Alzheimer's disease

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Alzheimer's Disease

 

Definition

Alzheimer's disease (AD) is the most common form of dementia, a neurologic disease characterized by loss of mental ability severe enough to interfere with normal activities of daily living, lasting at least six months, and not present from birth. AD usually occurs in old age, and is marked by a decline in cognitive functions such as remembering, reasoning, and planning.

Description

A person with AD usually has a gradual decline in mental functions, often beginning with slight memory loss, followed by losses in the ability to maintain employment, to plan and execute familiar tasks, and to reason and exercise judgment. Communication ability, mood, and personality also may be affected. Most people who have AD die within eight years of their diagnosis, although the interval may be as short as one year or as long as 20 years. AD is the fourth leading cause of death in adults after heart disease, cancer, and stroke.
Between two and four million Americans have AD; that number is expected to grow to as many as 14 million by the middle of the 21st century as the population ages. While a small number of people in their 40s and 50s develop the disease (called earlyonset AD), AD predominantly affects the elderly. AD affects about 3% of all people between ages 65 and 74, about 19% of those between 75 and 84, and about 47% of those over 85. Slightly more women than men are affected with AD, but this may be because women tend to live longer, leaving a higher proportion of women in the most affected age groups.
The cost of caring for a person with AD is considerable. The annual cost of caring for one AD patient in 1998 was estimated as about $18,400 for a patient with mild AD, $30,100 for a patient with moderate AD, and $36,100 for a patient with severe AD. The annual direct and indirect costs of caring for AD patients in the United States was estimated to be as much as $100 billion. Slightly more than half of people with AD are cared for at home, while the remainder are cared for in a variety of health care institutions.

Causes and symptoms

Causes

The cause or causes of Alzheimer's disease are largely unknown, though some forms have genetic links. Some strong leads have been found through recent research, however, and these have given some theoretical support to several new experimental treatments.
At first AD destroys neurons (nerve cells) in parts of the brain that control memory, including the hippocampus, which is a structure deep in the deep that controls short-term memory. As these neurons in the hippocampus stop functioning, the person's short-term memory fails, and the ability to perform familiar tasks decreases. Later AD affects the cerebral cortex, particularly the areas responsible for language and reasoning. Many language skills are lost and the ability to make judgments is affected. Personality changes occur, which may include emotional outbursts, wandering, and agitation. The severity of these changes increases with disease progression. Eventually many other areas of the brain become involved, the brain regions affected atrophy (shrink and lose function), and the person with AD becomes bedridden, incontinent, helpless, and non-responsive.
Autopsy of a person with AD shows that the regions of the brain affected by the disease become clogged with two abnormal structures, called neurofibrillary tangles and amyloid plaques. Neurofibrillary tangles are twisted masses of protein fibers inside nerve cells, or neurons. In AD, tau proteins, which normally help bind and stabilize parts of neurons, are changed chemically, become twisted and tangled, and no longer can stabilize the neurons. Amyloid plaques consist of insoluble deposits of beta-amyloid, (a protein fragment from a larger protein called amyloid precursor protein (APP), mixed with parts of neurons and non-nerve cells. Plaques are found in the spaces between the nerve cells of the brain. While it is not clear exactly how these structures cause problems, many researchers believe that their formation is responsible for the mental changes of AD, presumably by interfering with the normal communication between neurons in the brain and later leading to the death of neurons. By 2000, three drugs for the treatment of AD symptoms were approved by the U.S. Food and Drug Administration (FDA). They act by increasing the level of chemical signaling molecules in the brain, known as neurotransmitters, to make up for this decreased communication ability. All act by inhibiting the activity of acetyl-cholinesterase, which is an enzyme that breaks down acetylcholine, an important neurotransmitter released by neurons that is necessary for cognitive function. These drugs modestly increase cognition and improve one's ability to perform normal activities of daily living.
Exactly what triggers the formation of plaques and tangles and the development of AD is unknown. AD likely results from many interrelated factors, including genetic, environmental, and others not yet identified. Two types of AD exist: familial AD (FAD), which is a rare autosomal dominant inherited disease, and sporadic AD, with no obvious inheritance pattern. AD also is described in terms of age at onset, with early onset AD occurring in people younger than 65, and late-onset occurring in those 65 and older. Early onset AD comprises about 5-10 % of AD cases and affects people aged 30 to 60. Some cases of early onset AD are inherited and are common in some families. Early-onset AD often progresses faster than the more common late-onset type.
All cases of FAD, which is relatively uncommon, that have been identified to date are the early onset type. As many as 50% of FAD cases are known to be caused by three genes located on three different chromosomes. Some families have mutations in the APP gene located on chromosome 21, which causes the production of abnormal APP protein. Others have mutations in a gene called presenilin 1 located on chromosome 14, which causes the production of abnormal presenilin 1 protein, and others have mutations in a similar gene called presenilin 2 located on chromosome 1, which causes production of abnormal presenilin 2. Presenilin 1 may be one of the enzymes that clips APP into beta-amyloid; it also may be important in the synaptic connections between brain cells.

Key terms

Acetylcholine — —One of the substances in the body that helps transmit nerve impulses.
Dementia — —Impaired intellectual function that interferes with normal social and work activities.
Ginkgo — —An herb from the Ginkgo biloba tree that some alternative practitioners recommend for the prevention and treatment of AD.
Neurofibrillary tangle — —Twisted masses of protein inside nerve cells that develop in the brains of people with AD.
Senile plaque — —Structures composed of parts of neurons surrounding brain proteins called beta-amyloid deposits found in the brains of people with AD.
There is no evidence that the mutated genes that cause early onset FAD also cause late onset AD, but genetics appears to play a role in this more common form of AD. Discovered by researchers at Duke University in the early 1990s, potentially the most important genetic link to AD was on chromosome 19. A gene on this chromosome, called APOE (apolipoprotein E), codes for a protein involved in transporting lipids into neurons. APOE occurs in at least three forms (alleles), called APOE e2, APOE e3, and APOE e4. Each person inherits one APOE from each parent, and therefore can either have one copy of two different forms, or two copies of one. The relatively rare APOE e2 appears to protect some people from AD, as it seems to be associated with a lower risk of AD and a later age of onset if AD develops. APOE e3 is the most common version found in the general population, and only appears to have a neutral role in AD. However, APOE e4 appears to increase the risk of developing late onset AD with the inheritance of one or two copies of APOE e4. Compared to those without APOE e4, people with one copy are about three times as likely to develop late-onset AD, and those with two copies are almost four times as likely to do so. Having APOE e4 also can lower the age of onset by as much as 17 years. However, APOE e4 only increases the risk of developing AD and does not cause it, as not everyone with APOE e4 develops AD, and people without it can still have the disease. Why APOE e4 increases the chances of developing AD is not known with certainty. However, one theory is that APOE e4 facilitates beta-amyloid buildup in plaques, thus contributing to the lowering of the age of onset of AD; other theories involve interactions with cholesterol levels and effects on nerve cell death independent of its effects on plaque buildup. In 2000, four new AD-related regions in the human genome were identified, where one out of several hundred genes in each of these regions may be a risk factor gene for AD. These genes, which are not yet identified, appear to make a contribution to the risk of developing late-onset AD that is at least as important as APOE e4.
Other non-genetic factors have been studied in relation to the causes of AD. Inflammation of the brain may play a role in development of AD, and use of nonsteroidal anti-inflammatory drugs (NSAIDs) were once thought to reduce the risk of developing AD. Other agents once thought to reduce chances of dementia are now thought to increase its risk. In 2002, hormone replacement therapy (HRT), which combines estrogen and progestogen, was found to double the risk of developing dementia in postmenopausal women. Highly reactive molecular fragments called free radicals damage cells of all kinds, especially brain cells, which have smaller supplies of protective antioxidants thought to protect against free radical damage. Vitamin E is one such antioxidant, and its use in AD may be of possible theoretical benefit.
While the ultimate cause or causes of Alzheimer's disease still are unknown, there are several risk factors that increase a person's likelihood of developing the disease. The most significant one is, of course, age; older people develop AD at much higher rates than younger ones. There is some evidence that strokes and AD may be linked, with small strokes that go undetected clinically contributing to the injury of neurons. A 2003 Dutch study reported that symptomless, unnoticed strokes could double the risk of AD and other dementias. Blood cholesterol levels also may be important. Scientists have shown that high blood cholesterol levels in special breeds of genetically engineered (transgenic) mice may increase the rate of plaque deposition. There are also parallels between AD and other progressive neurodegenerative disorders that cause dementia, including prion diseases, Parkinson's disease, and Huntington's disease.
Numerous epidemiological studies of populations also are being conducted to learn more about whether and to what extent early life events, socioeconomic factors, and ethnicity have an impact on the development of AD. For example, a 2003 report showed that the more formal education a person has, the better his or her memory is, despite presence of AD. Other studies have related education level or participation in leisure activities such as playing cards or doing crossword puzzles to delayed onset of AD.
Many environmental factors have been suspected of contributing to AD, but epidemiological population studies have not borne out these links. Among these have been pollutants in drinking water, aluminum from commercial products, and metal dental fillings. To date, none of these factors has been shown to cause AD or increase its likelihood. Further research may yet turn up links to other environmental factors.

Symptoms

The symptoms of Alzheimer's disease begin gradually, usually with memory lapses. Occasional memory lapses are of course common to everyone, and do not by themselves signify any change in cognitive function. The person with AD may begin with only the routine sort of memory lapse—forgetting where the car keys are—but progress to more profound or disturbing losses, such as forgetting that he or she can even drive a car. Becoming lost or disoriented on a walk around the neighborhood becomes more likely as the disease progresses. A person with AD may forget the names of family members, or forget what was said at the beginning of a sentence by the time he hears the end.
As AD progresses, other symptoms appear, including inability to perform routine tasks, loss of judgment, and personality or behavior changes. Some people with AD have trouble sleeping and may suffer from confusion or agitation in the evening ("sunsetting" or Sundowner's Syndrome). In some cases, people with AD repeat the same ideas, movements, words, or thoughts. In the final stages people may have severe problems with eating, communicating, and controlling their bladder and bowel functions.
The Alzheimer's Association has developed a list of 10 warning signs of AD. A person with several of these symptoms should see a physician for a thorough evaluation:
  • memory loss that affects job skills
  • difficulty performing familiar tasks
  • problems with language
  • disorientation of time and place
  • poor or decreased judgment
  • problems with abstract thinking
  • misplacing things
  • changes in mood or behavior
  • changes in personality
  • loss of initiative
Other types of dementia, including some that are reversible, can cause similar symptoms. It is important for the person with these symptoms to be evaluated by a professional who can weigh the possibility that his or her symptoms may have another cause. Approximately 20% of those originally suspected of having AD turn out to have some other disorder; about half of these cases are treatable.

Diagnosis

Diagnosis of Alzheimer's disease is complex, and may require office visits to several different specialists over several months before a diagnosis can be made. While a confident provisional diagnosis may be made in most cases after thorough testing, AD cannot be diagnosed definitively until autopsy examination of the brain for plaques and neurofibrillary tangles.
The diagnosis of AD begins with a thorough physical exam and complete medical history. Except in the disease's earliest stages, accurate history from family members or caregivers is essential. Since there are both prescription and over-the-counter drugs that can cause the same mental changes as AD, a careful review of the patient's drug, medicine, and alcohol use is important. AD-like symptoms also can be provoked by other medical conditions, including tumors, infection, and dementia caused by mild strokes (multi-infarct dementia). These possibilities must be ruled out as well through appropriate blood and urine tests, brain magnetic resonance imaging (MRI), positron emission tomography (PET) or single photon emission computed tomography (SPECT) scans, tests of the brain's electrical activity (electroencephalographs or EEGs), or other tests. Several types of oral and written tests are used to aid in the AD diagnosis and to follow its progression, including tests of mental status, functional abilities, memory, and concentration. Still, the neurologic exam is normal in most patients in early stages.
One of the most important parts of the diagnostic process is to evaluate the patient for depression and delirium, since each of these can be present with AD, or may be mistaken for it. (Delirium involves a decreased consciousness or awareness of one's environment.) Depression and memory loss both are common in the elderly, and the combination of the often can be mistaken for AD. On the other hand, depression can be a risk factor for AD. A 2003 study showed that a history of depressive symptoms can be associated with nearly twice the risk of eventually developing AD. Depression can be treated with drugs, although some antidepressants can worsen dementia if it is present, further complicating both diagnosis and treatment.
An early and accurate diagnosis of AD is important in developing strategies for managing symptoms and for helping patients and their families planning for the future and pursuing care options while the patient can still take part in the decision-making process.
A genetic test for the APOE e4 gene is available, but is not used for diagnosis, since possessing even two copies does not ensure that a person will develop AD. In addition, access to genetic information could affect the insurability of a patient if disclosed, and also affect employment status and legal rights.

Treatment

Alzheimer's disease is presently incurable. Recent reports show that prompt intervention can slow decline from AD. The use of medications mentioned below as early as possible in the course of AD can help people with the disease maintain independent function as long as possible. The remaining treatment for a person with AD is good nursing care, providing both physical and emotional support for a person who is gradually able to do less and less for himself, and whose behavior is becoming more and more erratic. Modifications of the home to increase safety and security often are necessary. The caregiver also needs support to prevent anger, despair, and burnout from becoming overwhelming. Becoming familiar with the issues likely to lie ahead, and considering the appropriate financial and legal issues early on, can help both the patient and family cope with the difficult process of the disease. Regular medical care by a practitioner with a non-defeatist attitude toward AD is important so that illnesses such as urinary or respiratory infections can be diagnosed and treated properly, rather than being incorrectly attributed to the inevitable decline seen in AD.
People with AD often are depressed or anxious, and may suffer from sleeplessness, poor nutrition, and general poor health. Each of these conditions is treatable to some degree. It is important for the person with AD to eat well and continue to exercise. Professional advice from a nutritionist may be useful to provide healthy, easy-to-prepare meals. Finger foods may be preferable to those requiring utensils to be eaten. Regular exercise (supervised if necessary for safety) promotes overall health. A calm, structured environment with simple orientation aids (such as calendars and clocks) may reduce anxiety and increase safety. Other psychiatric symptoms, such as depression, anxiety, hallucinations (seeing or hearing things that aren't there), and delusions (false beliefs) may be treated with drugs if necessary.

Drugs

As of 2003, four drugs—tacrine (Cognex), donepezil hydrochloride (Aricept), and rivastigmine (Exelon)—have been approved by the FDA for its treatment. Tacrine has been shown to be effective for improving memory skills, but only in patients with mild-to-moderate AD, and even then in less than half of those who take it. Its beneficial effects are usually mild and temporary, but it may delay the need for nursing home admission. The most significant side effect is an increase in a liver enzyme known as alanine aminotransferase, or ALT. Patients taking tacrine must have a weekly blood test to monitor their ALT levels. Other frequent side effects include nausea, vomiting, diarrhea, abdominal pain, indigestion, and skin rash. The cost of tacrine was about $125 per month in early 1998, with additional costs for the weekly blood monitoring. Despite its high cost, tacrine appears to be cost-effective for those who respond to it, since it may decrease the number of months a patient needs nursing care. Donepezil is the drug most commonly used to treat mild to moderate symptoms of AD, although it only helps some patients for periods of time ranging from months to about two years. Donepezil has two advantages over tacrine: it has fewer side effects, and it can be given once daily rather than three times daily. Donepezil does not appear to affect liver enzymes, and therefore does not require weekly blood tests. The frequency of abdominal side effects is also lower. The monthly cost is approximately the same. Rivastigmine, approved for use in April of 2000, has been shown to improve the ability of patients to carry out daily activities, such as eating and dressing, decrease behavioral symptoms such as delusions and agitation, and improve cognitive functions such as thinking, memory, and speaking. The cost is similar to those of the other two drugs. However, none of these three drugs stops or reverses the progression of AD. Galantamine (Reminyl) works in the early and moderates stages of AD. It has fewer side effects than other drugs, with the exception of donepezil and must be taken twice a day. Three other drugs were being tested for AD treatment in mid-2003.
Estrogen, the female sex hormone, is widely prescribed for post-menopausal women to prevent osteoporosis. Studies once showed that estrogen was beneficial to women with AD, but in 2003, a large clinical trial called the Women's Health Initiative showed dementia among other negative effects of combined estrogen therapy.
Preliminary studies once suggested a reduced risk for developing AD in elderly people who regularly used nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen, and naproxen, although not acetaminophen. However, an important study published in 2003 showed that NSAIDs were not effective in preventing or slowing the progression of AD. The study authors recommended that people stop taking NSAIDs to slow dementia.
Antioxidants, which act to inhibit and protect against oxidative damage caused by free radicals, have been shown to inhibit toxic effects of beta-amyloid in tissue culture. Therefore, research is being conducted to see whether antioxidants may delay or prevent AD.
Another antioxidant, vitamin E, is also thought to delay AD onset. Hoever, it is not yet clear whether this is due to the specific action of vitamin E on brain cells, or to an increase in the overall health of those taking it.
Drugs such as antidepressants, anti-psychotics, and sedatives are used to treat the behavioral symptoms (agitation, aggression, wandering, and sleep disorders) of AD. Research is being conducted to search for better treatments, including non-drug approaches for AD patients.

Nursing care and safety

The person with Alzheimer's disease will gradually lose the ability to dress, groom, feed, bathe, or use the toilet by himself; in the later stages of the disease, he may be unable to move or speak. In addition, the person's behavior becomes increasingly erratic. A tendency to wander may make it difficult to leave him unattended for even a few minutes and make even the home a potentially dangerous place. In addition, some people with AD may exhibit inappropriate sexual behaviors.
The nursing care required for a person with AD is well within the abilities of most people to learn. The difficulty for many caregivers comes in the constant but unpredictable nature of the demands put on them. In addition, the personality changes undergone by a person with AD can be heartbreaking for family members as a loved one deteriorates, seeming to become a different person. Not all people with AD develop negative behaviors. Some become quite gentle, and spend increasing amounts of time in dreamlike states.
A loss of good grooming may be one of the early symptoms of AD. Mismatched clothing, unkempt hair, and decreased interest in personal hygiene become more common. Caregivers, especially spouses, may find these changes socially embarrassing and difficult to cope with. The caregiver usually will need to spend increasing amounts of time on grooming to compensate for the loss of attention from the patient, although some adjustment of expectations (while maintaining cleanliness) is often needed as the disease progresses.
Proper nutrition is important for a person with AD, and may require assisted feeding early on, to make sure the person is taking in enough nutrients. Later on, as movement and swallowing become difficult, a feeding tube may be placed into the stomach through the abdominal wall. A feeding tube requires more attention, but is generally easy to care for if the patient is not resistant to its use.
For many caregivers, incontinence becomes the most difficult problem to deal with at home, and is a principal reason for pursuing nursing home care. In the early stages, limiting fluid intake and increasing the frequency of toileting can help. Careful attention to hygiene is important to prevent skin irritation and infection from soiled clothing.
Persons with dementia must deal with six basic safety concerns: injury from falls, injury from ingesting dangerous substances, leaving the home and getting lost, injury to self or others from sharp objects, fire or burns, and the inability to respond rapidly to crisis situations. In all cases, a person diagnosed with AD should no longer be allowed to drive, because of the increased potential for accidents and the increased likelihood of wandering very far from home while disoriented. In the home, simple measures such as grab bars in the bathroom, bed rails on the bed, and easily negotiable passageways can greatly increase safety. Electrical appliances should be unplugged and put away when not in use, and matches, lighters, knives, or weapons should be stored safely out of reach. The hot water heater temperature may be set lower to prevent accidental scalding. A list of emergency numbers, including the poison control center and the hospital emergency room, should be posted by the phone. As the disease progresses, caregivers need to periodically reevaluate the physical safety of the home and introduce new strategies for continued safety.

Care for the caregiver

Family members or others caring for a person with AD have an extremely difficult and stressful job, which becomes harder as the disease progresses. Dementia caregivers spend significantly more time on caregiving than do people providing care for those with other types of illnesses. This type of caregiving also has a greater impact in terms of employment complications, caregiver strain, mental and physical health problems, time for leisure and other family members, and family conflict than do other types of caregiving. It is common for AD caregivers to develop feelings of anger, resentment, guilt, and hopelessness, in addition to the sorrow they feel for their loved one and for themselves. Depression is an extremely common consequence of being a full-time caregiver for a person with AD. Support groups are an important way to deal with the stress of caregiving. Becoming a member of an AD caregivers' support group can be one of the most important things a family member does, not only for him or herself, but for the person with AD as well. The location and contact numbers for AD caregiver support groups are available from the Alzheimer's Association; they also may be available through a local social service agency, the patient's physician, or pharmaceutical companies that manufacture the drugs used to treat AD. Medical treatment for depression may be an important adjunct to group support.

Outside help, nursing homes, and governmental assistance

Most families eventually need outside help to relieve some of the burden of around-the-clock care for a person with AD. Personal care assistants, either volunteer or paid, may be available through local social service agencies. Adult daycare facilities are becoming increasingly common. Meal delivery, shopping assistance, or respite care may be available as well.
Providing the total care required by a person with late-stage AD can become an overwhelming burden for a family, even with outside help. At this stage, many families consider nursing home care. This decision often is one of the most difficult for the family, since it is often seen as an abandonment of the loved one and a failure of the family. Careful counseling with a sympathetic physician, clergy, or other trusted adviser may ease the difficulties of this transition. Selecting a nursing home may require a difficult balancing of cost, services, location, and availability. Keeping the entire family involved in the decision may help prevent further stress from developing later on.
Several federal government programs may ease the cost of caring for a person with AD, including Social Security Disability, Medicare, and Supplemental Security Income. Each of these programs may provide some assistance for care, medication, or other costs, but none of them will pay for nursing home care indefinitely. Medicaid is a state-funded program that may provide for some or all of the cost of nursing home care, although there are important restrictions. Details of the benefits and eligibility requirements of these programs are available through the local Social Security or Medicaid office, or from local social service agencies.
Private long-term care insurance, special "reverse mortgages," viatical insurance, and other financial devices are other ways of paying for care for those with the appropriate financial situations. Further information on these options may be available through resources listed below.

Alternative treatment

Several substances are currently being tested for their ability to slow the progress of Alzheimer's disease. These include acetylcarnitine, a supplement that acts on the cellular energy structures known as mitochondria. Ginkgo extract, derived from the leaves of the Ginkgo biloba tree, appears to have antioxidant as well as anti-inflammatory and anticoagulant properties. Ginkgo extract has been used for many years in China and is widely prescribed in Europe for treatment of circulatory problems. A 1997 study of patients with dementia seemed to show that ginkgo extract could improve their symptoms, though the study was criticized for certain flaws in its method. Large scale follow-up studies are being conducted to determine whether Ginkgo extract can prevent or delay the development of AD. Ginkgo extract is available in many health food or nutritional supplement stores. Some alternative practitioners also advise people with AD to take supplements of phosphatidylcholine, vitamin B12, gotu kola, ginseng, St. Johnõs Wort, rosemary, saiko-keishi-to-shakuyaku (A Japanese herbal mixture), and folic acid.

Prognosis

While Alzheimer's disease may not be the direct cause of death, the generally poorer health of a person with AD increases the risk of life-threatening infection, including pneumonia. In addition, other diseases common in old age—cancer, stroke, and heart disease—may lead to more severe consequences in a person with AD. On average, people with AD live eight years past their diagnosis, with a range from one to 20 years.

Prevention

Currently, there is no sure way to prevent Alzheimer's disease. treatments discussed above may eventually be proven to reduce the risk of developing the disease. Avoiding risks such as hormone replacement therapy may help prevent development of AD.
Research on the prevention of AD is focusing on blocking the production of amyloid in the brain as well as breaking down beta-amyloid once it is released from cells but before it has a chance to aggregate into insoluble plaques. There also are promising studies being conducted to develop an AD vaccine, where immune responses may result in the elimination of the formation of amyloid plaques.
The Alzheimer's Disease Research Centers (ADCs) program promotes research, training and education, technology transfer, and multicenter and cooperative studies in AD, other dementias, and normal brain aging. Each ADC enrolls and performs studies on AD patients and healthy older people. Persons can participate in research protocols and clinical drug trials at these centers. Data from the ADCs as well as from other sources are coordinated and made available for use by researchers at the National Alzheimer's Coordinating Center, established in 1999.

Resources

Books

Cohen, Donna, and Carl Eisdorfer. The Loss of Self: A Family Resource for the Care of Alzheimer's Disease and Related Disorders. Revised. NewYork: W.W. Norton & Company, 2001.
Geldmacher, David S. Contemporary Diagnosis and Management of Alzheimer's Disease. Newtown, PA: Associates in Medical Marketing Co., Inc., 2001.
Gruetzner, Howard. Alzheimer's: A Caregiverõs Guideand Sourcebook. 3rd ed. New York: John Wiley & Sons, 2001.
Mace, Nancy L., and Peter V. Rabins. The 36-Hour Day: A Family Guide for Caring with Persons with Alzheimer Disease, Related Dementing Illnesses, and MemoryLoss in Later Life. New York: Warner Books, 2001.
Teitel, Rosette, and Marc L. Gordon. The Handholderõs Handbook: A Guide for Caregivers of Alzheimerõs and other Dementias. NewBrunswick, NJ: Rutgers University Press, 2001.

Periodicals

"Alzheimer's Could be Linked to Depression." GP (May 26, 2003): 4.
"Alzheimer's Could Reduced by Education." The Lancet (June 28, 2003): 2215.
"Contrary to Some Earlier Results, New Study Shows NSAIDs Do Not Slow Progression of Alzheimer's Disease." The Brown University Geriatric Psychopharmacology Update (July 2003): 1.
Gitlin, L.N., and M. Corcoran. "Making Homes Safer: Environmental Adaptations for People with Dementia." Alzheimer's Care Quarterly 1 (2000): 50-58.
Helmuth, L. "Alzheimer's Congress: Further Progress on aB-Amyloid Vaccine." Science 289, no. 5476 (2000): 375.
Josefson, Deborah. "Latests HRT Trial Results Show Risk of Dementia." British Medical Journal (June 7, 2003): 1232.
McReady, Norah. "Prompt Intervention May Slow Alzheimer's Decline." Family Practice News (May 1, 2003): 32-41.
Naditz, Alan. "Deeply Affected: As the Nation Ages, Alzheimer's Will Strike More People Close to Us." Contemporary Long Term Care (July 2003): 20-23.
"Researchers Believe "Silent" Strokes Boost Risk." GP (April 14, 2003): 9.

Other

Alzheimer's Disease Books and Videotapes. http://www.alzheimersbooks.com.
National Institute on Aging, National Institutes of Health. 2000: Progress Report on Alzheimer's Disease—Taking the Next Steps. NIH Publication No. 4859 (2000). 〈http://www.alzheimers.org/pubs/prog00.htm#References〉.

Alzheimer's disease

 [altz´hi-merz]
irreversible dementia characterized by intellectual deterioration, disorganization of the personality, and functional disabilities in carrying out activities of daily living. The official name is now dementia of the alzheimer type. It is categorized as either presenile (early onset) or senile (late onset) depending on whether or not it begins by the age of 65, and is subcategorized on the basis of accompanying features, including delirium, delusions, depressed mood, behavioral disturbances, or none (uncomplicated).

Diagnosis is tentatively made on the basis of the symptoms presented and their progression over a period of time. Confirmation of the diagnosis of Alzheimer's disease can be made only by postmortem examination of brain tissue. The defining characteristics noted on autopsy are neurofibrillary tangles in the cytoplasm of neurons, neuritic plaques or deposits resulting from degeneration in the neural processes, and granulovacuolar degeneration in the neurons.
Etiology. The cause or causes of Alzheimer's disease are under investigation. Postmortem studies have revealed below normal levels of choline acetyltransferase; altered levels of the neurotransmitters acetylcholine, somatostatin, substance P, and norepinephrine; and higher than normal deposits of aluminum in cerebral tissue. It is hypothesized that there is no single cause of the disease. Age is the most important risk factor. Many researchers believe that genetics plays a role. apolipoprotein e is also being actively studied as having a possible role.
Symptoms. Alzheimer's disease can progress slowly over a period of ten to fifteen years or it can become steadily worse in a matter of only a few years. In the early stages there are forgetfulness, especially of recent events, inability to learn or remember new information, impaired concentration, and deterioration in personal hygiene. Later as symptoms worsen, memory, language, and motor functions become increasingly impaired and the patient becomes more intellectually and physically disabled.

Perseveration, or continuous repetition of words or gestures, is characteristic of Alzheimer's disease in its later stages. Personality changes, incontinence, voracious appetite, and a compulsion to put everything in the mouth are other manifestations of the disease.
Treatment. At present there is no cure for Alzheimer's disease; therapies are aimed at relieving symptoms and managing behavior problems. There has been limited success in the use of drugs. tacrine, donepezil, rivastigmine, or galantamine may slow progression of symptoms in the early stages. Research in this area is ongoing.
Patient Care. As cognitive and psychomotor functions become more impaired, the impact on family members or other caregivers becomes more profound. They will need continued guidance and support as physical care of the patient escalates from a part-time to a full-time responsibility. In the early stages the patient may be able to handle basic self-care functions and can live in the community and take care of personal financial and marketing chores with minimal help. However, the forgetfulness that accompanies Alzheimer's disease places the patient at a safety risk because of the tendency to wander and get lost. Later, assistance with activities of daily living such as eating, grooming, and toileting will be required. Eventually the patient will be unable to handle the most basic tasks of personal care, and all motor abilities and forms of communication will be lost.

Family members and other caregivers encounter emotional outbursts and progressive intellectual and physical deterioration that make the tasks of care even more challenging. Part-time or full-time help in the home usually is needed to give some respite to caregivers. They will also need guidance in the management of incontinence and help in coping with role reversals and their own feelings about the loss they have suffered and the burden of care that they bear. Eventually, it may be necessary to institutionalize the person with Alzheimer's disease. This can bring on feelings of guilt and a sense of failure on the part of the caregiver.

Educational materials and information on clinical trials are available from the Alzheimer's Disease Education and Referral Center (ADEAR) by writing them at P.O. Box 8250, Silver Spring MD 20807-8250, calling them at 1-800-272-3900, or consulting their web site at http://www.alzheimer.org.

Alzheimer's disease

(älts′hī-mərz, ălts′-, ôlts′-, ôlz′-)
n.
A degenerative disease of the brain, occurring chiefly in elderly people and characterized by disorientation, memory failure, speech disturbances, and the progressive loss of mental capacity. It is associated with the formation of beta-amyloid plaques and neurofibrillary tangles in the cerebral cortex and loss of neurons.

Alzheimer's disease (AD)

[ôl′zīmərz]
Etymology: Alois Alzheimer, German neurologist, 1864-1915
a condition characterized by progressive mental deterioration, often with confusion, memory failure, disorientation, restlessness, agnosia, speech disturbances, inability to carry out purposeful movement, and hallucinosis. There are three phases of disease progression over time: (1) preclinical Alzheimer's characterized by changes that indicate the very earliest signs of disease; (2) mild cognitive impairment (MCI) or mild changes in memory and thinking abilities, enough to be noticed and measured, but not impairment that compromises everyday activities; (3) dementia due to Alzheimer's. The patient may become hypomanic, refuse food, and lose sphincter control without focal impairment. The disease sometimes begins in middle life with slight defects in behavior and memory, usually an inability to incorporate new knowledge with old knowledge, but the symptoms can worsen dramatically with age. When the symptoms are severe, patients are unable to perform activities of daily living or orient to surroundings and do not recognize loved ones. Typical pathological features are miliary amyloid plaques in the cortex and fibrillary degeneration (tangles) in layers containing pyramidal ganglion cells. The cerebral cortex atrophies with widening of the cerebral sulci, especially in the frontal and temporal regions. Diagnostic criteria consist of a failure in at least three cognitive functions, including memory, use of language, visuospatial skills, personality, and calculating skills. Measurement of biomarkers in blood and cerebrospinal fluid, as well as neuroimaging tests to characterize brain changes, are assessments recommended by the Alzheimer's Association. Treatment may involve medications that are thought to decrease the rate of decline. Also called senile dementia-Alzheimer type (SDAT).
clinical considerations Care is initially concerned primarily with promoting activity and sleep and preventing agitation, violence, and injury. Death usually occurs 8 to 12 years after the first symptoms appear. Late-stage care is focused on palliative measures.
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Alzheimer's disease

Alzheimer's disease

Alzheimer's dementia Neurology A progressive, neurodegenerative disease, which is the most common cause of dementia, and characterized by progressive mental deterioration accompanied by disorientation, memory and language defects, confusion, leading to progressive dementia, which may be accompanied by dysphasia, and apraxia; in the DSM-IV, AD '…is …a diagnosis of exclusion, and all other causes (of) cognitive defects … must first be ruled out.' AD affects 3% in those aged 65–74; 18% aged 75–84; 47% > age 85; AD has been linked to a form of apolipoprotein E, those with 1 defective APOE ε4 gene–located on chromosome 19 are at an ↑ risk of AD, and those with 2 copies have AD of early onset; A68 protein is present in AD brain homogenates, and linked to formation of neuritic plaques and neurofibrillary tangles–68 kD; one Alzheimer's amyloid precursor–APP may inhibit serine proteases, and is generated by alternative enzyme splicing, releasing an intact β fragment, possibly explaining the deposition of these fibrils in AD brains Management Tetrahydroaminoacridine-THA, aka tacrine, an acetylcholinesterase inhibitor, may improve the quality of life in AD Pts. See Tacrine.

Alzheimer's disease

A brain disorder that is by far the commonest cause of DEMENTIA. A common disorder with important genetic elements featuring severe brain shrinkage from loss of nerve tissue, accumulation of plaques of AMYLOID beta (A-beta) peptide in the brain cells and tangled masses of fibres of tau protein. The A-beta peptide is cleaved from the natural AMYLOID PRECURSOR PROTEIN (APP). A mutation of the gene on chromosome 21 for APP is a cause of Alzheimer's disease. Mutations in the genes for presenilin 1 and 2, which have a role in the cleavage of A-beta peptide from APP can also cause the disease. There is progressively worsening dementia. People with DOWN'S SYNDROME develop this disorder 10 to 30 years earlier than other people. Down's syndrome is caused by an extra chromosome 21 and features slow accumulation of A-beta peptide. Acetylcholinesterase inhibitor drugs can help temporarity as can glutamate inhibitors such as memantine. Research is progressing on ways of inhibiting the production of A-beta. (Alois Alzheimer, German neurologist, 1864–1915).

Alzheimer's disease

a form of senile dementia in humans which may be associated with genes on chromosome 21.

Alzheimer’s Disease

DRG Category:57
Mean LOS:4.8 days
Description:MEDICAL: Degenerative Nervous System Disorders without Major CC

Alzheimer’s disease (AD) is a degenerative disorder of the brain that is manifested by dementia and progressive physiological impairment. It is the most common cause of dementia in the elderly but is not a normal part of aging. More than 4 million Americans suffer from AD. AD causes two-thirds of the dementia cases in the United States, and the prevalence of dementia doubles every 5 years in people older than 65, reaching 30% to 50% at age 85. It involves progressive decline in two or more of the following areas of cognition: memory, language, calculation, visuospatial perception, judgment, abstraction, and behavior. Dementia of the Alzheimer’s type (DAT) accounts for approximately half of all dementias. The average time from onset of symptoms to death is 8 to 10 years. The pathophysiological changes that occur in DAT include the following:

  • Presence of neurofibrillary tangles, neuritic plaques, and amyloid angiopathy
  • Accumulation of lipofuscin granules and granulovacuolar organelles in the cytoplasm of the neurons
  • Structural changes in the dendrites of the neurons and in the cell bodies
  • Predominant neuronal degeneration in the cortical association areas of the basal ganglia
  • Gross cortical atrophy and widening of the sulci
  • Enlargement of the ventricles
  • Decrease in neurotransmitters (acetylcholine, dopamine, norepinephrine, serotonin), somatostatin, and neuropeptide substance P

Causes

The cause of AD is unknown, but knowledge about the hereditary links is growing (see Genetic Considerations). Patients with Down syndrome eventually develop DAT if they live long enough. There is a higher than normal concentration of aluminum in the brain of a person with DAT, but the effect is unknown. A distinct protein, AZ-50, has been identified at autopsy in the brains of patients with DAT. This protein has been isolated from neurons that were not yet damaged, suggesting that its presence early in the degenerative process might cause the neuronal damage. The life expectancy of a patient with DAT is reduced 30% to 60%.

Genetic considerations

AD is not caused by a single gene. The genetic contributions to the disease are complex because more than one gene mutation can cause AD, and genes on multiple chromosomes are involved. There are two basic types of AD from a genetic standpoint: familial and sporadic (associated with late-onset disease). Familial AD (FAD) is a rare form of AD that has an early onset before age 65 and affects less than 10% of AD patients. FAD is caused by gene mutations on chromosomes 1, 14, and 21 (definitively, within the PSEN2, PSEN1, and APP genes, respectively) and has an autosomal dominant inheritance pattern. Therefore, if one of these mutated genes is inherited from a parent, the person will almost always develop early-onset AD.

The majority of AD cases are late onset (developing after age 65), have no known cause, and show no clear inheritance pattern. Late-onset AD is linked with the apolipoprotein E (ApoE) gene on chromosome 19. It is involved with making ApoE, a substance that transports cholesterol in the bloodstream. The ApoE gene comes in several different alleles, but the three alleles that occur most frequently are ApoE epsilon 2, 3, and 4 (e2, e3, and e4). The e4 allele of the ApoE gene is considered a risk factor for AD and appears to influence the age of onset of the disease. No one really understands the degree of risk of AD based on ApoE status. Specific polymorphisms in the A2M, LRP1, TF, HFE, NOS3, VEGF, ABCA2, and TNF genes are also associated with AD. Scientists continue to search for genetic risk factors for late-onset AD on regions of chromosomes 1, 3, 7, 8, 9, 10, 12, 19, 20, and X. Recent genome-wide association studies (GWAS) identified three polymorphisms significantly associated with AD at the CR1 (1q32), CLU (8p21), and PICALM (11q14) loci. CLU, which encodes clusterin/apolipoprotein J, was identified independently by two separate groups of researchers and therefore likely represents a true genetic risk factor.

Gender, ethnic/racial, and life span considerations

The onset of DAT may occur at any age but is rare before age 50; the average onset occurs after age 65. Approximately 3% of men and women ages 65 to 74 have AD. More females than males have the disease. It is difficult to determine if there are racial and ethnic differences in the prevalence of AD. However, a unique issue for older blacks/African Americans is that, in contrast with other ethnic/racial groups, they are disproportionately affected by stroke, high blood pressure, and diabetes. These diseases can increase the risk of developing AD.

Global health considerations

Prevalence rates in Canada and the United States in people older than 65 years is approximately 6% to 7%. Lower rates are reported in China and Nigeria, and higher rates are reported in India. Data are not available for most developing countries.

Assessment

History

DAT is a slowly progressing disease, and secondary sources are used for diagnosis because the patient is often unaware of a thought-processing problem. Past medical history should be evaluated for previous head injury, surgery, recent falls, headache, and family history of DAT.

Physical examination

The history will help determine which stage the disease process has reached at the time of patient assessment. The following four-stage scale reflects the progressive symptoms of DAT:

  • Stage 1 is characterized by recent memory loss, increased irritability, impaired judgment, loss of interest in life, decline of problem-solving ability, and reduction in abstract thinking. Remote memory and neurological examination remain unchanged from baseline.
  • Stage 2 lasts 2 to 4 years and reveals a decline in the patient’s ability to manage personal and business affairs, an inability to remember shapes of objects, continued repetition of a meaningless word or phrase (perseveration), wandering or circular speech patterns (circumlocution dysphasia), wandering at night, restlessness, depression, anxiety, and intensification of the cognitive and emotional changes of stage 1.
  • Stage 3 is characterized by impaired ability to speak (aphasia), inability to recognize familiar objects (agnosia), inability to use objects properly (apraxia), inattention, distractibility, involuntary emotional outbursts, urinary or fecal incontinence, lint-picking motion, and chewing movements. Progression through stages 2 and 3 varies from 2 to 12 years.
  • Stage 4, which may last approximately 1 year, reveals a patient with a masklike facial expression, no communication, apathy, withdrawal, eventual immobility, assumed fetal position, no appetite, and emaciation.

The neurological examination remains almost normal except for increased deep tendon reflexes and the presence of snout, root, and grasp reflexes that appear in stage 3. In stage 4, there may be generalized seizures and immobility, which precipitate flexion contractures.

Appearance may range from manifesting normal patient hygiene in the early stage to a total lack of interest in hygiene in the later stages. Some patients also demonstrate abusive language, inappropriate sexual behaviors, and paranoia. The Folstein Mini-Mental State examination is a quick evaluation tool that can assist in diagnosis and monitoring of the disease’s progression.

Psychosocial

The nurse needs to assess the family for its ability to cope with this progressive disease, to provide physical and emotional care for the patient, and to meet financial responsibilities. A multidisciplinary team assessment approach is recommended for the patient and family.

Diagnostic highlights

Diagnostic tests will generally be completed to rule out a treatable condition that could be causing dementia, such as thyroid disease, stroke, vitamin deficiency, brain tumor, drug and medication effects, infection, anemia, and depression. Imaging studies such as computed tomography (CT) and magnetic resonance imaging (MRI) help exclude other possible causes for dementia, but clinical criteria rather than biological testing are used to make the diagnosis of AD.

TestNormal ResultAbnormality with ConditionExplanation
Brain biopsy upon autopsyNegativePositive for cellular changes that are associated with the diseaseNo diagnostic test is definitive for AD. Clinical criteria for diagnosis of DAT: (1) presence of at least two cognitive deficits, (2) onset occurring between ages 40 and 90, (3) progressive deterioration, (4) all other causes ruled out

Other Tests: Most patients will receive neuroimaging (CT, MRI) as part of the diagnostic work-up to rule out other conditions such as subdural hematoma, brain tumors, stroke, or other conditions. Supporting tests include CT scan, MRI, and positron emission tomography (PET). During the early stages of dementia, CT and MRI may be normal, but in later stages, an MRI may show a decrease in the size of the cerebral cortex or of the area of the brain responsible for memory, particularly the hippocampus. Genetic testing for the ApoE gene is available, and the presence of the gene is a risk factor for AD. Genetic tests may be helpful in diagnosis, but further studies are needed to confirm their reliability.

Primary nursing diagnosis

Diagnosis

Self-care deficit related to impaired cognitive and motor function

Outcomes

Self-care: Activities of daily living—Bathing, Hygiene, Eating, Toileting; Cognitive ability; Comfort level; Role performance; Social interaction skills; Hope

Interventions

Self-care assistance: Bathing and hygiene; Oral health management; Behavior management; Body image enhancement; Emotional support; Mutual goal setting; Exercise therapy; Discharge planning

Planning and implementation

Collaborative

The initial management of the patient begins with education of the family and caregivers regarding the disease, the prognosis, and changes in lifestyle that are necessary as the disease progresses. Basic collaborative principles include:

  • Keep requests for the patient simple
  • Avoid confrontation and requests that might lead to frustration
  • Remain calm and supportive if the patient becomes upset
  • Maintain a consistent environment
  • Provide frequent cues and reminders to reorient the patient
  • Adjust expectations for the patient as he or she declines in capacity

Pharmacologic highlights

Generally, therapy is focused on symptoms with an attempt to maintain cognition.

Medication or Drug ClassDosageDescriptionRationale
Donepezil5–10 mg PO qdCholinesterase inhibitor; elevates acetylcholine concentration in cerebral cortex by slowing degradation of acetylcholine released by intact neurons; other drugs in this class include galantamine and rivastigmineImproves cognitive symptoms; improves cognitive function in the early stages of the disease only; drug effects diminish as the disease progresses
AntidepressantsVaries with drugSelective serotonin reuptake inhibitors; increases activity of serotonin in the brainTreat depression, anxiety, and irritability
Atypical antipsychoticsVaries with drugRisperidone, olanzapine, quetiapine, aripiprazole, clozapine, ziprasidoneTreat psychosis but should be avoided in people with the risk of stroke and weight gain; drugs are expensive and may increase mortality but might be better tolerated; use must be weighed carefully

Other Therapies: Other drugs and preparations currently being investigated are memantine, ginkgo biloba, vitamin E, estrogen, and NSAIDs. Secondary treatments are aimed at treating depression, psychosis, and agitation. To control night wandering and behavioral outbursts, physicians prescribe mild sedatives such as diphenhydramine. Barbiturates are avoided because they can precipitate confusion. Depression is treated with antidepressants (trazodone), and agitation is controlled by anxiolytics (oxazepam or diazepam). Psychotic behaviors are treated with antipsychotics (chlorpromazine or haloperidol). Consider hospitalization for any unstable medical condition, such as an infectious or metabolic process, that may complicate the patient's treatment. If the patient becomes a danger to himself or herself or a danger to others, a short hospitalization may be indicated to adjust psychotropic medications.

Independent

Promote patient activities of daily living to the fullest, considering the patient’s functional ability. Give the patient variable assistance or simple directions to perform those activities. Anticipate and assess the patient’s needs mainly through nonverbal communication because of the patient’s inability to communicate meaningfully through speech. Emotional outbursts or changes in behavior often are a signal of the patient’s toileting needs, discomfort, hunger, or infection.

To maximize orientation and memory, provide a calendar and clock for the patient. Encourage the patient to reminisce, since loss of short-term memory triggers anxiety in the patient. Emotional outbursts usually occur when the patient is fatigued, so it is best to plan for frequent rest periods throughout the day.

Maintain physical safety of the patient by securing loose rugs, supervising electrical devices, and locking doors and windows. Lock up toxic substances and medications. Supervise cooking, bathing, and outdoor recreation. Be sure that the patient wears appropriate identification in case he or she gets lost. Terminate driving by removing the car keys or the car. Provide a safe area for wandering. Encourage and anticipate toileting at 2- to 3-hour intervals. Change incontinence pads as needed, but use them only as a last resort. Bowel and bladder programs can be beneficial in the early stage of the disease.

Provide structured activity during the day to prevent night wandering. If confusion and agitated wandering occur at night, provide toileting, fluids, orientation, night lights, and familiar objects within a patient’s view. Some patients respond calmly when given the security of a stuffed animal or a familiar blanket.

Families should be referred to the Alzheimer’s Association Web site (http://www.alz.org/index.asp) and the many pamphlets and books available to provide information on this disease. Encourage family members to verbalize their emotional concerns, coping strategies, and other aspects of caregiver role strain. Discuss appropriate referrals to local support groups, clergy, social workers, respite care, day care, and attorneys. Provide information about advanced directives (living wills and durable power of attorney for health care).

Evidence-Based Practice and Health Policy

Wilson, R., Rochon, E., Mihailidis, A., & Leonard, C. (2012). Examining success of communication strategies used by formal caregivers assisting individuals with Alzheimer’s disease during an activity of daily living. Journal of Speech, Language and Hearing Research, 55, 328–341.

  • There is minimal evidence to support effectiveness of various verbal and nonverbal communication strategies, such as slowed speech rate, verbatim repetition, use of gestures, and guided touch, to improve completion of tasks associated with activities of daily living among patients with AD.
  • Findings from one study among 12 AD caregiver dyads revealed that saying encouraging comments was associated with decreased duration of the task (hand washing) (r = 0.56, p = 0.056) and pointing to an object was associated with task success rate (r = 0.57, p = 0.056).
  • Asking open-ended questions and verifying questions were associated with an increased average time to complete the task (r = 0.81, p = 0.002 and r = 0.63, p = 0.028).

Documentation guidelines

  • Any changes in cognitive function: Confused orientation (time, place, person), emotional outbursts, forgetfulness, paranoia, decreased short-term memory, impaired judgment, loss of speech, disturbed affect, decline of problem-solving ability, and reduction in abstract thinking
  • Response to medications (anxiolytics, antipsychotics, cholinesterase inhibitors, antidepressants, sedatives)
  • Verbal and nonverbal methods that effectively meet or communicate the patient’s needs
  • Caregiver response to patient behaviors and information about DAT
  • Ability to perform the activities of daily living

Discharge and home healthcare guidelines

medications.
Be sure the caregiver understands all medications, including the dosage, route, action, and adverse effects.

safety.
Explain the need to supervise outdoor activity, cooking, and bathing. Lock doors and windows, and lock up medications and toxic chemicals. Make sure the patient wears identification to provide a safe return if she or he becomes lost. Commercially made products are available that trigger an alarm if the patient wanders out of safe territory.

Alzheimer's disease insidious dementia of unknown cause, presenting in middle or old age; leading to generalized deterioration and death within 10 years; presents initially as exaggerated signs of ageing (e.g. acute short-term memory loss, difficulty in naming and recognizing familiar objects, indecision) and later by reduced language expression and comprehension, lack of self-care, delusions and ultimately total lack of communication, immobility, incontinence and coma; central nervous system changes include development of senile plaques and neurofibrillary triangles and alterations in cholinergic neurotransmission

Alzheimer's disease,

n.pr a presenile dementia characterized by con-fusion, memory failure, disorientation, restlessness, agnosia, hallucinosis, speech disturbances, and the inability to carry out purposeful movement. The disease usually begins in later middle life with slight defects in memory and behavior that become progressively more severe. Also known as primary progressive aphasia.

Patient discussion about Alzheimer's disease

Q. My father is 84 and he was diagnosed with Alzheimer’s disease. I would like to share with all of you a common question that I hear a lot regarding Alzheimer. My father is 84 and he was diagnosed with Alzheimer’s disease. Is there anything I can do to affect how long I stay mentally sharp or is it solely determined by my genes?

A. This is a question that I hear a lot and the answer is Yes. What we do also counts. It is not just genetics. While there is currently no medication that cures Alzheimer’s disease, there is quite a bit of science that shows that although our genes count, our brain health is not completely predetermined. Research shows us that certain behaviors and life style support brain health and prolong mental acuity. Important contributors to brain health are being socially active, physically active, and cognitively active. We need to continue to challenge our mind even when we are no longer in school or are retired. We need to keep a healthy nutrition, make sure we get adequate sleep, and engage in enjoyable activities and life style that help reduce stress levels. Being happy and feeling good about ourselves is also important.

Q. How can alzheimer's disease be slowed down? My father has alzheimer's disease, but only not for a long time. Is it still possible to stop it from progressing? how to do it? He is still ok, recognizing everybody just not remember many things.

A. There are several drugs (including choline esterase inhibitors etc.) using to slow down mild-moderate Alzheimer’s disease, although these medications can't totally prevent the progression of the disease. Vitamin E is also generally recommended to Alzheimer disease patients. However, these drugs must be prescribed by a doctor so consulting one may be wise.

You may read more here:
http://www.nlm.nih.gov/medlineplus/alzheimersdisease.html

Q. how do you know if you have early onset of alzheimers? i'm 47. i do have extreme tremors at times and memory l i was told this could be what i have by a psychiatrist. What else can cause me to have these symptoms at my age and how do i know?

A. any time ;)

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