control, and eventually
need constant care.
This stage of complete
dependency may last
for years before the
patient dies. The
average length of time
from diagnosis to death
is 4 to 8 years, although
it can take 20 years or
more for the disease to
run its course.
Today, human clinical trials involve dozens
of compounds. Under scrutiny are such
well-known drugs as Non-Steroidal
Anti-Inflammatory Drugs (NSAIDS) for their
possible effectiveness against cognitive
decline and AD and wholly new molecules
designed to interrupt underlying mechanisms
of the disease. These studies target three
main treatment goals: prevent AD altogether or slow its
development; maintain cognitive function in the short-term; and
manage the difficult behavioral problems, such as agitation,
aggression, wandering, and sleep disorders, associated with the
disease.
Currently available compounds being
tested include NSAIDs and aspirin,
antioxidants such as vitamin E, combined
folate/B6/B12 supplementation, and
ginkgo biloba, which is being tested in a
trial supported mainly by the NIH's
National Center for Complementary and
Alternative Medicine. In addition, estrogen
replacement therapy is being evaluated to see if it might
prevent AD in women with a family history of the disease.
As a result of greater understanding of
the genetic, molecular, and cellular
factors involved in AD, the design and
testing of new therapeutic approaches
is gaining momentum as well.
Secretase-inhibiting drugs are a focus
in the private sector and both public
and privately funded researchers have
stepped up efforts to further study and
test a new vaccine against AD, which
may protect against the formation of
amyloid plaques altogether. The NIA
has issued a request for new research
applications to conduct further
vaccine-related basic research. These
studies, in animal models, should help
to further understand the mechanisms
and long-term effects of vaccines
against AD. One pharmaceutical
company is in the very early stages of
testing a vaccine in humans.

It has been estimated that over 4
million Americans have Alzheimer
disease. This number is expected to
triple during the next 20 years as the
baby boomer generation ages. In most
cases, Alzheimer disease develops in
people over the age of 65, though
there is a rare, early-onset form of the
disease that may strike people as
young as 30. Nearly all people who
have Down syndrome develop
Alzheimer disease if they live into their
forties.
Risk Factors
It is possible to develop Alzheimer disease with or without the risk
factors. However, the more risk factors you have, the greater your
likelihood of developing Alzheimer disease.
There are still many questions regarding the exact cause(s) of Alzheimer,
so risk factors are still being identified. Currently, risk factors for
Alzheimer disease include:


age
gender
genetic factors
medical conditions
down syndrome
high cholesterol and hypertension
B-vitamin deficiency
mental activity and education
environment
Risk Factors
AGE
Age is the most important known risk factor for developing Alzheimer
disease. The number of people with Alzheimer disease doubles every five years
beyond age 65 until age 85, when almost 50% of all people have the disease.

GENDER
Alzheimer disease affects both men and women, but women may have a
slightly higher risk of developing the disease than men.

GENETIC FACTORS
There has been a clear genetic link established for an early-onset form of
Alzheimer disease (occurs in people during their 30s, 40s and early 50s), and
a genetic link is suspected for late-onset Alzheimer disease. However, a
specific gene has not yet been identified. One gene that has been implicated as
being a major risk factor for late-onset Alzheimer disease is the ApoE4 gene.
Scientists continue to study the role of genetic factors in the development of
this disease.

MEDICAL CONDITIONS
There are some studies that suggest that people who suffered a serious,
traumatic head injury at some time in their lives may be at higher risk of
developing Alzheimer disease.
Risk Factors
DOWN SYNDROME
Nearly all people with Down syndrome who live to be age 40 or older develop
Alzheimer disease. Women who give birth before age 35 to a child with Down
syndrome are also at higher risk of developing Alzheimer disease.

HIGH CHOLESTEROL & HYPERTENSION
Recent research suggests that people who have high cholesterol and high
blood pressure may be at increased risk of developing Alzheimer disease.

B-VITAMIN DEFFICIENCY
Low levels of the vitamin B12 and folate have been linked to a development of
Alzheimer disease.

MENTAL ACTIVITY & EDUCATION
Some research has suggested that people who have higher education levels
and continue to be mentally active and engaged in their later years are less
likely to develop Alzheimer disease.

ENVIRONMENT
Some theories suggest that Alzheimer disease may be linked to exposure to
certain environmental factors, such as toxins, certain viruses and bacteria,
certain metals, or electromagnetic fields, but there is currently no conclusive
evidence to support these theories.

Reducing Your Risk
At this time, there are no screening tests or screening
guidelines for Alzheimer disease. Testing is usually
not initiated until symptoms become apparent to
either the patient or a family member.

Because the causes of Alzheimer disease are
unknown, there are currently no guidelines for
reducing your risk of Alzheimer disease. Scientists
are studying medications and lifestyle factors (such
as diet, mental activity, and exercise) that may help
ward off Alzheimer disease. As our understanding of
Alzheimer disease grows, your doctor may have
more information regarding steps for reducing your
risk of Alzheimer disease as you age.