Course Price  $30.00 Contact Hours  4 Instructions   Study the course, then take the test. You can also print the course and test questions and return later to take the test.

Quicklinks Print this course Take the test How to take a course

Alzheimer's Disease

Nancy Evans, BS

Wild Iris Medical Education is an approved provider (#PA-54) of continuing nursing education by the Washington State Nurses Association, an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation. Our courses fulfill continuing nursing education requirements in all 50 states.
Wild Iris Medical Education (CBRN Provider #12300) is approved as a provider of continuing education for RNs, LVNs, and respiratory therapists by the California Board of Registered Nursing.
Nurse practitioners may apply these contact hours to pharmacy continuing education and prescriptive authorization.

There is no one biological marker in Alzheimer's patients that is consistent from person to person. Every individual with presumed AD has a brain that moves along the continuum of brain aging in a unique way. Peter Whitehouse, MD, PhD, 2008

What we call Alzheimer's disease (AD) is an age-related, irreversible brain disorder that gradually erases memory, thinking, and understanding. Over time, as neurons die in widespread areas of the brain's cerebral cortex, mild sporadic memory loss evolves into severe cognitive dysfunction as well as behavior and personality changes and, eventually, loss of physical function.

The course of AD and the rate of decline vary from person to person. On average, clients with AD live for 8 to 10 years after diagnosis but may live as long as 20 years.

Medial view of the human brain showing major landmarks. Courtesy of Alzheimer's Disease Education and Referral Center.

Alzheimer's disease is one of a group of disorders called dementias, which are characterized by progressive cognitive and behavioral changes. Symptoms commonly appear after age 60, beginning with loss of recent memory and followed by faulty judgment and personality changes. People in the early stages of AD often think less clearly and may be easily confused.

In progressive stages of the disease, people who have AD may forget how to do simple tasks, such as how to dress themselves or eat with proper utensils. In the late stages, people with AD are unable to function on their own and become completely dependent on others for their everyday care. Finally, the disease is so debilitating that people become bedfast and succumb to other illnesses and infections. Pneumonia is the most common cause of death in AD.

Although the risk of developing AD increases with age, AD and other dementia symptoms are the result of many interacting factors over many years of life—environmental, genetic, lifestyle factors—that affect brain function. Alzheimer's disease has become the most dreaded diagnosis in modern society, and it is predicted to explode among our aging population. However, a recent study by Langa and colleagues (2008) offers reason to hope that what we call AD may be preventable, not by medications but by lifestyle changes that begin early in life.

This study indicates that the rates of cognitive impairment among older Americans are declining (Langa et al., 2008). Researchers reported that cognitive impairment among people age 70 and older dropped from 12.2 percent in 1993 to 8.7 percent in 2002. Higher levels of education and more affluent financial status appeared to protect against cognitive impairment. Researchers suggest that improved treatment for stroke and cardiovascular disease during that time period may have contributed to the decreased rates of cognitive impairment. The proportion of college-educated elderly also increased during that time from 11 percent to 17 percent.

The Langa study also confirms other research showing the benefits of higher education and more affluent financial status, which are typically markers for better nutrition, better general health, access to healthcare, and increased longevity. These findings suggest preventing AD and other chronic health problems may depend on efforts related to social and environmental justice and public health rather than new drug development. For example, African Americans and Hispanic Americans are twice as likely to live in poverty as whites and Asian Americans, and this disparity affects health status and the ability to obtain high-quality healthcare (Commonwealth Fund, 2008).

EPIDEMIOLOGY

First described by German psychiatrist Alois Alzheimer in 1906, AD was then a rare disease. But as life expectancy in the United States has risen to more than 77 years, so have the number of persons with a probable diagnosis of AD. Age is the greatest risk factor for AD, and the disease is more common among women than men because women live longer than men.

More than 5 million Americans have AD, 20 percent of them between the ages of 75 and 84, more than 40 percent of them age 85 and older. People over 85 constitute one of the fastest growing segments of the population and, as this population continues to grow, so will the number of people with AD. By 2030 the number of people age 65 and older who have AD is expected to reach 7.7 million, an increase of more than 50 percent over the number currently affected (Alzheimer's Association, 2008).

African Americans and Hispanic Americans are at high risk for AD because, compared to the general public, they have a higher risk of diabetes, high blood pressure, and stroke. Latinos are one of the fastest growing population groups with the disease.

A recent survey showed that African Americans and Hispanic Americans are concerned about AD but are not aware of the link to heart disease and stroke. Half of those surveyed reported that nothing can be done to reduce the risk of AD and to maintain cognitive function. They believe that AD is a normal part of aging (Connell et al., 2007).

Alzheimer's disease inflicts a heavy economic burden on families and on society as a whole. According to the Alzheimer's Association, the costs of caring for individuals with AD total at least $100 billion annually. The average lifetime cost for an individual with AD is estimated at $174,000 (Alzheimer's Association, 2008).

One recent study found that as the functional status of a person with AD or other dementia declines, healthcare costs increase. Each impairment in activities of daily living (ADL) increases healthcare costs nearly $2,000 per person and each impairment in independent activities of daily living (IADL) increases costs more than $500 per person (Hill et al., 2006).

The staggering cost of AD for families—home healthcare, adult daycare, caregiver respite, and long-term care—are seldom covered by medical insurance or Medicare, which is intended to cover the acute healthcare needs of people over 65 and disabled people under 65. Medicare Part A mainly covers the following services:

• Inpatient hospital care with deductible
• Skilled nursing care facility for up to 120 days after 3 days or more of hospitalization if need exists
• Limited home healthcare, including part-time skilled nursing care, physical therapy, speech-language therapy, home-health aide services, durable medical equipment (such as wheelchairs, hospital beds, oxygen, and walkers) and supplies and other services if need exists; AD alone is not sufficient to justify services. Patient must pay 20 percent of costs for durable medical equipment, which must be prescribed by a doctor.
• Companion care services, if accompanied by a need for skilled nursing care after a hospital stay of three days or longer and is overseen by a skilled professional (such as a registered nurse). This is only covered for a designated amount of time following a hospital stay.
• Hospice care if terminally ill and the patient's physician and a hospice medical director certify that life expectancy is six months or less; this applies both to home care and nursing home care. By choosing hospice care, the patient waives the right for Medicare to pay for other services to treat the terminal illness.

Medicare Part B covers 80 percent of the costs for the following services:

• Evaluation and diagnosis after deductible. This includes the use of positron emission tomography (PET) scans for Medicare beneficiaries with suspected AD or other dementia if other diagnostic methods have been inconclusive.
• Physician visits for treatment of AD after deductible. It is important that the physician use code 331 when completing insurance forms; otherwise, Medicare will cover only 50 percent of the physician's bills.
• Physical therapy, occupational therapy or speech therapy, psychotherapy or behavioral management therapy by a mental health professional, and skilled home-care services (such as skilled nursing, speech or physical therapy).

Medicare does not pay for prescription drugs for Alzheimer's, adult day care, room and board at assisted-living facilities or nursing homes. Medicare policy related to Alzheimer's disease may change so it is advisable to consult the Medicare websites for the latest information.

Clients who have long-term care insurance, which may cover home healthcare, or those who are eligible for state-funded Medicaid programs, have some coverage for these services, but many families must pay all or most of the cost themselves.

Seven out of 10 people with AD are cared for at home and 3 out of 4 caregivers are women—wives, daughters or other women, many of whom are juggling childcare, jobs, and other responsibilities. Caring at home for someone with AD inflicts extraordinary emotional, physical, and financial stress on families. According to the Alzheimer's Association (2006), the average annual cost of nursing home care is $42,000 but it can exceed $70,000 annually in some areas of the country. "In caring for their loved ones, family caregivers save taxpayers an estimated $306 billion in long-term care costs each year" (National Family Caregivers Association & Family Caregiver Alliance, 2006).

PATHOPHYSIOLOGY

Alzheimer's is the opposite of cancer. Cancer is runaway cell growth. Alzheimer's is runaway cell death. Sandra Steingraber Origins of Dementia, Part 2

Aging itself is a major risk factor for developing AD, but aging is not the cause of the disease. Normal aging involves changes throughout the body, and the brain is not exempt. Even in normal aging some neurons die; some shrink and are less effective, especially in areas of the brain related to learning, memory, and executive function (the abilities required to plan, organize, and carry out tasks).

As we age, tangles develop in neurons, and plaques may accumulate in particular regions of the brain. Inflammation and oxidative stress increase with age. These age-related changes in the brain vary from person to person, and a healthy individual may experience only a slight decline in memory.

Research indicates that people with dementia suffer from a mix of disease processes, most commonly AD and cerebral infarcts (strokes) but also other conditions such as Parkinson's, hemorrhages, tumors, or traumatic brain injury (Schneider et al., 2007). According to Dallas Anderson, of the National Institute on Aging, "We know that people can have Alzheimer's pathology without having symptoms"(National Institute on Aging, 2007).

Plaques

Three decades of research have begun to shed light on how AD steadily destroys brain function. A protein called amyloid precursor protein (APP), produced by healthy neurons, is severed by two enzymes, called beta and gamma secretase. This process creates a short, sticky protein called beta amyloid.

Instead of dissolving in the fluid that surrounds the neurons, beta amyloid protein folds into insoluble clumps called fibrils. The fibrils stick together, resulting in plaques on the surface of the neuron. Beta amyloid plaques are one of two characteristic lesions of AD.

A beta-amyloid protein in a healthy cell. Courtesy of Alzheimer's Disease Education and Referral Center.

The beta-amyloid protein being cleaved by beta and gamma secretase enzymes. Courtesy of Alzheimer's Disease Education and Referral Center.

A beta-amyloid plaque forming outside the cell. Courtesy of Alzheimer's Disease Education and Referral Center.

Tangles

The other lesion that characterizes AD is called a neurofibrillary tangle that forms inside the neuron itself. Normally, healthy neurons connect with each other through slender appendages or branches called neurites. The neurites contain microtubules that maintain the shape of the cell and serve as its life support system, carrying nutrients and neurotransmitters.

A neurofibrillary tangle, which forms inside the cell. Courtesy of Alzheimer's Disease Education and Referral Center.

The walls of the microtubules are reinforced by tau proteins, which act like the rungs on a ladder. In AD, the tau proteins loosen and form neurofibrillary tangles. Without the reinforcing effect of the tau proteins, the microtubules disintegrate, cutting off life support to the neuron, which then shrivels and dies.

Disruption of Neurotransmitters

Alzheimer's disease reduces the production of certain neurotransmitters in the brain that normally act as chemical messengers, transmitting nerve impulses. These neurotransmitters include acetylcholine, norepinephrine, serotonin, and somatostatin. Reduction of acetycholine is first apparent in the entorhinal cortex, which is adjacent to the hippocampus, an area of the brain associated with recent memory and storage of new information.

ETIOLOGY

Alzheimer's disease is a complex disease with no single, clear-cut cause, and therefore no sure means of prevention and no "silver bullet" cure or treatment. A number of scientists suggest that AD is an ecological disease related to the interaction of genetic, environmental, and lifestyle factors over many years, causing changes in brain structure and function.

Neurologist Peter Whitehouse writes … what I used to call Alzheimer's is not a single condition waiting to be fixed. It includes various processes that affect us all to one degree or another as we age. Some of these processes start early in life …. In fact, exposure of very young children to the increasing number of environmental toxins, such as lead, should be part of our program of prevention" (Whitehouse, 2008).

Alzheimer's disease is classified in two ways: by heritability and by age of onset. Familial AD (FAD) follows a certain inheritance pattern, whereas sporadic AD, according to current research, does not show an inheritance pattern.

Alzheimer's disease is also classified as either early-onset or and late-onset. Early-onset AD occurs in people younger than 65 and is called pre-senile dementia. Late-onset AD, the most common form of the disease, occurs after age 65 and is referred to as senile dementia Alzheimer's type (SDAT). Fortunately, early-onset AD is rare (about 5% to 10% of cases) and affects people between the ages of 30 and 65. It often progresses more rapidly than late-onset AD. Some forms of early-onset AD are inherited.

… it is imperative to remember that the presence of ApoE-4 increases susceptibility to Alzheimer's but does not cause the disease by itself. In other words, these are not inevitability genes; they are only susceptibility genes and may increase risk. Peter Whitehouse, 2008

Genetic Factors

Research to date indicates that most familial AD has an early onset and that about half of all cases of FAD are known to be caused by mutations (defects) in three genes located on three different chromosomes:

• Mutations in the APP gene on chromosome 21.
• Mutations in the presenilin 1 gene on chromosome 14.
• Mutations in the presenilin 2 gene on chromosome 1.

Everyone inherits two copies of each of these genes—one from each parent. A parent carrying a defective version of one of these genes has a 50-50 chance of transmitting the defective gene to each of his or her children. A single defective version of any one of these three genes will cause early AD nearly 100 percent of the time.

This type of inheritance pattern is called autosomal dominant inheritance. The total known number of these cases is small—between 100 and 200 worldwide. There is no scientific evidence that links these mutations with the more common sporadic, late-onset AD.

Even though autosomal dominant inheritance of genetic mutations does not appear to cause late-onset AD, research indicates that other genetic factors may increase the risk for developing the sporadic form of the disease. Scientists at Duke University's Alzheimer's Disease Center found that inheritance of one or two copies of the apolipoprotein E epsilon 4 (APOE e4) gene version on chromosome 19 increases the risk of late-onset AD (Strittmatter et al., 1993).

In contrast, APOE e2 lowers the risk of AD, and APOE e3 has no effect. Different versions of particular genes cause variations in inherited characteristics such as eye color or blood type. Everyone inherits two gene versions of the APOE gene. For instance, one person may inherit two e4 versions, and another e2/e3. The APOE variations cause changes in the manufacture of the APOE protein, one function of which is to help distribute blood cholesterol throughout the body.

The APOE protein is found in the neurons of healthy brains, but in excess amounts in the brains of people with AD and those with trisomy-21 (Down syndrome) (Bird, 2006). Studies of large populations have shown that the number of copies of the APOE e4 allele inherited influences the age of onset of AD. For example, on average, someone with two copies of APOE e4 would tend to have an earlier age of onset of AD than someone with only a single copy.

A retrospective study of 111 families in which both parents had a clinical diagnosis of AD found that nearly 23 percent of their adult children also developed AD. Many of the children are younger than 70 years of age, which means that more of them will develop AD as they age (Jayadev et al., 2008).

Scientists at Smart Genetics, a Philadelphia company, have developed a direct-to-consumer test to determine what combination of APOE genes an individual carries. Available on the Internet for $399, this test has proved controversial among geneticists, who argue that the test can do nothing to prevent or delay the onset of AD in those who are in high-risk groups. Others contend that some people would prefer to have the test results to better plan their lives. Smart Genetics' plan for the test includes genetic counseling for consumers provided by a board-certified genetic counselor.

The presence of a genetic predisposition does not ensure that AD will develop. A person may have one or two copies of the APOE e4 gene version and never develop AD, and someone else may lack APOE e4 alleles and still develop AD. The APOE e4 gene version thus increases the risk of AD, but it does not cause the disease.

Scientists recently reported that genetic factors accounted for 58 to 79 percent of cases of AD, based on the largest twin study to date, which employed the Swedish Twin Registry. However, the authors did not rule out the importance of environmental factors. They concluded "…we confirmed that heritability for AD is high and that the same genetic factors are influential for both men and women. However, nongenetic risk factors also play an important role and might be the focus for interventions to reduce disease risk or delay disease onset" (Gatz et al., 2006).

In early 2003 Swiss researchers identified a second gene called CYP46 that, when mutated, also may increase the risk of developing late-onset sporadic AD (Papassotiropoulos et al., 2003). This gene plays a key role in removing cholesterol from the brain. Mutations in this gene lead to the buildup of beta-amyloid plaques in the brain. Someone with both the CYP46 mutation and the APOE e4 mutation has more than twice the risk of developing AD as someone with only the APOE e4 mutation.

Continuing research suggests that there may be other genes that contribute to both early- and late-onset AD. For example, the gene encoding ubiquilin 1 (UBQLN1) is one of several candidate genes for AD, located on chromosome 9q22. Mutations in this gene may influence alternative splicing of this gene in the brain (Bertram et al., 2005).

In 2007 scientists reported that certain versions of the gene SORL1 increase the risk of developing AD. This analysis was based on examination of DNA from more than 6,000 people from various ethnic groups (Rogaeva et al., 2007).

Other Risk Factors and Possible Preventive Strategies

A 2006 report from the National Institutes of Health's Cognitive and Emotional Health Project (CEHP) identified a number of factors that affect cognitive and emotional health (Hendrie et al., 2006). Based on an analysis of 36 large longitudinal cohort studies, this report shows that the following factors contribute to declines in cognitive function:

• Increasing age
• Hypertension
• Diabetes
• Stroke, or transient ischemic attacks (TIAs)
• Presence of infarcts or white-matter lesions
• Low mood (depression)
• Higher body mass index (BMI)

Smoking is also a risk factor for AD, not only because of its association with cardiovascular disease and diabetes (Willi et al., 2007), but also because of the toxic chemicals and metals present in the tobacco smoke. Many of these substances such as benzene, formaldehyde, arsenic, lead, and cadmium are known neurotoxins.

Factors that protect cognitive function include:

• Higher levels of education
• Higher socioeconomic status (SES)
• Emotional support
• Better baseline cognitive function
• Better lung capacity
• More physical exercise
• Moderate alcohol use
• Use of vitamin supplements

Many research studies show that people with higher IQ, more education, and a more active engagement in social networks have a reduced risk of developing AD, even though their autopsies reveal the plaques and tangles characteristic of the disease (Perneczky et al., 2006). Based on these findings, scientists have developed the concept of cognitive reserve. This concept suggests that more years of education and social engagement develop more efficient, more extensive neural networks for processing information that are less vulnerable to pathologic disruption.

Cognitive reserve differs from brain reserve, which assumes that the brain itself is different (larger or containing more neurons) rather than the processing networks (Stern, 2006; Roe et al., 2007; Fotenos et al., 2008). Mortality studies support this concept. However, once the cognitive reserve is no longer able to compensate for the physical damage, the trajectory to dementia and death is steep and swift (Hall et al., 2007).

Traumatic brain injury is considered a risk factor for AD (Plassman et al., 2000), as is depression. In fact, head injury in early adulthood increases the lifetime risk of depression (Holsinger et al., 2002). The high incidence of traumatic brain injury among Iraq War veterans puts them at higher risk for AD than others in their age cohort. In a study of postmortem data, the brains of patients with AD who had a history of recurrent major depressive disorder showed increased hippocampal plaques and neurofibrillary tangles compared with the brains of other patients with AD who had no history of depression (Rapp et al., 2006).

Strategies to prevent head trauma include:

• Driving safely and using seatbelts when driving or riding in a motor vehicle
• Wearing a helmet when biking, skating, skiing, skateboarding, or rollerblading
• Using handrails on stairs and steps
• Wearing shoes and slippers with nonskid soles

Chronic stress may also be implicated in AD because of the hormonal imbalances it creates, particularly the dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis. Stress causes the hypothalamus to release corticotrophin-releasing hormone (CRH), which triggers the pituitary to signal the adrenal glands to release cortisol, the stress hormone.

Poorly controlled diabetes can result in an overactive HPA axis and excessive cortisol production in the adrenal gland, which may explain the association between diabetes and AD (National Institute on Aging, 2008). People at high risk for AD may be most sensitive to the effects of high stress, according to a study by Yale researchers. They found that for some aspects of memory, highly stressful experiences had a detrimental effect only on those individuals who carried the APOE-a4 allele (Peavy et al., 2007).

Plasma homocysteine, known to be a cardiovascular risk factor, may also increase the risk of AD (Ravaglia et al., 2005). Plasma homocysteine is associated with a deficiency of B vitamins such as folate, vitamin B12, and vitamin B6. Trials are underway to see if oral supplements of these vitamins can prevent or delay the development of AD. There is some evidence that a high-fat diet and high cholesterol levels also may increase the risk of AD; however, more study is needed before this link can be clearly established.

Exposures to environmental toxicants such as lead may also increase the risk of AD. Research in rodents and primates suggest that early life exposure to lead may predispose the brain to AD in later life (Bolin et al., 2006; Wu et al., 2008; Basha et al., 2005). This is a concern not only for Baby Boomers but for anyone born before lead was banned in house paint (1978) and in gasoline (beginning in the 1970s) because some of that lead is stored in our bones. Women face a higher risk of endogenous lead exposure during pregnancy and at menopause because there is a significant release of bone lead associated with increased bone turnover (Vahter et al., 2004).

Occupational studies also indicate that exposure to lead during adult life increases the risk of dementia in later life, particularly in those who have at least one APOE e4 allele (Stewart et al., 2002; Schwartz, 2000). Although blood lead levels have declined dramatically in children under age 6, levels in older adults are higher, primarily due to occupational exposure (CDC, 2005). Occupational lead exposures occur largely in battery manufacturing (primarily storage battery production), construction, and mining.

Exposure to other metals such as aluminum, methylmercury, iron, zinc, and copper may also increase the risk of AD (Fattoretti et al., 2004; House et al., 2004; Grant et al., 2004; Sparks & Schreurs, 2003). In 2008 British researchers reported finding elevated levels of magnetic iron oxides in postmortem examination of brain tissue of people with AD. In some cases, the levels were 15 times as high as in the brain tissue of those without AD and highest among females with AD (Pankhurst et al., 2008). Exposure to pesticides, many of which are known neurotoxins in children, may also contribute to the risk of AD in later life (Baldi et al., 2003).

Extremely low-frequency electromagnetic fields* (ELF-EMF) appear to be a possible risk factor for AD according to a growing body of evidence (Garcia et al., 2008; Davanipour et al., 2007; Röösli et al., 2007; Feychting et al., 2003; Hankansson et al., 2003). These findings are based primarily on epidemiologic studies of workers with chronic exposures.

*Electromagnetic fields (EMF) are a type of low-intensity electromagnetic radiation that includes power-frequency radiation from power lines and electrical appliances as well as radiofrequency radiation from cell phones, personal data assistants (PDAs), and other wireless technologies, as well as cellular antennas and broadcast towers.

Everyone in the developed world is exposed to EMF every day from electrical and electronic appliances and power lines. The expansion of wireless technologies throughout the world is also increasing human exposure to radiofrequency radiation [see earlier definition], which research indicates may contribute to higher rates of neurodegenerative diseases such as AD, Parkinson's disease, and ALS (Lou Gehrig's disease) (The BioInitiative Report, 2007).

POSSIBLE PREVENTIVE STRATEGIES

Preventing AD would save untold suffering of patients and families, not to mention billions of dollars. Research studies to identify factors that increase or decrease the risk of developing AD are a first step toward making primary prevention a reality. For example, lifestyle choices related to diet and exercise that reduce the risk of diabetes, hypertension, cardiovascular disease (including atrial fibrillation), stroke, and obesity could also reduce the risk of AD as well as alter the course of the disease.

Researchers report that physical exercise at midlife reduced the risk of dementia three decades later. Light exercise such as gardening or walking and regular exercise involving sports reduced the odds of developing dementia compared with hardly any exercise (Andel et al., 2008).

A growing body of evidence is showing that what is good for the heart is also good for the brain. For example, a study of patients with AD showed that those with hypertension at the time of diagnosis lost memory 100 percent faster over a three-year period than those with normal blood pressure. In those with atrial fibrillation, the rate of memory loss was 75 percent faster than in those with normal heartbeats (Mielke et al., 2007); therefore, effective treatment of hypertension and atrial fibrillation may slow the progression of AD and thus protect cognitive function.

Preliminary research evidence suggests that certain foods and dietary supplements may also be protective against AD. These include green tea, aged garlic, vitamins C and E (Zandi et al., 2004), and melatonin. Investigation continues on these and other nutritional approaches to preventing AD.

Two recent studies demonstrate the positive effects of a Mediterranean diet, which includes plenty of fish, fresh fruits and vegetables, and olive oil, together with a moderate amount of wine (Scarmeas et al., 2006; Scarmeas et al., 2007). These studies showed that the Mediterranean diet not only reduced the risk of developing AD but also reduced mortality among people diagnosed with AD. Some types of fish are high in mercury (tuna, swordfish, shark), however, which may increase the risk of AD, so consumers need to choose carefully.

The Alzheimer's Association encourages people to exercise, eat a "brain-healthy" diet, stay socially engaged, and make other wise choices to protect their aging brains. In June 2006, the National Institute on Aging released a 36-page booklet explaining in clear layperson's language what people can do to reduce their risk of AD. Called Genes, Lifestyles, and Crossword Puzzles: Can Alzheimer's Disease Be Prevented?, the booklet is available online at http://www.nia.nih.gov.

Occupational studies implicating metals, pesticides, and electromagnetic fields point to the need to reduce or eliminate worker and public exposure to these agents. Protecting children from early exposure to lead and other metals could also reduce the number of AD cases in the future.

SCREENING

As more imaging studies and other tests for AD become available, some health professionals advocate widespread screening of older adults. Some experts recommend screening every patient over age 75. This stance is controversial, however, when, according to the Alzheimer's Association (2008): "No treatment is available to delay or stop the deterioration of brain cells in Alzheimer's disease." In addition, there is no evidence of benefit in screening people with no symptoms of memory problems, and there are potential risks of negative consequences. These risks include false positives that make cause depression or anxiety, possible stigma, as well as loss of long-term care insurance, loss of employment, or loss of a driver's license. There is agreement, however, that testing is useful for patients who are experiencing memory problems.

Bouzani and colleagues (2007) recommend that primary-care physicians focus on "dementia red flags" rather than routine screening. These red flags include medication adherence problems, more than seven prescribed medications, agitation, multiple falls, and more than two hospitalizations or emergency department visits in the past year:

Pressures to institute screening of unproven benefit could divert much needed resources from the health and social care systems and have an overall negative impact on care for patients with dementia and other illnesses, when dementia screening becomes indicated. The goal should continue to be the best possible care for most patients, which currently does not include screening for dementia. (Bouzani et al., 2007)

The pathology of [AD] defies precise definition at present. This is because its individual components occur to some extent in normal aging. Esiri & Nagy, 2002

CLINICAL DIAGNOSIS

Alzheimer's disease remains a diagnosis of exclusion, ruling out other conditions that may cause similar symptoms, such as stroke, hypothyroidism, hypercalcemia, depression, nutritional deficiencies (including B12), normal-pressure hydrocephalus, head trauma, brain tumor, Parkinson's disease, dehydration, brain infections (HIV, encephalitis, meningitis), syphilis, and chronic effects of alcohol or other medications.

Definitive diagnosis of AD is still only possible at autopsy: "The truth is we can only make a 'probable' diagnosis of AD once we have eliminated all other causes" and even then "pathologists must ask the clinician whether the patient was demented or not in their life in order to consider a diagnosis of Alzheimer's in death" (Whitehouse, 2008).

Mini-Mental Status Examination

The Mini-Mental Status Examination (MMSE; see table below) is a quick evaluation tool used to assess people with cognitive impairment or memory loss. It measures an individual's reality orientation, registration abilities, attention and calculation skills, recall, language, and visuoconstruction (seeing and copying designs) abilities.

The highest possible score is 30 points. Those who score less than 24 need further evaluation for possible AD or other dementia, depression, delirium, or schizophrenia. Those who score 20 or less generally have one of these disorders.

Although widely used, the MMSE may misclassify patients in minority populations or those with low educational levels. A number of alternative screening strategies have been developed—most recently, the Alzheimer's Disease Screen for Primary Care (ADS-PC). This two-stage strategy uses two brief tests in the first-stage rapid screen: memory impairment screen (MIS) and animal fluency.

Only those who fail the rapid screen undergo the second-stage testing, which uses free and cued selective reminding (FCSR). ADS-PC appears to be more sensitive in detecting early dementia, and more accurate in classifying African American patients than the MMSE, but these results were not found in patients with low educational levels (Grober et al., 2008).

THE MINI-MENTAL STATUS EXAM
Indications Cognitive Function Assessment Documentation of subsequent cognitive function decline
Questions (Total of 30 points)
Category	Points	Questions
1. Orientation	10	Year, season, date, day of week, and month State, county, town, or city Hospital or clinic, floor
2. Registration	3	Name three objects: apple, table, penny - Speak each one distinctly and with a brief pause - Patient repeats all three (one point for each) Repeat process until all three objects learned Record number of trials needed to learn all three
3. Attention and Calculation	5	Spell WORLD backwards: DLROW - Points given up to first misplaced letter - Example: DLORW scored as 2 points only
4. Recall	3	Recite the three objects memorized in number 2 (Registration)
5. Language	9	Patient names two objects when they are displayed - Example: pencil and watch (1 point each) Repeat a sentence: "No ifs, ands, or buts" Follow three-stage command: - Take a paper in your right hand - Fold it in half - Put it on the floor Read and obey the following: - Close your eyes - Write a sentence - Copy the design (picture of two overlapped pentagons

According to a National Institute on Aging report (NIA, 2006), "Tests that measure delayed recall, verbal fluency, and overall cognitive status are highly accurate in distinguishing between cognitively healthy individuals and people with mild AD." In a large prospective Canadian study of initially nondemented patients, neuropsychological tests accurately predicted conversion to Alzheimer's disease after 5 and 10 years (Tierney et al., 2005).

Laboratory Findings

Ruling out other physical and psychological disorders that can mimic the symptoms of AD involves a number of laboratory tests including a complete blood count (CBC) to rule out anemia. Blood glucose testing is done because AD disturbs glucose metabolism. Thyroid function tests are performed to rule out hypothyroidism. Electrolyte and vitamin B12 levels should also be measured and hepatic and renal function should be assessed (Kawas, 2003).

A lumbar puncture may be done to measure soluble amyloid beta protein precursor (sBPP) in cerebrospinal fluid, which is decreased in those with AD. Normal sBPP levels are >450 U/L (Pagana & Pagana, 2005).

Imaging Studies

Improved imaging techniques have enabled researchers to see the effects of AD on brain structure and function. Magnetic resonance imaging (MRI) studies, particularly functional MRI (fMRI), have shown that AD causes some brain structures, particularly the hippocampus, to shrink during the early stage of the disease (Thompson et al., 2003).

Positron emission tomography (PET) and single photon emission tomography (SPECT) scanning allow scientists to visualize brain activity during cognitive operations such as memorizing, recalling, speaking, reading, and learning. Researchers at the University of Pittsburgh have developed a new agent to be used with PET scans that binds to the abnormal amyloid plaque in the brain. Called Pittsburgh compound B (PIB), this agent highlights actual pathologic changes in the brain as early as 10 years before serious memory loss occurs (UPMC, 2008). These techniques can help identify persons at risk for developing AD even before symptoms appear. Although there is yet no prevention or cure for AD, early screening and diagnosis enable the patient and family to plan for future care and options while the patient can still participate in decisions.

A PET scan of a normal brain. Courtesy of Alzheimer's Disease Education and Referral Center.

A PET scan of a person with advanced AD. Note the decreased brain activity (indicated by loss of orange, yellow, and green colors). Courtesy of Alzheimer's Disease Education and Referral Center.

People with mild cognitive impairment (MCI) are an increased focus of research, including studies at the University of South Florida's Alzheimer's Disease Center, one of two centers funded by the National Institute on Aging (NIA).

In 2001 the American Academy of Neurology (AAN) established the following criteria for an MCI diagnosis:

• An individual's self-report of memory problems, preferably confirmed by another person
• Measurable, greater-than-normal memory impairment detected with standard memory assessment tests
• Normal general thinking and reasoning skills
• Ability to perform normal daily activities (Alzheimer's Association, 2008)

Only about half of people with MCI will go on to develop AD.

Researchers at Duke University estimate that more than 5 million elder Americans have cognitive impairment without dementia. This is a public health concern because cognitive impairment, even without dementia, increases the chance of disability, higher healthcare costs, and possible progression to AD or other dementia (Plassman et al., 2008).

A prospective study of more than 700 people in Sweden determined that cognitive impairment with no dementia may be caused by factors other than the neurodegenerative process of AD. These include frailty-related factors such as hip fracture or polypharmacy (use of more than five medications) and neuropsychiatric factors such as depression and use of psychoactive drugs. The study also showed that people who were less engaged in social activities and mental stimulation were more likely to develop cognitive impairment (Monastero et al., 2007).

Even mild cognitive impairment can disrupt family life and relationships. Care partners may need to take on new responsibilities, reducing the time for personal interests and activities. The person affected with MCI may resent loss of independence. Families need information and support to help coping with the situation. For more information, see Mild Cognitive Impairment: What Do We Do Now? online at http://www.gerontology.vt.edu/docs/Gerontology_MCI_final.pdf.

Two subtypes of MCI have been established: amnestic MCI, characterized by memory problems, and nonamnestic MCI, which affects cognitive functions other than memory, such as language, attention, critical thinking, reading, and writing. Experts estimate that MCI may affect more than 20 percent of the population over age 65. People diagnosed with MCI are at increased risk of developing AD or other dementia.

Researchers in the Alzheimer's Disease Cooperative Study compared participants with amnestic MCI to persons with AD and determined that those with amnestic MCI had impaired memory but other cognitive functions were not impaired. Cognitive and functional test scores of the people with amnestic MCI fell between the scores of healthy people and those with AD (Grundmann et al., 2004).

Initial research on amnestic MCI suggested that treatment with drugs approved for AD may slow its progression to AD. In a three-year, placebo-controlled clinical trial, more than 750 patients with amnestic MCI were randomized into three treatment groups: one group received donepezil (Aricept), the second received Vitamin E, and the third group received a placebo. The study showed that donepezil reduced the risk of developing AD during the first year (Petersen et al., 2005). However, by the end of the three-year study, the risk was the same as for those in the placebo group.

Vitamin E showed no significant benefit at any time. Although the benefits of donepezil were relatively short term, delaying progression to AD by a year represents a significant reprieve for both patients and caregivers in terms of maintaining function and quality of life as well as reducing healthcare costs.

Two subsequent trials of the AD drug galantamine (Razadyne) to treat MCI showed no significant benefit in improving function or preventing progression to AD. In addition, scientists reported a significant increase in deaths among patients taking galantamine as compared with those receiving a placebo. In April 2005 the FDA mandated a labeling change acknowledging the increased risk of death. According to the Alzheimer's Association (2008), data from these studies "have not been published, but are posted on line."

Functional Assessment

Caring for someone with AD should include periodic assessment of the person's ability to function as the disease progresses. Researchers at Duke University developed the Functional Dementia Scale shown below to help caregivers monitor functional abilities and plan appropriate interventions.

FUNCTIONAL DEMENTIA SCALE
Circle one rating for each item 1 = None or little of the time 2 = Some of the time 3 = Good part of the time 4 = Most or all of the time		Patient: Observer: Position or relation to patient: Facility: Date:
Question	Rating	Task
1.	1 2 3 4	Has difficulty completing simple tasks on own, eg, dressing, bathing, doing arithmetic.
2.	1 2 3 4	Spends time either sitting or in apparently purposeless activity
3.	1 2 3 4	Wanders at night or needs to be restrained to prevent wandering
4.	1 2 3 4	Hears things that are not there
5.	1 2 3 4	Requires supervision or assistance in eating
6.	1 2 3 4	Loses things
7.	1 2 3 4	Appearance is disorderly if let to own devices
8.	1 2 3 4	Moans
9.	1 2 3 4	Cannot control bowel function
10.	1 2 3 4	Threatens to harm others
11.	1 2 3 4	Cannot control bladder function
12.	1 2 3 4	Needs to be watched so doesn't injure self, eg, careless smoking, leaving the stove on, falling
13.	1 2 3 4	Destructive of materials around self, eg, breaks furniture, throws food trays, tears up magazines
14.	1 2 3 4	Shouts or yells
15.	1 2 3 4	Accuses others of doing self bodily harm or stealing possessions (when you are sure the accusations are not true)
16.	1 2 3 4	Is unaware of limitations imposed by illness
17.	1 2 3 4	Becomes confused and is not oriented to place
18.	1 2 3 4	Has trouble remembering
19.	1 2 3 4	Has sudden changes of mood, eg, gets upset, angry, or cries easily
20.	1 2 3 4	If left alone, wanders aimlessly during the day or needs to be restrained to prevent wandering
Source: Moore, 1983.

STAGES OF ALZHEIMER'S DISEASE

Although AD is most commonly diagnosed after age 65, the brain changes characteristic of the disease may begin 10 to 20 years before symptoms appear. Buildup of beta amyloid plaques, development of neurofibrillary tangles, and consequent death of neurons ultimately shrink the hippocampus, the critical structure in memory.

The symptoms of AD are usually described in three stages: early-stage (mild), mid-stage (moderate), and late-stage (severe). The object of treatment is to slow progression of the disease and maintain maximum physical and mental function as long as possible.

Early Stage

Early-stage (mild) AD first affects memory, language, and reasoning. This stage is typically marked by one or more of the following symptoms:

• Memory loss
• Confusion about location of familiar places (getting lost begins to occur)
• Taking longer to accomplish normal daily tasks
• Trouble handling money and paying bills
• Making bad decisions due to impaired judgment
• Loss of spontaneity and sense of initiative
• Mood and personality changes, increased anxiety

Medial view of the brain with early damage to the hippocampus and portions of the frontal lobe in blue. Courtesy of Alzheimer's Disease Education and Referral Center.

Clinical diagnosis of AD is usually made during the early stage, when the person appears to be physically healthy but is having increasing difficulty making sense of the environment. The affected person and the family may mistake early signs of AD for normal age-related changes. Deciding to seek diagnostic testing can be a major hurdle for the person and the family.

Mid-Stage

Mid-stage (moderate) AD involves areas of the cerebral cortex that control language, reasoning, sensory processing, and conscious thought. These regions continue to atrophy, resulting in more pronounced and widespread symptoms.

Behavior problems, such as wandering and agitation, require more intensive supervision and care. Symptoms of this stage usually include:

• Increasing memory loss and confusion
• Shortened attention span
• Problems recognizing friends and family members
• Difficulty with language; problems with reading, writing, numbers
• Difficulty organizing thoughts and thinking logically
• Inability to learn new things or to cope with new or unexpected situations
• Restlessness, agitation, anxiety, tearfulness, wandering, especially in the late afternoon or at night
• Loss of ability to tell time; late-day time disorientation and confusion, called "sundowning"
• Repetitive statements or movement, occasional muscle twitches
• Hallucinations, delusions, suspiciousness or paranoia, irritability
• Loss of impulse control (sloppy table manners, undressing at inappropriate times or places, vulgar language)
• Perceptual-motor problems (trouble getting out of a chair or setting the table)

Mid-stage AD may be the time when family caregivers begin to need respite care as their loved one's need for intensive supervision increases. Adult daycare can benefit both caregivers and people with AD. Using adult daycare offers caregivers relief from the physical and emotional stress of providing 24/7 care, and it provides a safe, secure environment for the patient, with social activities and peer support, plus meals and snacks.

According to ElderCare Online (http://www.ec-online.net), family caregivers should consider using adult daycare when the person with AD:

• Can no longer structure his or her own daily activities
• Is isolated and desires companionship
• Can't be safely left alone at home

New research shows that adult daycare may ease the transition between care at home and eventual placement in a nursing home. Many people with AD suffer accelerated cognitive decline after being placed in a nursing home but a new study from researchers at Rush University Medical Center suggests that those who had used daycare services fared better than those making an abrupt transition (Wilson et al., 2007).

Medial view of the brain with mild-to-moderate AD in blue. Note the spread of damage forward into the frontal lobe and backward into the temporal lobe. Courtesy of Alzheimer's Disease Education and Referral Center.

Late Stage

Late-stage (severe) AD involves widespread plaques and tangles throughout the brain and further atrophy in the hippocampus and other areas of the cortex. Patients cannot recognize family and loved ones or communicate in any way. They are completely dependent on others for care. Other symptoms can include:

• Weight loss
• Seizures, skin infections, difficulty swallowing
• Groaning, moaning, or grunting
• Increased sleeping
• Lack of bladder and bowel control

Medial view of the brain with severe AD indicated in blue. Note the increased damage in the hippocampus (dark blue) and the spread of the disease throughout the frontal, temporal, occipital, and parietal lobes. Courtesy of Alzheimer's Disease Education and Referral Center.

At the end of life, patients are partly or completely bedfast. Death comes most often in the form of aspiration pneumonia. Unable to swallow properly, the patient breathes food or liquids into the lungs.

MEDICAL AND PHARMACOLOGIC MANAGEMENT

It is more important to de-emphasize the role of medications in caring for brain aging and focus on other forms of non-medical, humanistic interventions to promote quality of life. Peter Whitehouse, 2008

Care and treatment of the person with AD will change over time as the disease progresses. Care planning should begin at the time of diagnosis and should involve the patient and the family. The plan includes:

• Consideration of cholinesterase inhibitor therapy to temporarily improve cognition or slow the rate of cognitive decline. (see Drug Treatment Guidelines below)
• Management of co-morbid conditions, especially sensory deficits
• Treatment of behavioral symptoms and mood disorders
• Support and resources for patient and caregiver
• Discussion of advance directives (see Ethical Considerations below)
• Compliance with state-mandated reporting requirements for driving impairment and elder abuse (see Ethical Considerations below) (Cummings et al., 2002)

Until it becomes necessary to institutionalize the patient, the primary caregiver will most likely be the spouse (usually the wife) or a child (usually a daughter). That caregiver and other family members involved need education and support to help manage the care as the patient's symptoms and needs change.

People with AD generally receive care in the primary care setting, which often has limited resources and results in less than optimal quality of care. In a randomized controlled trial, researchers at Indiana University studied the effectiveness of collaborative care for patients with AD compared with usual care. The collaborative care intervention patients received care from an interdisciplinary team led by an advanced-practice nurse working with the patient's family caregiver and integrated with primary care.

Standard protocols were used to initiate treatment and identify, monitor, and treat behavioral and psychological symptoms of dementia, emphasizing nonpharmacologic management. Assessed at 6, 12, and 18 months of the study, patients receiving collaborative care had significantly fewer behavioral and psychological symptoms of dementia (measured by the Neuropsychiatric Inventory [NPI]) than those receiving usual care.

Family caregivers also benefited, showing significant reduction in distress and improvement in depression. Researchers reported that these improvements "were achieved without significantly increasing the use of antipsychotics or sedative-hypnotics" (Callahan, et al, 2006).

Drug Treatment

In March 2008 the American College of Physicians (ACP) and the American Academy of Family Physicians (AAFP) issued new guidelines on pharmacologic treatment of dementia, based on a comprehensive review of the scientific literature. (Qaseem et al., 2008).Their cautious recommendations include the following:

1. Clinicians should base the decision to initiate treatment with FDA-approved drugs for dementia on an individualized assessment of the patient.
2. The choice of drugs should be based on tolerability, adverse effect profile, ease of use, and cost of medication.

Five drugs have been approved by the Food and Drug Administration (FDA) for treatment of dementia symptoms. Four are cholinesterase inhibitors (used in mild to moderate AD) and the fifth is a neuropeptide modifying agent, memantine (Mamenda) used in more severe AD.

The cholinesterase inhibitors are:

• Donepezil (Aricept)
• Rivastigmine (Exelon)
• Galantamine (Razadine)
• Tacrine (Cognex)

Tacrine, the first drug approved for AD, has been largely replaced by the other cholinesterase inhibitors because the risk of liver damage outweighed minimal benefit of improved cognition. All of these drugs interfere with the action of acetylcholinesterase, an enzyme that normally breaks down the neurotransmitter acetylcholine.

"Major contraindications of cholinesterase inhibitors and memantine include, but are not limited to uncontrolled asthma, angle-closure glaucoma, the sick sinus syndrome, and left bundle-branch block" (Quaseem et al., 2008).

CHOLINESTERASE INHIBITORS FOR COGNITIVE DEFICITS IN AD

Drug	Suggested dosage	Side effects	Specific cautions
Donepezil (Aricept)	Initial dosage: 5 mg QD; if necessary, dosage can be increased to 10 mg QD after 4–6 weeks	Mild side effects including nausea, vomiting, and diarrhea; can be reduced by taking medication with food. Initial increase of agitation in some patients, which typically subsides after a few weeks	Conflicting evidence about possible interactions with cimetidine (Tagamet), theophylline, warfarin (Coumadin), and digoxin (Lanoxin)
Rivastigmine* (Exelon)	Initial dosage: 1.5 mg BID is generally well-tolerated; can be increased as tolerated but not more quickly than by 1.5 mg BID every 4 weeks to maximum of 6 mg BID. BID dosing is as efficacious as TID dosing and has comparable tolerability.	Nausea, vomiting and diarrhea, headaches, dizziness, abdominal pain, fatigue, malaise, anxiety and agitation; effects can be reduced by taking the medication with food. Eating disorders/weight loss.	Weight loss Interacting drugs include aminoglycosides and procainamide (Procanbid)
Galantamine (Razadine)	Initial dosage: 4 mg BID taken with morning and evening meals for 4 weeks; dosage then increased to 8 mg BID for at least 4 weeks. An increase to 12 mg BID may be considered on an individual basis.	Mild side effects including nausea, vomiting and diarrhea; side effects can be reduced by taking the medication with food. Anorexia, weight loss and dizziness. No apparent association with sleep disturbances, which can occur with other cholinergic medications.	Contraindicated in patients with hepatic or renal impairment
*Rivastigmine in a transdermal patch was approved by FDA in July 2007. The once-daily patch delivers 9.5 mg of the drug over 24 hours. Family caregivers in the clinical trials preferred the patch to capsules because it improved compliance with less interference in daily life, and had a low incidence of gastrointestinal side effects (Winblad et al., 2007). Source: Qaseem et al., 2008).

All of the FDA approved drugs may slow the progression of AD for a few months or even a few years, but they are not a cure. They may help some patients with activities of daily living (ADL) and with behavioral symptoms such as delusions and agitation, and may even improve memory and speaking skills. However, physicians need to be realistic in explaining to the patient and the family the limitations of drug therapy.

Some of the side effects of Alzheimer's drugs, such as nausea, vomiting, and diarrhea, may resolve within a few weeks. If they do not resolve, or if no significant improvement is seen with three months of drug therapy, the medication should be discontinued. Each patient responds differently to drug therapy. Thus, if one drug fails to elicit a response, another may.

Memantine (Namenda) is most commonly used in moderate to severe AD. Approved by FDA in 2003, memantine is an N-methyl-D-aspartate (NMDA) antagonist, which reduces overstimulation of the NMDA receptor by glutamate. Treatment with memantine resulted in statistically significant but not clinically important cognitive improvement in patients with mild to moderate AD. The side effects profile is similar to that of the cholinesterase inhibitors (nausea, dizziness, diarrhea) but memantine also caused agitation in some patients (Qaseem et al., 2008).

A number of older drugs have shown some promise in slowing the progression of AD. One study showed that daily intake of 2,000 IU of vitamin E or 10 mg of selegiline (Eldepryl) slowed the progression of symptoms in patients with AD. Based on this study, some physicians now recommend high-dose vitamin E supplements (1,400–2,000 IU daily) as part of standard treatment. However, those patients taking blood-thinning drugs such as Coumadin are advised not to take vitamin E. Some studies suggest that vitamin C may also delay AD progression.

At one time, hormone replacement therapy (HRT) in women was believed to delay the onset of AD. However, the Women's Health Initiative Study showed that HRT actually increased the risk of dementia among postmenopausal women (Shumaker et al., 2003). Thus HRT is not recommended for treatment or prevention of AD. Ginkgo biloba is widely touted by manufacturers in the popular media as improving memory; however, research to date does not support that claim.

Scientists continue to search for new and better treatments for AD. A small study in Australia showed that patients given a metal-binding compound called iodochlorhydroxyquin (Clioquinol) showed significant improvement in cognitive function among the most severely affected patients. The drug prevents zinc and copper ions from binding to beta amyloid, reducing the buildup of plaques (Ritchie et al., 2003).

A large trial was launched in 2004 to see if either of two nonsteroidal anti-inflammatory drugs (NSAIDs) could prevent AD in older adults with a family history of the disease. The two drugs were naproxen (Aleve, Naprosyn and Anaprox) and celecoxib (Celebrex). Recruitment for the trial was suspended later that same year when another NSAID, rofecoxib (Vioxx), a drug in the same subclass as celecoxib, was withdrawn from the market due to increased risk of cardiovascular problems. Researchers are continuing to monitor the approximately 2,400 participants who have been taking naproxen, celecoxib, or a placebo for up to three years.

Clinical trials also are underway on vitamins B6 and B12 and the cholesterol-lowering drugs known as statins. To date, results of the statin trials for AD are contradictory. While some small early studies showed some benefit in reducing the risk of AD, others showed evidence of cognitive impairment with statin use (King et al., 2003; Wagstaff et al., 2003; Patatanian & Gales, 2005).

A 12-year prospective study of 929 older Catholic clergy who were all free of dementia at baseline found that statin use did not affect the incidence of AD or improve cognition (Arvanitakis et al., 2008). According to Stanford researcher B.A. Golomb (2005), "the elderly may be more vulnerable to known adverse effects of statins, and evidence provides cause for concern that new risks may supervene, including cancer, neurodegenerative disease, and heart failure."

A firm conclusion regarding the effects of cholesterol or statins on human brain and cognitive function has not been well established, and it is premature to recommend statins for prevention and/or treatment of AD. Patanian & Gales, 2005

Co-Existing Health Problems

People with AD often have other health problems common to older adults, such as impaired hearing and vision, dental problems, hypertension, congestive heart failure, diabetes, hypothyroidism, genitourinary conditions, and arthritis. Any of these conditions, alone or in combination, can further diminish the patient's ability to function in the world.

For example, people who do not see or hear well may be easily confused in unfamiliar situations. Couple those limitations with AD, and the confusion intensifies. Recognition and treatment of any and all co-existing conditions can help improve the patient's ability to function and quality of life.

Impaired vision is not uncommon among institutionalized older adults. It can diminish quality of life and sometimes lead to depression. Basic eye care services to detect and correct impaired vision can improve quality of life and increase residents' participation in activities, hobbies, and social interaction (Owsley et al., 2007). Because people with AD may be unable to communicate about their visual impairment, it may go undetected.

A study of nursing home patients with AD found that more than 90 percent of the 85 residents in the study needed eye glasses for correction of presbyopia, myopia, or both. Nearly one-third of these residents had not been using glasses since entering the nursing home because the glasses had been lost, damaged, or were no longer adequate to correct their vision.

Based on these finding, the researchers offered three recommendations to prevent uncorrected visual acuity among nursing home residents with dementia: (1) label eyewear in appropriate populations to provide rapid identification if glasses are misplaced; (2) recommend that an extra pair of glasses be made available if the current pair is lost or damaged, and (3) ensure that all residents have annual or biannual eye exams. Visual acuity is essential to maintaining functional independence as long as possible, reducing the burden on nursing staff, and improving the patients' overall quality of life (Koch et al., 2005).

Many older adults suffer from depression and patients with AD are no exception. Unless treated, depression can further impair function. Antidepressants with limited anti-cholinergic side effects such as citalopram (Celexa) and sertraline (Zoloft) have been shown to be effective in treating depression in patients with dementia (Lyketsos et al., 2003). Effective treatment of the patient's depression has a secondary benefit of reducing caregiver stress.

Depressed patients with AD also may benefit from regular exercise. Researchers compared the effects of an exercise-behavior intervention with routine care in 153 patients with AD between the ages of 55 and 93 years who were living at home. Over a three-month period, one group of patients and their caregivers attended 12 one-hour exercise sessions. The other group received routine care. In the intervention group, caregivers learned behavior management techniques, including identification of activities that patients enjoyed.

The goal of the intervention was for patients to engage in moderate-intensity exercise for a minimum of 30 minutes daily. After three months, patients in the intervention group had reduced rates of depression and improved physical health and function. Those in the routine care group declined on both function and depression scales. A 24-month follow-up found that significant functional improvement persisted in the treatment group, while behavioral problems in the routine-care group had led to increased institutionalization (Teri et al., 2003).

A more recent study of nursing home residents with AD yielded similar findings. Ninety participants were randomized to three behavioral intervention groups: supervised walking, comprehensive exercise (walking plus strength training, balance, and flexibility exercises) and social conversation. Interventions were provided 5 days a week for 16 weeks; each session lasted 30 minutes.

At the end of that time, the comprehensive exercise group showed higher positive and lower negative affect and mood than either of the other two groups. The social conversation group evidenced the least positive and most negative mood and affect (Williams & Tappen, 2007). These researchers did a similar study of 45 nursing home residents with moderate to severe AD and found that depression was reduced in all three groups, most markedly in the exercise group (Williams & Tappen, 2008).

To maintain mobility in patients with AD, walking exercises and the use of wheelchair alternatives (such as walkers with a built-in seat) should be used to delay dependence on wheelchairs. Wheelchairs "only rarely improve mobility, and standard sling-bottom wheelchairs are not comfortable for long-term sitting" (Volicer, 2007). Those who cannot walk even with assistance need to have comfortably padded lounge chairs that can be easily tilted and repositioned.

NURSING MANAGEMENT

We do not know to what degree the patient is able to understand at any stage of this illness, but who is to say that the inability to communicate represents the real person who may still be struggling inside (Wolanin-Phillips, 1981). Care of the patient with AD demands ongoing assessment, planning, intervention, and evaluation throughout the course of the disease.

A comparative study of two nursing home units using different approaches to dementia care found that a humanized or person-centered approach not only improves the quality of life for patients but may also extend the length of their lives. One unit used a task-oriented maintenance approach to care that emphasized disease progression and pathology. The other unit used a more flexible person-centered approach that looked beyond physical and cognitive abilities and focused instead on a person's will to live and relationships with others. Those in the person-centered unit were found to be happier, with better quality of life, and longer life, while those in the unit emphasizing disability and disease progression were heavily medicated and often failed to thrive (McLean, 2006).

Another patient-centered approach to care of patients with severe AD is the Namaste Care program, developed by medical social worker Joyce Simard (2007). Namaste (Nah-mah-STAY) means "to honor the spirit within." Namaste programming uses a multisensory approach to care of patients who can no longer engage with others but still respond to touch, sounds, and visual cues.

Soft background music plays in the unit when the day begins and throughout the day. Each morning residents are dressed in soft comfortable clothing and groomed. Staff check hearing aids, clean glasses, and assess residents for pain. After breakfast, residents are taken to the Namaste care room and tucked into comfortable recliner chairs with soft quilts. The tucking in seems to help residents feel secure. Other techniques include gentle brushing of residents' hair, use of moisturizers and massage, and aromatherapy.

At day's end, residents are returned to their rooms and fall asleep listening to soft music. Families are encouraged to be part of these activities and, because they see that their loved ones are peaceful rather than agitated or anxious, they have a more positive experience and visit more often. Staff in Namaste units receive special training and report improved morale and special pride in their work (Lourde, 2007).

Fundamental to all care of the person with AD is the creation of a supportive environment (Box 1). Whether at home or in an institution, the goals are the same: to maximize the person's functional abilities and quality of life and to provide competent, compassionate care that acknowledges and respects the patient and family. Ideally, that care would be multidisciplinary, including medicine, nursing, and social work. Nurses contribute a wealth of expertise in Alzheimer's care as caregivers, counselors, and case managers.

Case managers are particularly important for patients with AD who live alone or with a spouse who is unable to act as caregiver. These patients are at high risk for injury or self-neglect. The case manager can serve as an advocate and primary support person, accompanying the patient to medical appointments and coordinating community services. If a person has advanced AD, the case manager can apply for a court-appointed conservator to establish guardianship and surrogate decision-making authority.

The challenges of caring for someone with AD include communicating effectively with the person; managing behavior problems such as agitation, wandering, and sleep disturbance; assisting with ADLs while helping maintain the person's independence; and planning activities that will help maintain well-being and prevent boredom. Meeting these challenges may become more difficult as the disease progresses.

COMMUNICATION ISSUES

Give us time to speak, wait for us to search around that untidy heap on the floor of the brain for the word we want to use. Try not to finish our sentences. Just listen, and don't let us feel embarrassed if we lose the thread of what we say. Christine Bryden, Diagnosed with Alzheimer's at age 46

Communicating with the person who has AD begins with patience, respect, and understanding. Remember that the patient is not deliberately being difficult. Face the patient, make eye contact, and speak directly in a calm, even tone. If patients have hearing problems, be sure they are wearing a hearing aid. Keep sentences simple; focus on one idea at a time.

Minimize questions because they may make the patient feel anxious or threatened. If the patient doesn't understand, offer nonverbal cues, such as pointing, demonstrating the desired action (eating, drinking), or nodding. Even though patients may be unable to speak, they may still understand—so do not talk about the patient to others in the patient's presence.

Nonverbal communication, especially touch, between caregiver and patient is also important. Patients who may be unable to respond verbally will respond to a smile, kind gesture, and caring touch. Some patients may need reminders during a meal to begin or continue eating, for example, by placing the spoon in the patient's hand.

Careful observation of the patient's facial expressions, eye contact or lack of eye contact, and body language can help the caregiver assess comfort or pain, anger, hostility, and misunderstanding. For example, increased motor activity and shaking fists suggest frustration or anger. Experience and patience over time helps caregivers gain skill interpreting these nonverbal signals.

Patients with AD may ask the same question repeatedly because they do not remember the answer given. Respond to the question, then try to distract the patient with an activity or a change of topic or a change of scene. Activities or events should not be discussed with the patient until they are about to happen; otherwise, the patient may retain the idea that something is going to happen but forget the details, triggering more questions.

BEHAVIOR MANAGEMENT

At one time, the recommendation was to bring patients back to reality by correcting their misconceptions. Now the rule is the opposite. As one staff member put it: If you can't bring them back to a better reality than they are experiencing in their heads, let them be. Pipher, 1999

Behavioral symptoms of Alzheimer's disease include agitation, vocal outbursts, wandering, and sleep disturbance. Although medications are available to treat these disorders—antidepressants, antipsychotic drugs, and sedatives—all have side effects and may interact with other medications, and most show limited efficacy. The U.S. Food and Drug Administration (FDA) has issued a public health advisory because use of "atypical" antipsychotic drugs (eg, olanzapine, risperidone, quetiapine) in people with dementia was associated with a slightly increased risk of death (FDA, 2005).

A meta-analysis of 15 trials of atypical antipsychotics found other adverse events, including urinary tract infection, incontinence, worsened cognitive test scores, and an increased risk of cerebrovascular events including stroke, especially with risperidone (Schneider et al., 2006). In view of these findings, nondrug approaches should be attempted before resorting to medications.

Agitation

Agitation is always related to fear or lack of control (Wolanin-Phillips, 1981). Caregivers need education and training to respond effectively to the agitated patient without becoming agitated themselves.

Speaking softly and calmly, the caregiver can gently and quietly take control of the situation. Ask the patient if he or she needs to use the bathroom. If not, try to determine what the patient needs: an extra blanket, a drink of water, food, or a warm hug.

Another approach to the problem of agitation is the three Rs: repeat, reassure, and redirect (Sultzer & Cummings, 1993). Using this approach, the caregiver repeats an instruction or answer to a question, reassures the patient, and redirects the patient to a different activity to divert attention from the problem.

Research has shown music therapy to be effective in relieving the behavioral and psychological symptoms of AD, and in some case improving cognitive and social skills. In one recent study of patients with moderate to severe AD, those who received music therapy over a 6-week period exhibited reduced activity disturbances, aggressiveness, and anxiety compared to those in the control group (Svansdottir & Snaedal, 2006). In another study, researchers observed the effect of stimulating, familiar background music on patients with AD. They found that the music significantly increased positive social behaviors and decreased negative behaviors related to agitation (Ziv et al., 2007).

Vocal Outbursts

Disruptive vocal outbursts—screaming, swearing, crying, shouting, negative comments to staff and/or other patients, self-talk—become increasingly common as AD progresses. Men generally display more aggressive vocalizations, such as swearing, while women typically exhibit more agitated vocalizations, such as crying or complaining. Until these behaviors diminish in the final stages of the disease, they present an ongoing challenge to caregivers.

Managing vocal outbursts effectively demands special intervention training and education for staff. Inadequate behavior management training for staff can result in overmedication of the patient, inappropriate use of restraints, physically combative behavior, or isolation of the patient. The staff may suffer stress and burnout, leading to high turnover. Learning to manage these disruptive outbursts successfully respects the patient's human dignity and builds confidence, improved morale, and job satisfaction in the staff.

Staff need to remember that the patient is not deliberately misbehaving; these are not temper tantrums. Staff should not take remarks or attacks personally, nor should they try to reason with the patient. Instead of focusing on the problem, staff need to acknowledge that the dementia is causing the problems.

Behavior problems such as vocal outbursts and wandering are major reasons why family caregivers decide to seek long-term care for their loved one. Staff can gain valuable insights from the family into the patient's behavioral history, which will aid in planning effective interventions. Together with psychological and medical evaluations, this behavioral history can alert staff to important triggers for behavioral problems.

Experienced staff often can anticipate outbursts and intervene to prevent them. Signs of an impending outburst vary from person to person, but these events are often preceded by restlessness, refusals, and blushing. Emotional triggers can include fear, anger, depression, grief, confusion, helplessness, loneliness, sadness, impatience, and frustration. Environmental factors such as poor lighting, seasonal changes, over-stimulation or lack of stimulation, loud noises, or excessive heat, can also trigger outbursts.

Outbursts may also signal physical illness or discomfort, including pain, hunger, thirst, incontinence, constipation, infection, or fatigue. Once the outburst has subsided, a thorough physical assessment may reveal the underlying physical problem, which can then be remedied.

Managing outbursts triggered by environmental or physical factors is simpler than dealing with outbursts that stem from an unknown emotional or psychological cause. With training and experience, however, staff can better manage and even prevent vocal outbursts. Interventions begin with distracting and diverting the patient, taking him or her to a quiet room, or taking a walk. This disconnects the patient from the problem and makes possible other interventions such as:

• Prompting the patient to reminisce.
• Engaging the patient in group activities such as games, singing, or listening to music.
• Touching the patient, hugging or holding hands.
• Giving the patient something to hold, a soft doll or a stuffed animal.
• Showing movies or interactive videos such as sing-alongs.
• Using headphones to listen to soothing sounds such as mountain brooks or the ocean.
• Playing audiotapes of the spouse or other family members recalling happy times together.

The techniques listed above are most effective as prevention measures. Once an outburst occurs, distraction is necessary to disconnect the patient from the problem. Otherwise, there is a risk of reinforcing inappropriate behaviors, which may result in more frequent outbursts.

Wandering

Wandering is a major behavior problem in patients with AD, more so than in patients with other types of dementias. For that reason, all persons diagnosed with AD should be registered in the Alzheimer's Association nationwide Safe Return Program (Alzheimer's Association, 2006). Registration includes an identification bracelet that should be worn at all times.

Agitation, restlessness, and sleep disturbances all lead to wandering, particularly at night, increasing the risk of injury to the patient and others. Wandering is generally one of two types: goal-directed, in which the patient attempts to reach an impossible goal such as going home or going to the store, and non-goal-directed, in which the patient wanders aimlessly. Wandering patterns include:

• Moving to a specific location
• Lapping or circling alone a path or track
• Pacing back and forth
• Wandering at random

Confusion and failing memory can lead to wandering because the patient is unable to keep a clear destination in mind. Wandering may also represent a search for social interaction when the patient can no longer communicate verbally. Unable to sleep, the patient walks to keep busy, or to find a loved one. Wandering in the late afternoon or early evening may be triggered by a fading memory of leaving work to go home.

Wandering may also be caused by a physical need, such as toileting. Staff can use large-print signs to mark destinations with a drawing of the activity. Placing a photo of the patient as a younger adult on the room door may help a wanderer find "home."

Wanderers are more likely to have delusions, hallucinations, and severe depressions. Long-term use of neuroleptics, such as haloperidol (Haldol), chlorpromazine (Thorazine), or thioridazine (Mellaril) can induce aimless wandering. Men are more likely to wander than women are, and wandering often increases as AD progresses.

The family can help staff identify and anticipate wandering in the newly admitted resident. Staff needs to learn as much as possible about the resident's lifestyle prior to diagnosis with AD, what kind of work the person did, previous patterns of exercise, stress, and response to touch. Once a wanderer is identified, the facility can have photographs made and distributed to other units, and assign special clothing or identification bands.

To prevent wandering outside the facility, staff can conceal or camouflage doors by:

• Placing a Velcro cloth strip or panel across doors
• Painting doorknobs the same color as doors
• Installing grid patterns on floors in front of doors

Safety locks, alarm systems, and personal monitoring devices can also help control persistent wanderers. Staff should use the least-restrictive methods possible to reduce, redirect, or prevent wandering. Interventions for goal-directed wandering involve distracting the person. A calm, gentle, and respectful approach helps to establish trust.

Approach the person from the front and use simple commands to change direction if necessary and guide the wanderer away from the exit. Diversions such as listening to music, looking at pictures, or exercising may be effective. Staff should avoid negative or harsh commands such as "Don't go out there!" and should not argue with the person.

Wandering in a safe area can be good exercise for the person with AD and helps manage non-goal-directed wandering. Many facilities are designed with these safe areas in the form of sheltered courts, gardens, lounges, or pathways.

Education and training for staff can help them identify and anticipate problem behaviors and learn diversionary strategies to manage these behaviors. Gaining competence builds confidence in staff and enhances the quality of life for residents with AD.

Sleep Disturbance

Patients with AD often have disturbed sleep patterns due to medications, sleep apnea, and disruption in their biorhythms. New research shows that exposing patients to a few hours of bright light each day, both morning and evening, helps them sleep longer at night and maintain a more normal sleeping schedule. Light therapy can include natural light outdoors or in a sunny room, or artificial light that is brighter than ordinary indoor light. Researchers at the University of California at San Francisco found that 1 hour of exposure to morning light plus an evening dose of 5 mg melatonin helped normalize sleep-wake cycles in institutionalized patients with AD (Dowling et al., 2008).

Exercise and physical activity, such as walking during the day, also helps patients sleep better at night. The activities should be as vigorous as possible within the limitations of the client. Those who are bedfast can still benefit from passive exercise.

Daytime napping can interfere with sleep at night. Napping may signal boredom or depression and the need for more stimulating daytime activity. Limiting fluid intake during the evening will reduce the need to urinate at night.

ACTIVITIES OF DAILY LIVING

Although senile dementia, like the dying process, may be irreversible and progressive, the living involved during the process can still be hopeful, filled with good feelings and moments of satisfaction. Wolanin-Phillips, 1981

Habit memory outlives all other types of memory in AD because it is stored in an area of the brain unaffected until the late stage. One woman recalled her mother's deterioration from AD: "She finally quit smoking because she forgot to smoke, but she would pat her breast pocket (where she carried her cigarettes) and then go through the motions of smoking, holding up two fingers, putting them to her mouth, inhaling, and then blowing out, but without any cigarette." Habit memory enables patients in the early and mid-stages of AD to remain physically able to manage ADL, but they may need reminders about hygiene and grooming.

Establishing and maintaining a routine in ADL helps the patient retain learned habits longer and therefore need less assistance. Once the routine becomes automatic, the patient no longer needs to stop and think what to do next. A fixed routine for eating and toileting also reduces the incidence of incontinence.

Bathing can be a challenge because patients with AD may be frightened by showers. If it is not possible to offer a bath instead, using a shower bench with a hand-held shower may be less threatening. The bathroom should be prepared in advance, with water at the correct temperature.

Dressing can be simplified by offering one or two choices, or just laying out the garments to be worn. If the patient wants to wear the same clothes every day, make duplicates available so that favorite clothes can be laundered. Many older patients, with or without AD, feel embarrassed when completely undressed, so removing and replacing one article of clothing at a time may work better.

As the disease progresses, patients forget about hygiene and grooming and may even forget to eat. Sleep patterns are disrupted; day and night are confused. Caregivers need to monitor nutrition and fluid intake as well as elimination because the patient no longer responds to thirst, hunger, or signals to defecate. Incontinence increases as health deteriorates. In moderate and late-stage AD, the patient needs someone to plan and provide personal care.

Eating habits and behaviors change during the course of AD, and may be caused by physiologic or psychological factors. In early-stage AD, depression related to the diagnosis may result in anorexia and weight loss. Patients may forget to eat or refuse to eat. Confusion and agitation may lead to extreme eating behaviors such as gorging.

Physiologic factors affecting eating behaviors may include dental problems such as uncomfortable dentures, missing teeth, and/or periodontal (gum) disease. Neurofibrillary tangles and plaques can affect the function of the hypothalamus, which regulates appetite and hunger signals. Many persons with AD lose their sense of smell, which affects taste and appetite. Some medications can also affect appetite.

In addition to depression, other psychological factors that affect eating behaviors include new and unfamiliar environments, which create confusion and agitation, distractions such as loud noises, unappealing food, and unusual odors such as urine.

Weight loss is common among patients with AD, regardless of quality of care. Wandering, restlessness, and agitation expend energy and interfere with food intake. In mid- and late-stage AD, patients are unable to feed themselves or to chew and swallow the food when placed in their mouths. Patients who are unable to swallow properly can be come dehydrated and can aspirate food, leading to aspiration pneumonia.

It is essential to maintain the nutritional well-being of the patient with AD (Box 2). Monitoring the patient's nutritional status for weight loss and possible nutritional deficiencies should include:

• Oral assessment to check for denture problems, missing teeth, and gum problems, with referral for any treatment needed.
• Review of medications to check for drugs such as Digoxin that may affect appetite
• Vision problems that could cause confusion at mealtime
• Assessment for depression

PHYSICAL AND SOCIAL ACTIVITIES

As horizons of experience narrow, small pleasures in life become more and more important. In dementia care, those pleasures and gratifications that are small loom large. Stephen G. Post, 2000

Physical activity plus social and cognitive stimulation help maintain general well-being and prevent boredom and agitation in people with AD—especially in the early stage of the disease. Walking in safe areas also helps people sleep better at night. Someone who enjoyed dancing may still find pleasure in that activity.

Those living at home can help with household tasks appropriate to their abilities and interests. For example, a woman who is no longer able to cook a meal may be able to peel the potatoes, shell the peas, or set the table. Gardening or other hobbies, arts and crafts, or pets can all be enjoyable sources of stimulation.

Activities should be tailored to the individual's personality. Shy, introverted people should not be required to participate in group activities, whereas more outgoing individuals may be happiest in a group. Those who enjoy music, either as listeners or performers, can find pleasure in listening to the radio or to recorded music. Group sing-a-longs may awaken pleasant memories of familiar songs.

People with AD who formerly liked to read may still like to leaf through magazines or books, especially those with interesting pictures. Television can be entertaining for some; for others, it can be frustrating and upsetting when they are no longer able to understand the story.

Simple games can provide enjoyment for people with AD. One Japanese study found that the cognitive and daily performance abilities of patients with Alzheimer's disease regress to the level of a child between 4 and 5 years old (Shoji et al., 2002). Although the person with AD should not be treated as a child, keeping this developmental level in mind when planning recreational activities can be helpful.

A limited activities budget does not have to limit creativity when planning entertaining and stimulating activities for people with AD. (See Activities on a Shoestring: http://www.angelfire.com/in/shoestring2.)

CARING FOR THE CAREGIVERS

Alzheimer's disease exacts a heavy toll on the emotional, physical, and financial resources of the family, especially the primary caregiver, usually a spouse or a daughter. Even though the family member willingly assumes the role of caregiver, the physical and emotional energy required can exhaust the most devoted individual. In a recent survey of 400 caregivers, two common themes emerged: anticipatory grief and ambiguous loss. Anticipatory grief is the pain and sadness of losing a loved one before death actually occurs. Ambiguous loss is the unsettling feeling of interacting with someone who is physically alive but seems no longer socially or emotionally present (Frank, 2008).

Caregivers also face loss of their previous role in the relationship while dealing with responsibilities formerly shouldered by or shared with the patient. If an adult daughter or son is the caregiver, he or she joins the "sandwich generation," caught between the parent's needs and the demands of career and family at home.

The time commitment required to care for a person with AD is daunting. An Alzheimer's Association survey showed that caregivers who live with a relative with AD spend about one hundred hours weekly providing care. Caregivers who are employed outside the home devote an average of 40 hours weekly to providing care—equivalent to a second full-time job. Half of all caregivers reported not having enough time for themselves. The caregiver is always on call; theirs is a 36-hour day (Mace & Rabins, 2006).

As AD progresses, the physical energy required to care for the increasingly dependent patient may deplete the caregiver's capacity. By mid-stage AD, the patient needs help with bathing, dressing, and a host of other activities. According to the Alzheimer's Association, 45 percent of caregivers report not getting enough sleep. Hospitalization rates are high for caregivers.

The lives of the caregiver and the patient are inextricably linked in a long, painful dance toward death. When the caregiver's quality of life suffers, it affects the quality of care for the person with AD. Without help and support from family, friends, health professionals, and community resources, caregivers are at great risk for:

• Emotional distress, such as depression and anxiety
• Fatigue and sleep deprivation
• Social isolation, when relatives and friends stop calling or visiting
• Family conflict
• Substance abuse

Just as education and training for staff can improve care and quality of life for patients, educational interventions for family members can make a positive difference in the caregivers' ability to cope with their difficult task. A long-term study in New York city found that caregivers receiving enhanced counseling and support, including support group participation, and continuous access to ad-hoc telephone counseling reported significantly better self-rated health than the control group. The benefits of the intervention lasted for two years (Mittelman et al., 2007).

Caregiver support and counseling may also help delay nursing home placement by as much as 18 months (Mittelman et al., 2006). Caregivers' guides also are available from many hospitals and government agencies including the National Institute on Aging:
http://www.nia.nih.gov/Alzheimers/Publications/caregiverguide.htm.

Better understanding of the dementia and techniques to cope with it can reduce caregivers' burdens and the negative reactions to disruptive behaviors common to AD. Reducing the burdens of caregiving can delay the need for nursing home care.

Caregivers may benefit from the following suggestions from the National Family Caregivers Association:

• Believe in Yourself.
• Protect Your Health.
• Reach Out for Help.
• Speak Up for Your Rights.

ETHICAL CONSIDERATIONS

Alzheimer's disease raises a host of ethical issues that, ideally, the physician discusses with the patient and the family at the time of diagnosis. These issues include:

• Driving
• Advance directives
• CPR vs. DNR
• Nutrition and hydration
• Hospice care

That the patient or the family may suspect Alzheimer's disease does not lessen the impact of the diagnosis, so it is up to the physician or other healthcare professional to raise these issues and help prepare families to discuss them while the patient can still share in the process.

The patient who lives alone but has intact relationships with geographically distant family members may consent to have the diagnosis shared with those relatives. If the patient is alone or has no local family member, friend, or significant other, a case manager can fill that role and can apply for a court-appointed conservator to establish guardianship and surrogate decision-making authority (Snyder, 2001).

Driving

Safe driving requires mental alertness, quick reflexes, and good judgment, all of which are eroded by AD, often before the patient or the family is aware of the problem. One recent study found that persons mildly impaired with AD and their caregivers underestimated their difficulties with driving, both on a questionnaire and on a standardized road test judged by an independent evaluator (Wild & Cotrell, 2003). The drivers with AD also rated significantly worse than healthy elders on 9 out of 10 driving behaviors.

A three-year study of older drivers, two-thirds of whom had early AD, showed that at baseline persons with AD had had more accidents and showed poorer performance on road tests compared with control subjects. While scientists found that some individuals with very mild dementia can continue driving for extended periods of time, regular follow-up assessments at least every 6 months are needed to ensure safety (Ott et al., 2008).

Families are usually the first to notice unsafe driving behaviors in the person with AD but often find it difficult to convince the person that he or she should stop driving. Helpful information is available from the following websites:

• http://www.thehartford.com/alzheimers
• http://www.nhtsa.dot.gov
• http://www.niapublications.org/agepages/PDFs/Older_Drivers.pdf
• http://www.floridagranddriver.com/reportUnsafeDriver.cfm

Once the diagnosis of AD is established, the physician needs to encourage the patient to stop driving. Some patients do this willingly; others are reluctant to give up the independence that driving represents, thereby creating a significant threat to personal and public safety. Those who refuse to quit driving even though they pose a hazard must be prevented from driving by other means, either by hiding the car keys or disabling the car.

Although many states encourage physicians and other health professionals to report people with conditions that may affect their ability to drive safely, only California has a public policy specifically requiring the reporting of individuals who have Alzheimer's disease. In Florida, any physician, person, or agency knowing of a licensed driver's (or applicant's) mental or physical disability to drive is authorized to report this to the department of highway safety and motor vehicles (Florida GrandDriver, 2008). The form to be used is available at http://www.flhsmv.gov/forms/72190.html.

PREVENTION OF ELDER ABUSE

Abuse of older adults is a well-kept secret in America. According to the National Administration on Aging, hundreds of thousands of elders are abused, neglected, and exploited by family members and others. Many cases go unreported. Abuse may be physical, verbal/psychological, financial, sexual, or neglect. People with Alzheimer's disease or other cognitive impairment are at higher risk than other older adults. Most known perpetrators of abuse and neglect are family members, usually an adult child or a spouse.

Caring for a person with AD can lead to stress, depression, feelings of isolation, financial worries, and substance abuse, any or all of which can lead to elder abuse. Violent behavior by the patient may also lead to physical abuse by the caregiver.

Respite care for the patient and support group and counseling for the caregiver can help to prevent elder abuse. In severe cases of abuse, it is usually necessary to separate the patient from the caregiver, initiate legal action, and find a safe facility for the patient.

Signs of abuse include bruises, skin wounds, burns or fractures, and lack of explanation for falls and injuries. Physical signs of neglect include severe weight loss, dehydration, poor personal hygiene, and pressure ulcers (bedsores).

LEGAL CONSIDERATIONS

Getting legal affairs in order—drawing up advance directives, powers of attorney, wills, or trusts should be done as soon as possible after diagnosis, while the patient is able to express personal wishes and participate in decisions. Referral to the local chapter of the Alzheimer's Association can help families find attorneys who specialize in elder law or estate planning.

This referral should not be made abruptly but as a suggestion, emphasizing that every adult, regardless of health status, should make such a plan. This helps ensure that one's wishes are respected in end-of-life care and disposition of property after death. Otherwise, families will need to make difficult decisions without knowing the patient's wishes.

Advance Directives

An advance directive specifies a person's preferences for care in the event that he or she is unable to communicate those wishes—for example, in the advanced stages of AD. A living will is one type of advance directive. In an advance directive, the person can also name a representative to see that his or her wishes concerning care are carried out. This is sometimes called a durable power of attorney for healthcare.

Physicians should have copies of advance directives available or be able to refer families to a source for the appropriate forms. Federal law requires hospitals to inform patients that they have a right to complete an advance directive (the Patient Self-Determination Act), but advance directives are regulated by state law and may differ from state to state.

Family Caregiver Alliance (http://www.caregiver.org) can provide state-specific information and appropriate forms for advance directives. Advance directives are used by almost half (46.6%) of all Floridians with severe cognitive impairment, compared with 37.6 percent of their counterparts nationwide (Brown University, 2004).

CPR vs. DNR Orders

One type of advance directive is a do-not-resuscitate order (DNRO), which informs medical personnel that a patient does not want to have cardiopulmonary resuscitation (CPR) performed in the event of cardiac or respiratory arrest. These DNROs are also regulated by state law.

A DNRO order should be posted prominently, either on the head or foot of the bed, or, if the patient is at home, on the refrigerator, and also be included in the patient's chart. The DNRO should be readily available in the event of an emergency to ensure that the patient's wishes will be honored. Some patients prefer the additional safeguard of wearing a bracelet or necklace to alert care providers that a DNRO is in force.

Nutrition and Hydration

In the late stages of AD, patients may become unable to consume sufficient oral feedings to prevent weight loss. If the patient's advance directive indicates that he or she does not want artificial nutrition and hydration (ANH), caregivers must respect that decision. However, if the decision was not made earlier, this is the time when the patient's surrogate (also called a proxy) decision maker, together with the physician and other members of the health team, must decide together whether to initiate tube feedings.

Deciding whether to have ANH means weighing the potential benefit and the burden to the patient. The physician and care providers need to help families understand that forgoing ANH is not "killing" or "starving" the patient.

The Ethics Advisory Panel of the Alzheimer's Association (2000) recommends assisted oral feeding coupled with hospice care, when needed, as the compassionate alternative to tube feeding. This recommendation is based on several studies that point out tube feeding:

• Is associated with in creased diarrhea and related discomforts
• Results in increased use of physical restraints to prevent patients from pulling tubes out of their abdomens
• Does not usually improve nutritional status
• Does not lower the incidence of aspiration pneumonia or skin breakdown
• Does not improve longevity
• Denies the patient the gratification of tasting preferred foods

The Alzheimer's Association emphasizes that "assisted oral feeding should be available to all persons with advanced Alzheimer's as needed. Neglect in this area should not be tolerated, and concerted efforts are called for to educate and support professional and family caregivers in techniques of assisted oral feeding."

Eventually, the ability to swallow is lost, at which time the patient is considered terminal. This is a normal part of the final stage of AD, and research suggests that those patients who forgo ANH do not seem to feel thirsty or hungry. Without ANH, patients have less trouble with fluid in the lungs, which causes shortness of breath, or fluid in the throat, which means less need for suctioning.

Research also indicates that forgoing ANH actually increases the body's natural pain-relieving hormones, called endorphins, making the patient more comfortable and less likely to experience pain (Lynn & Harrold, 1999). The only side effect of dehydration at the end of life is dry mouth, which can be relieved by good mouth care, ice chips, or moistened sponge swabs.

Antibiotics

Patients with advanced AD or other dementias are frequently given antibiotics as they near the end of life, primarily for lower respiratory infection. There is concern that this practice (1) often does not benefit the patient, and (2) may contribute to the development of drug-resistant superbugs in nursing homes. A new study by Boston researchers found that more than 40 percent of the residents who died during the study had received antibiotics in the last two weeks of life. Nearly half the time, the antibiotics were administered intravenously (D'Agata & Mitchell, 2008).

The use of antibiotics near the end of life is another issue that ideally needs to be discussed during the preparation of the patient's advance directive. If that has not occurred, then health professionals need to discuss antibiotics with the family if an infection develops. Even if antibiotic treatment extends the patient's life a few days or weeks, it does not increase their comfort, which should be the primary concern (Volicer, 2007).

Because advanced dementia is currently incurable, it should be considered a terminal illness, similar to terminal cancer. Therefore, palliative care may be the most appropriate strategy for management of advanced dementia. The goals of palliative care are maintenance of quality of life, dignity, and comfort …. L. Volicer, 2007

Hospice Care

Hospice is a philosophy of care that emphasizes physical comfort, pain and symptom management, and death with dignity. It encompasses the spiritual and psychosocial aspects of care, both for the patient and the family, and includes bereavement support for the surviving family members.

During the terminal stages of AD, hospice care can be particularly beneficial to patients and families. Each year, more than half a million terminally ill people enter hospice programs for end-of-life care. Most of them are people with cancer. Unfortunately, few clients with AD receive hospice care, accounting for only about 7 percent of the annual hospice census.

Physicians and other health professionals need to educate families about the benefits of hospice care for their loved one with AD and for themselves. Ideally, this education would begin at the time of diagnosis, when the patient is still capable of expressing preferences about end-of-life care.

Hospice care involves a team of health professionals, including doctors, nurses, social workers, clergy, therapists, and trained volunteers. Hospice care is most often given in a patient's own home, but it can also be given in nursing homes or hospitals. A few communities may have separate facilities designated for hospice care.

To qualify for insurance reimbursement (including Medicare) for hospice services, a physician and a hospice medical director must certify that the patient has less than six months to live. Medicare covers the cost of hospice care in every state, as does most private long-term care insurance.

Dementia will always have a deeply tragic aspect, both for those who are affected and for those who are close to them. There is, however, a vast difference between a tragedy, in which persons are actively involved and morally committed, and a blind and hopeless submission to fate. Tom Kitwood, 1997

Posted July 17, 2008

Expires July 1, 2010

Copyright © 2008 Wild Iris Medical Education. All rights reserved.