Most of us worry from time to time that we are losing our memory and other mental abilities (Glauberman, 2014). You rush out the door without your keys, you meet a familiar person and cannot remember her name, or you forget that you have seen a particular film. Actually such mishaps are a common and quite normal feature of stress or of aging. As people move through middle age, these memory difficulties and lapses of attention increase, and they may occur regularly by the age of 60 or 70 (see MindTech below). Sometimes, however, people have memory and other cognitive changes that are far more extensive and problematic.

In Chapter 6 you saw that problems in memory and related cognitive processes can occur without biological causes, in the form of dissociative disorders. More often, though, cognitive problems do have organic roots, particularly when they appear late in life. The leading such disorders among the elderly are delirium, major neurocognitive disorder, and mild neurocognitive disorder.

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Delirium is a major disturbance in attention and orientation to the environment (see Table 18-1). As the person’s focus becomes less clear, he or she has great difficulty concentrating and thinking in an organized way, leading to misinterpretations, illusions, and on occasion, hallucinations (Lawlor & Bush, 2014; Eeles & Bhat, 2010). Sufferers may believe that it is morning in the middle of the night or that they are home when actually they are in a hospital room.

This state of massive confusion typically develops over a short period of time, usually hours or days (APA, 2013). Delirium may occur in any age group, including children, but is most common in elderly people. Fewer than 0.5 percent of the nonelderly population experience delirium, compared with 1 percent of people over 55 years of age and 14 percent of those over 85 years of age (Tune & DeWitt, 2011). When elderly people enter a hospital to be treated for a general medical condition, 1 in 10 of them shows the symptoms of delirium. At least another 10 percent develop delirium during their stay in the hospital (Bagnall & Faiz, 2014; Inouye, 2006; Inouye et al., 2003). Around 17 percent of patients admitted for surgery develop delirium (de Castro et al., 2014). That number rises to 23 percent among those admitted suddenly for acute surgery. Sixty percent of nursing home residents older than 75 years of age have some delirium, compared with 35 percent of similar people living independently with the assistance of home health services (Tune & DeWitt, 2011).

Fever, certain diseases and infections, poor nutrition, head injuries, strokes, and stress (including the trauma of surgery) may all cause delirium (Lawlor & Bush, 2014; Eeles & Bhat, 2010; Wetterling, 2005). So may intoxication by certain substances, such as prescription drugs. Partly because older people face so many of these problems, they are more likely than younger ones to experience delirium. If a clinician accurately identifies delirium, it can often be easy to correct—by treating the underlying infection, for example, or changing the patient’s drug prescription. However, the syndrome typically fails to be recognized for what it is (Lawlor & Bush, 2014; Ames et al., 2010). One pioneering study on a medical ward, for example, found that admission doctors detected only 1 of 15 consecutive cases of delirium (Cameron et al., 1987). Incorrect diagnoses of this kind may contribute to a high death rate for older people with delirium (Dasgupta & Brymer, 2014; Trzepacz & Meagher, 2008)

People with a neurocognitive disorder experience a significant decline in at least one (often more than one) area of cognitive functioning, such as memory and learning, attention, visual perception, planning and decision making, language ability, or social awareness (APA, 2013). Those who have certain types of neurocognitive disorders may also undergo personality changes—they may behave inappropriately, for example—and their symptoms may worsen steadily.

If the person’s cognitive decline is substantial and interferes significantly with his or her ability to be independent, a diagnosis of major neurocognitive disorder is in order. If the decline is modest and does not interfere with independent functioning, the appropriate diagnosis is mild neurocognitive disorder (see Table 18-2).

There are currently 44 million people with neurocognitive disorders around the world, with 4.6 million new cases emerging each year (Hollingworth et al., 2011). The number of cases is expected to reach 135 million by 2050 unless a cure is found (Sifferlin, 2013). The occurrence of neurocognitive disorders is closely related to age (see Figure 18-2). Among people 65 years of age, the prevalence is around 1 to 2 percent, increasing to as much as 50 percent among those over the age of 85 (Zhao et al., 2014; Apostolova & Cummings, 2008).

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As you read earlier, Alzheimer’s disease is the most common type of neurocognitive disorder, accounting for around two-thirds of all cases (Burke, 2011; Farlow, 2010). Around 5 million people in the United States currently have this disease, a number that is expected to triple by the year 2050 (Wesson et al., 2011). Alzheimer’s disease sometimes appears in middle age (early onset), but in the vast majority of cases it occurs after the age of 65 (late onset), and its prevalence increases markedly among people in their late 70s and early 80s (Zhao et al., 2014). At least 17 percent of those with Alzheimer’s also experience major depressive disorder (Chi et al., 2014; Mathys & Belgeri, 2010).

Alzheimer’s disease is a gradually progressive disease in which memory impairment is the most prominent cognitive dysfunction (APA, 2013). Technically, sufferers receive a DSM-5 diagnosis of mild neurocognitive disorder due to Alzheimer’s disease during the early and mild stages of the syndrome and major neurocognitive disorder due to Alzheimer’s disease during the later, more severe stages (see Table 18-3).

Alzheimer’s disease is named after Alois Alzheimer, the German physician who formally identified it in 1907. Alzheimer first became aware of the syndrome in 1901 when a new patient, Auguste D., was placed under his care:

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Although some people with Alzheimer’s disease may survive for as many as 20 years, the time between onset and death is typically 8 to 10 years (Advokat et al., 2014; Soukup, 2006). It usually begins with mild memory problems, lapses of attention, and difficulties in language and communication (Farlow, 2010). As symptoms worsen, the person has trouble completing complicated tasks or remembering important appointments. Eventually sufferers also have difficulty with simple tasks, forget distant memories, and have changes in personality that often become very noticeable. For example, a gentle man may become uncharacteristically aggressive.

People with Alzheimer’s disease may at first deny that they have a problem, but they soon become anxious or depressed about their state of mind; many also become agitated. A woman from Virginia describes her memory loss as the disease progresses:

As the neurocognitive symptoms intensify, people with Alzheimer’s disease show less and less awareness of their limitations. They may withdraw from others during the late stages of the disorder, become more confused about time and place, wander, and show very poor judgment. Eventually they become fully dependent on other people. They may lose almost all knowledge of the past and fail to recognize the faces of even close relatives. They also become increasingly uncomfortable at night and take frequent naps during the day (Ames et al., 2010; Edelstein et al., 2008). During the late phases of the disorder, they require constant care.

People with Alzheimer’s usually remain in fairly good health until the later stages of the disease. As their mental functioning declines, however, they become less active and spend much of their time just sitting or lying in bed. This makes them prone to develop illnesses such as pneumonia, which can result in death (Park et al., 2014; Ames et al., 2010). Alzheimer’s disease is currently responsible for close to 84,000 deaths each year in the United States, a number that is 40 percent higher than it was a decade ago (NCHS, 2014). It is the sixth leading cause of death in the country, the third leading cause among the elderly (CDC, 2013, 2010).

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In most cases, Alzheimer’s disease can be diagnosed with certainty only after death, when structural changes in the person’s brain, such as excessive senile plaques and neurofibrillary tangles, can be fully examined. Senile plaques are sphere-shaped deposits of a small molecule known as the beta-amyloid protein that form in the spaces between cells in the hippocampus, cerebral cortex, and certain other brain regions, as well as in some nearby blood vessels. The formation of plaques is a normal part of aging, but it is exceptionally high in people with Alzheimer’s disease (Zhao et al., 2014; Selkoe, 2011, 2000, 1992). Neurofibrillary tangles, twisted protein fibers found within the cells of the hippocampus and certain other brain areas, also occur in all people as they age, but again people with Alzheimer’s disease form an extraordinary number of them.

Scientists do not fully understand what role excessive numbers of plaques and tangles play in Alzheimer’s disease, but they suspect they are very important. Today’s leading explanations for this disease center on these plaques and tangles and on the various factors that may contribute to their formation.

What Are the Genetic Causes of Alzheimer’s Disease?To understand the genetic theories of Alzheimer’s disease, we must first appreciate the nature and role of proteins. Proteins are fundamental components of all living cells, including, of course, brain cells. They are large molecules made up of chains of carbon, hydrogen, oxygen, nitrogen, and sulfur. There are many different kinds of proteins, each with a different function. Collectively, they are essential for the proper functioning of an organism.

The plaques and tangles that are so plentiful in the brains of Alzheimer’s patients seem to occur when two important proteins start acting in a frenzied manner. Abnormal activity by the beta-amyloid protein is, as we noted above, key to the repeated formation of plaques (Zhao et al., 2014; Fändrich et al., 2011). Abnormal activity by another protein, tau, is key to the excessive formation of tangles (Zhao et al., 2014; Obulesu et al., 2011). One of the leading theories holds that the many plaques formed by beta-amyloid proteins cause tau proteins in the brain to start breaking down, resulting in tangles and the death of many neurons (Hughes, 2011; Obulescu et al., 2011).

What causes this chain of events? Genetic factors are a major culprit. However, the genetic factors that are responsible differ for the early-onset and late-onset types of Alzheimer’s disease.

EARLY-ONSET ALZHEIMER’S DISEASEAs we noted earlier, Alzheimer’s disease occurs before the age of 65 in relatively few cases. Such cases typically run in families. Researchers have learned that this form of Alzheimer’s disease can be caused by abnormalities in the genes responsible for the production of two proteins—the beta-amyloid precursor protein (beta-APP) and the presenilin protein. Apparently, some families transmit mutations, or abnormal forms, of one or both of these genes—mutations that lead ultimately to abnormal beta-amyloid protein buildups and, in turn, to plaque formations (Zhao et al., 2014; Wesson et al., 2011).

LATE-ONSET ALZHEIMER’S DISEASEThe vast majority of Alzheimer cases develop after the age of 65. Such cases typically do not run in families and are often called sporadic Alzheimer’s disease. This late-onset form of the disease appears to result from a combination of genetic, environmental, and lifestyle factors. However, the genetic factor at play in late-onset Alzheimer’s disease is different from those involved in early-onset Alzheimer’s disease.

A gene called the apolipoprotein E (ApoE) gene, located on chromosome 19, is normally responsible for the production of a protein that helps carry various fats into the bloodstream. This gene comes in various forms. About 30 percent of the population inherit the form called ApoE-4, and those people may be particularly vulnerable to the development of Alzheimer’s disease (Shu et al., 2014; Hollingworth et al., 2011). Apparently, the ApoE-4 gene form promotes the excessive formation of beta-amyloid proteins, helping to spur the formation of plaques and, in turn, the breakdown of the tau protein, the formation of numerous tangles, the death of many neurons, and, ultimately, the onset of Alzheimer’s disease.

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Although the ApoE-4 gene form appears to be a major contributor to the development of Alzheimer’s disease, it is important to recognize that not everyone with this form of the gene develops the disease. Other factors—perhaps environmental, lifestyle, or stress-related—may also have a significant impact in the development of late-onset Alzheimer’s disease (Nation et al., 2011; Tran et al., 2011).

AN ALTERNATIVE GENETIC THEORY OF ALZHEIMER’S DISEASEAs you have just read, the leading genetic theories of Alzheimer’s disease point to gene forms, such as ApoE-4, that produce abnormal beta-amyloid proteins buildups and plaque formations, which, in turn, lead to abnormal activity of tau proteins and the formation of numerous tangles. In recent years, however, some researchers have come to believe that abnormal tau protein activity is not always the result of these abnormal beta-amyloid protein buildups (Peterson et al., 2014; Karch, Jeng, & Goate, 2013). These researchers have identified other gene forms in Alzheimer’s patients that seem to be directly associated with tau protein abnormalities and tangle formations. Thus it may be that there are multiple genetic causes for the formation of numerous tangle formations and the onset of Alzheimer’s disease: (1) gene forms that start the ball rolling by first promoting beta-amyloid protein formations and plaques, and (2) gene forms that more directly promote tau protein abnormalities and tangle formations.

How Does Brain Structure Relate to Alzheimer’s Disease?We know that genetic factors may predispose people to Alzheimer’s disease, but we still need to know what abnormalities in brain structure eventually result from such factors—that is, which brain structure abnormalities help promote Alzheimer’s disease. Researchers have identified a number of possibilities. To understand these, we need first to appreciate some basic information about the operation and biology of memory.

The human brain has two memory systems that work together to help us learn and recall. Short-term memory, or working memory, gathers new information. Long-term memory is the accumulation of information that we have stored over the years, information that first made its way through the short-term memory system. The information held in short-term memory must be transformed, or consolidated, into long-term memory if we are to hold on to it. Remembering information that has been stored in long-term memory is called retrieval, which is described as going into one’s long-term memory to bring it out for use again in short-term, or working, memory.

Certain brain structures seem to be especially important in memory. Among the most important structures in short-term memory is the prefrontal cortex, located just behind the forehead. When animals or humans acquire new information, their pre-frontal cortex becomes more active (Jiang et al., 2000), enabling them to hold information temporarily and to continue working with the information as long as it is needed. Among the most important structures in transforming short-term memory into long-term memory are the temporal lobes (which include the hippocampus and amygdala) and the diencephalon (which includes the mammillary bodies, thalamus, and hypothalamus). Research indicates that Alzheimer’s disease involves damage to or improper functioning of one or more of these brain areas (van der Flier et al., 2005; Caine et al., 2001) (see Figure 18-3).

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What Biochemical Changes in the Brain Relate to Alzheimer’s Disease?Memory researchers have also identified biochemical changes that occur in cells as memories form. In order for new information to be acquired and stored, certain proteins must be produced in key brain cells. Several chemicals—for example, acetylcholine, glutamate, RNA (ribonucleic acid), and calcium—are responsible for the production of the memory-linked proteins. If the activity of any of these chemicals is disturbed, the proper production of proteins may be prevented and the formation of memories interrupted (Canas et al., 2014; Wu et al., 2008). For example, by blocking the activity of glutamate, animal researchers have prevented the operation of short-term memory. Similarly, by blocking the cellular production of RNA or of calcium, they have interrupted the formation of long-term memories (Berridge, 2011).

Some research suggests that abnormal activity by these various chemicals may contribute to the symptoms of Alzheimer’s disease. Studies have found, for example, that acetylcholine and glutamate are in low supply, or at least function differently, in the brains of Alzheimer’s victims, and other studies suggest that Alzheimer’s victims have an imbalance in the breakdown of calcium (Canas et al., 2014).

Other Explanations of Alzheimer’s DiseaseSeveral lines of research suggest that certain substances found in nature may act as toxins, damage the brain, and contribute to the development of Alzheimer’s disease. For example, researchers have detected high levels of zinc in the brains of some Alzheimer’s patients (Xu et al., 2014; Schrag et al., 2011). This finding has gained particular attention because in some animal studies zinc has been observed to trigger a clumping of the beta-amyloid protein, similar to the plaques found in the brains of Alzheimer’s patients.

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Another line of research suggests that the environmental toxin lead may contribute to the development of Alzheimer’s disease (Lee & Freeman, 2014; Ritter, 2008). Lead was phased out of gasoline products between 1976 and 1991, leading to an 80 percent drop of lead levels in people’s blood. However, many of today’s elderly were exposed to high levels of lead in the 1960s and 1970s, regularly inhaling air pollution from vehicle exhausts—an exposure that might have damaged or destroyed many of their neurons. Several studies suggest that this earlier absorption of lead and other pollutants may be having a negative effect on the current cognitive functioning of these individuals (Richardson et al., 2014; Ritter, 2008; Hu et al., 2005).

One study, for example, examined elderly people and scanned their shinbones for lead (Schwartz & Stewart, 2007). Interpreting shinbone levels of lead as indicators of the person’s lifetime exposures to lead, the researchers found that the higher a person’s lifetime lead exposure, the more poorly he or she performed on memory and language tests. An important question here is: Why would cognitive dysfunction first appear decades after exposure to the toxin? Medical researcher Philip Landrigan (2007) suggests, “If a substance destroys brain cells in early life, the brain may cope by drawing on its reserve capacity until [eventually] it loses more cells with aging…. Only then would symptoms like forgetfulness or tremors begin.”

Two other explanations for Alzheimer’s disease have also been offered. One is the autoimmune theory. On the basis of certain irregularities found in the immune systems of people with Alzheimer’s disease, several researchers have speculated that changes in aging brain cells may trigger an autoimmune response (that is, a mistaken attack by the immune system against itself) that helps lead to the disease (Marchese et al., 2014; Zipp & Aktas, 2006). The other explanation is a viral theory. Because Alzheimer’s disease resembles Creutzfeldt-Jakob disease, another type of neurocognitive disorder that is known to be caused by a slow-acting virus, some researchers propose that a similar virus may cause Alzheimer’s disease (Head, 2013; Doty, 2008; Prusiner, 1991). To date, however, no such virus has been detected in the brains of Alzheimer’s victims.

Assessing and Predicting Alzheimer’s DiseaseAs you read earlier, most cases of Alzheimer’s disease can be diagnosed with absolute certainty only after death, when an autopsy is performed. However, brain scans, which reveal abnormalities in the living brain, now are used commonly as assessment tools and often provide clinicians with considerable confidence in their diagnoses of Alzheimer’s disease (Rabin, 2013; Yamasaki et al., 2012; Berti et al., 2011). In addition, several research teams currently are trying to develop tools that can identify those people who are likely to develop Alzheimer’s disease and other types of neurocognitive disorders.

One promising line of work, for example, comes from the laboratory of neuroscientist Lisa Mosconi and her colleagues (Mosconi, 2013; Mosconi et al., 2010, 2008; de Leon et al., 2007). Using a special kind of PET scan, this research team examined activity in certain parts of the hippocampus in dozens of elderly research participants and then conducted follow-up studies of them for up to 24 years. (Recall that the hippocampus plays a major role in memory.) Eventually, 43 percent of the study’s participants developed either a mild or major neurocognitive disorder due to Alzheimer’s disease. The researchers found that those who developed such cognitive impairments had displayed lower hippocampus activity on their initial PET scans than the participants who remained healthy. Overall, the PET scans, administered years before the onset of symptoms, predicted mild neurocognitive impairment with an accuracy rate of 71 percent and major neurocognitive impairment with an accuracy rate of 83 percent.

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As you will see shortly, the most effective interventions for Alzheimer’s disease and other types of neurocognitive disorders are those that help prevent these problems, or at least ones that are applied early. Clearly, then, it is essential to have tools that identify the disorders as early as possible, preferably years before the onset of symptoms (Rabin, 2013). That is what makes the research advances in assessment and diagnosis so exciting.

Other Types of Neurocognitive DisordersThere are a number of neurocognitive disorders in addition to Alzheimer’s disease (APA, 2013) (see PsychWatch on pages 626–627). Vascular neurocognitive disorder, for example, follows a cerebrovascular accident, or stroke, during which blood flow to specific areas of the brain was cut off, thus damaging the areas (Jia et al., 2014; Ames et al., 2010). In many cases, the patient may not even be aware of the stroke (Moorhouse & Rockwood, 2010). Like Alzheimer’s disease, this disorder is progressive, but its symptoms begin suddenly rather than gradually. Moreover, the person’s cognitive functioning may continue to be normal in areas of the brain that have not been affected by the stroke, in contrast to the broad cognitive deficiencies usually displayed by Alzheimer’s patients. Some people have both Alzheimer’s disease and vascular neurocognitive disorder.

Frontotemporal neurocognitive disorder, also known as Pick’s disease, is a rare disorder that affects the frontal and temporal lobes. It has a clinical picture similar to Alzheimer’s disease, but the two diseases can be distinguished at autopsy.

Neurocognitive disorder due to prion disease, also called Creutzfeldt-Jakob disease, has symptoms that include spasms of the body. As we observed earlier, this disorder is caused by a slow-acting virus that may live in the body for years before the disease develops. Once launched, however, the disease has a rapid course.

Neurocognitive disorder due to Huntington’s disease is an inherited progressive disease in which memory problems, along with personality changes and mood difficulties, worsen over time. People with Huntington’s have movement problems, too, such as severe twitching and spasms. Children of people with Huntington’s disease have a 50 percent chance of developing it.

Parkinson’s disease, the slowly progressive neurological disorder marked by tremors, rigidity, and unsteadiness, can result in neurocognitive disorder due to Parkinson’s disease, particularly in older people or those whose cases are advanced.

Yet other neurocognitive disorders may be caused by HIV infections, traumatic brain injury, substance abuse, or various medical conditions such as meningitis or advanced syphilis.

What Treatments Are Currently Available for Alzheimer’s Disease and Other Neurocognitive Disorders?Treatments for the cognitive features of Alzheimer’s disease and most other types of neurocognitive disorders have been at best modestly helpful. A number of approaches have been applied, including drug therapy, cognitive techniques, behavioral interventions, support for caregivers, and sociocultural approaches.

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DRUG TREATMENTThe drugs currently prescribed for Alzheimer’s patients are designed to affect acetylcholine and glutamate, the neurotransmitters that play important roles in memory. Such drugs include tacrine (trade name Cognex), donepezil (Aricept), rivastigmine (Exelon), galantamine (Reminyl), and memantine (Namenda). The short-term memory and reasoning ability of some Alzheimer’s patients who take these drugs improve slightly, as do their use of language and their ability to cope under pressure (Jessen, 2014; Wang et al., 2014). Although the benefits of the drugs are limited and the risk of harmful effects (particularly those from tacrine) is sometimes high, these drugs have been approved by the FDA. Clinicians believe that they may be of greatest use to people in the early, mild stage of Alzheimer’s disease. Another approach, taking vitamin E, either alone or in combination with one of these drugs, also seems to help slow down further cognitive decline among people in the mild stage of Alzheimer’s disease (Dysken et al., 2014, 2009). Numerous other possible drug treatments are being investigated currently (Medina & Avila, 2014).

The drugs just discussed are each prescribed after a person has developed Alzheimer’s disease. In contrast, studies suggest that certain substances now available on the marketplace for other kinds of problems may help prevent or delay the onset of Alzheimer’s disease. For example, some studies have found that women who took estrogen, the female sex hormone, for years after menopause cut their risk of developing Alzheimer’s disease in half (Li, Cui, & Shen, 2014; Kawas et al., 1997). Other studies have suggested that the long-term use of nonsteroidal anti-inflammatory drugs such as ibuprofen and naprosyn (drugs found in Advil, Motrin, Nuprin, and other pain relievers) may help reduce the risk of Alzheimer’s disease, although recent findings on this possibility have been mixed (Advokat et al., 2014).

COGNITIVE TECHNIQUESCognitive treatments have been used in cases of Alzheimer’s disease, with some temporary success. In Japan, for example, a number of people with the disease meet regularly in classes, performing simple calculations and reading essays and novels aloud. Proponents of this approach claim that it serves as a mental exercise that helps rehabilitate those parts of the brain linked to memory, reasoning, and judgment. Similarly, some research suggests that cognitive activities, including computer-based cognitive stimulation programs, may help prevent or delay the onset of Alzheimer’s disease (Szalavitz, 2013; Wilson et al., 2012; Schmiedek et al., 2010). One study of 700 people in their 80s found that those research participants who had pursued cognitive activities over a five-year period (for example, writing letters, following the news, reading books, or attending concerts or plays) were less likely to develop Alzheimer’s disease than were mentally inactive participants (Wilson et al., 2012, 2007).

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BEHAVIORAL INTERVENTIONSBehavioral interventions have also been somewhat successful in helping Alzheimer’s patients. It has become increasingly clear across many studies that physical exercise helps improve cognitive functioning—for people of all ages and states of health (Szabo et al., 2011). There is evidence that regular physical exercise may also help reduce the risk of developing Alzheimer’s disease and other types of neurocognitive disorders (Borisovskaya, Pascuali, & Borson, 2014; Nation et al., 2011). Correspondingly, physical exercise is often a part of treatment programs for people with the disorders.

Behavioral interventions of a different kind have been used to help improve specific symptoms displayed by Alzheimer’s patients. The approaches typically focus on changing everyday patient behaviors that are stressful for the family, such as wandering at night, loss of bladder control, demands for attention, and inadequate personal care (Lancioni et al., 2011; Lindsey, 2011; Knight et al., 2006). The behavioral therapists use a combination of role-playing exercises, modeling, and practice to teach family members how and when to use reinforcement in order to shape more positive behaviors.

SUPPORT FOR CAREGIVERSCaregiving can take a heavy toll on the close relatives of people with Alzheimer’s disease and other types of neurocognitive disorders (Kang et al., 2014; Llanque et al., 2014). Almost 90 percent of all people with Alzheimer’s disease are cared for by their relatives (Alzheimer’s Association, 2014, 2007). It is hard to take care of someone who is becoming increasingly lost, helpless, and medically ill. And it is very painful to witness mental and physical decline in someone you love.

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One of the most frequent reasons for the institutionalization of people with Alzheimer’s disease is that overwhelmed caregivers can no longer cope with the difficulties of keeping them at home (Di Rosa et al., 2011;Apostolova & Cummings, 2008). Many caregivers experience anger and depression, and their own physical and mental health often declines (Kang et al., 2014; Pinquart & Sörensen, 2011; Kantrowitz &Springen, 2007). Clinicians now recognize that one of the most important aspects of treating Alzheimer’s disease and other types of neurocognitive disorders is to focus on the emotional needs of the caregivers, including their needs for regular time out, education about the disease, and psychotherapy (Mittelman & Bartels, 2014; McKenzie & Teri, 2011). Some clinicians also provide care-giver support groups.

SOCIOCULTURAL APPROACHESSociocultural approaches play an important role in treatment (Pongan et al., 2012; Brooks, 2005; Kalb, 2000) (see MediaSpeak below). A number of day-care facilities for patients with neurocognitive disorders have been developed, providing treatment programs and activities for outpatients during the day and returning them to their homes and families at night. There are also many assisted-living facilities in which those suffering from neurocognitive impairment live in cheerful apartments, receive needed supervision, and take part in various activities that bring more joy and stimulation to their lives. These apartments are typically designed to meet the special needs of the residents—providing more light, for example, or enclosing gardens with circular paths so the residents can go for strolls alone without getting lost. Studies suggest that such facilities often help slow the cognitive decline of residents and enhance their enjoyment of life. In addition, a growing number of practical devices, such as tracking beacons worn on the wrists of Alzheimer’s patients and shoes that contain a GPS tracker, have been developed to help locate patients who may wander off (Schiller, 2014, Quick, 2011; Neergaard, 2007).

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Given the progress now unfolding in the understanding and treatment of Alzheimer’s disease and other types of neurocognitive disorders, researchers are looking forward to enormous advances in the coming years. The brain changes responsible for these disorders are tremendously complex, but most investigators believe that exciting breakthroughs are just over the horizon. Ironically, just when significant progress is being made and genuine reason for hope has emerged, the public seems to be losing patience. In one survey of more than 3,000 adults across the United States, only 48 percent of the respondents believed that at least “some” progress has been made toward curing Alzheimer’s disease (Shriver, 2011). In contrast, 74 percent and 81 percent of them believed that at least some progress has been made toward curing cancer and heart disease, respectively.