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.

Overview
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
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 e4type 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-Lcarnitine 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.