ATrain Education


Continuing Education for Health Professionals

Elders and Their Care

Module 7


Dementia is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. It is estimated that as many as 6.8 million people in the United States have dementia, and at least 1.8 million of those are severely affected. Studies in some communities have found that almost half of all people age 85 and older have some form of dementia. Although it is common in very elderly individuals, dementia is not a normal part of the aging process. Many people live into their 90s and even 100s without any symptoms of dementia (NINDS, 2011).

People with dementia have significantly impaired mental functioning that interferes with normal activities and relationships. They can lose their ability to solve problems and maintain emotional control, and may experience personality changes and behavioral problems such as agitation, delusions, and hallucinations.

Memory loss is a common symptom of dementia but by itself does not mean a person has dementia. Dementia is diagnosed only if two or more brain functionssuch as memory, language, perception, reasoning, or judgment, among othersare significantly impaired.

Although memory and other cognitive functions change with age, age-related cognitive change is not dementia. Memory may not be as sharp and there may be word-finding difficultiesit may take longer to do certain mental tasks such as memorizing a string of words or numbers. Multi-tasking may be a thing of the past. Older adults with age-related cognitive changes can however read, operate a computer, manage their finances, and prepare their own mealsthey do not forget what a coffee pot is or how to operate a microwave. They understand when they are in danger and know that they should call for help or get out of a house if there is a fire.

Mild cognitive impairment (MCI) is a condition in which people have memory problems that are noticeably worse than age-related changes. However, people with MCI do not have the problems associated with dementia such as personality and cognitive changes. Some people with MCI do go on to develop AD, but not everyone does.

Differentiating Dementia from Other Conditions

The symptoms of a number of medical conditions mimic those of dementia and this must be considered when evaluating a person experiencing cognitive changes. Gerontology specialists speak of the “Three Ds”dementia, delirium, and depressionbecause these are the most prevalent reasons for cognitive impairment in older adults. Delirium and depression can cause cognitive changes that may be mistaken for dementia, and healthcare providers and caregivers should learn to distinguish among the three conditions.


Delirium is a sudden, severe confusion with rapid changes in brain function. Delirium develops over hours or days and is temporary and reversible. It can occur after general anesthesia, from infections (eg, UTI, pneumonia), from fluid/electrolyte or acid/base disturbances, or from other conditions that deprive the brain of oxygen. Pain can also contribute to delirium, as can the medications used to treat pain. Being in an unfamiliar environment such as adult daycare or a nursing home can also contribute to delirium.


Depression is caused by neurochemical imbalances in the brain. It can lead to cognitive impairment, which should improve when the depression is treated. People with depression are aware of the date and time; however, they may answer “I don’t know” to orientation questions and may not make eye contact. They may have a flat affect (show little expression) and may speak in a monotone. A smile does not rule out the presence of depression; people who are depressed may smile while describing the hopelessness of life. Irritability or verbal expression of pessimism, sadness, or hopelessness may indicate depression. Depression commonly occurs in the early stages of Alzheimer’s disease (AD) as individuals become aware of their loss of cognitive function.

Other Conditions

There are other conditions that can cause dementia-like symptoms; many of these conditions are reversible with appropriate treatment (NINDS, 2011):

  • Reactions to medications or interactions between medications
  • Metabolic problems and endocrine abnormalities
    • Thyroid abnormalities
    • Hypoglycemia
    • Too little or too much sodium or calcium
    • Pernicious anemia
  • Nutritional deficiencies.
    • Thiamine deficiency (vitamin B1)can occur with chronic alcoholism and can seriously impair mental abilities, in particular memories of recent events
    • Dehydrationcan cause mental impairment that resembles dementia.
  • Infectionscan cause neurologic symptoms, including confusion or delirium due to fever or other side effects of the body’s fight to overcome the infection
  • Subdural hematomas
  • Poisoningexposure to lead, heavy metals, or other poisonous substances Symptoms may or may not resolve after treatment, depending on how badly the brain is damaged.
  • Abuse of alcohol, prescription medications, and recreational drugs
  • Brain tumors
  • Anoxiaa diminished supply of oxygen to the brain. Recovery depends on the severity of the oxygen deprivation.
  • Heart and lung problemschronic lung disease or heart problems that prevent the brain from receiving adequate oxygen can starve brain cells and lead to the symptoms of dementia

Dementia Screening

[This section is taken largely from NINDS, 2011.]

For people with AD or other progressive dementias, early diagnosis allows them to plan for the future while they are still able to make decisions. There are a number of strategies for the assessment and diagnosis of dementia. Screening begins with a detailed patient history to determine when the symptoms began and to determine the person’s overall medical condition.

The physical examination helps to rule out treatable causes of dementia and identify signs of stroke or other disorders that can contribute to dementia. Look for signs of illness, such as heart disease or kidney failure, that can overlap with dementia. A review of medications is necessary to determine whether any medications or medication interactions are causing or contributing to the symptoms of dementia.

The neurologic examination assesses balance, motor control, sensory functions, and reflexes, and looks for the presence of any neurologic condition (eg, movement disorders, stroke) that may affect the patient’s diagnosis or is treatable with drugs.

Cognitive tests measure memory, language skills, math skills, and other abilities related to mental functioning. The Mini-Mental State Examination (MMSE) may be used to examine orientation, memory, and attention, the ability to name objects, follow verbal and written commands, write a sentence spontaneously, and copy a complex shape.

Brain scans are used to identify strokes, tumors, or other problems that can cause dementia. Cortical atrophydegeneration of the brain’s cortexis common in many forms of dementia and may be visible on a brain scan. Brain scans also can identify changes in the brain’s structure and function that suggest AD.

Electroencephalograms (EEGs) may be used in people with suspected dementia. Many patients with moderately severe to severe AD have abnormal EEGs. An EEG may also be used to detect seizures, which occur in about 10% of AD patients as well as in many other disorders.

A variety of laboratory tests are available to diagnose dementia or rule out other conditions, such as kidney failure, that can contribute to symptoms. A partial list of these tests includes a complete blood count, blood glucose test, urinalysis, drug and alcohol tests (toxicology screen), cerebrospinal fluid analysis (to rule out specific infections that can affect the brain), and analysis of thyroid and thyroid-stimulating hormone levels.

A psychiatric evaluation may be obtained to determine if depression or another psychiatric disorder may be causing or contributing to a person’s symptoms.

Types of Dementia

[This section is taken largely from NINDS, 2011.]

Even though Alzheimer’s disease is fairly common, it is not the only thing that causes dementia. Symptoms differ with each type of dementia, depending upon the part of the brain that is affected. Frontal-temporal dementia (FTD), which affects the front part of the brain, is the most common dementia in those under the age of 60; FTD is responsible for 5% to 10% of all cases of dementia.

Vascular dementia, which is caused by small repeated strokes, occurs in people with longstanding, inadequately controlled, high blood pressure. It is responsible for about 20% to 30% of all cases of dementia. Lewy Body dementia, which often accompanies Parkinson’s disease, can cause hallucinations and mental changes. It is responsible for a little less than 5% of all cases of dementia. Acquired immune deficiency syndrome (AIDS) can also cause a form of dementia called AIDS-related dementia.

The relative frequencies of dementia types are increasingly open to debate and the borders between the types are becoming less distinct as we learn more about dementia and brain anatomy. Studies have examined the agreement between the diagnosis made while the person was alive and the pathology found in the brain post mortem. These have suggested that mixed pathologies are more common than “pure” pathologiesmeaning most people have a mixture of two or more types of dementia. This is particularly true for Alzheimer’s disease and vascular dementia, and for Alzheimer’s disease and dementia with Lewy Bodies (ADI, 2009).

The less common types of dementia (frontotemporal dementia, Creutzfeldt Jacob disease, and Huntington disease) are often misdiagnosed in life as Alzheimer’s disease. Population-based studies have suggested that frontotemporal dementia and vascular dementia are relatively common diagnoses in men who have an early onset of dementia. Alzheimer’s disease tends to predominate over vascular dementia among older people with dementia, particularly women (ADI, 2009).

Alzheimer’s Disease

The most common type of dementia, Alzheimer’s disease (AD), is caused by the formation of abnormal proteins within the brain called plaques and tangles. Damage typically begins in an area of the cerebrum called the hippocampus, which is responsible for the formation of new memories. In fairly rapid succession, plaques and tangles spread forward to the temporal and frontal lobes, affecting language, judgment, learning, comprehension, orientation, and emotions. Although almost everyone with AD is elderly, it is not considered to be a normal part of aging.

The Human Brain

image: human brain

Source: Courtesy of the Alzheimer’s Association. Used with permission.

In most people, symptoms of AD appear after age 60. However, there are some early-onset forms of the disease that are usually linked to a specific gene defect, which may appear as early as age 30. AD causes a gradual decline in cognitive abilities, usually during a span of 7 to 10 years. Nearly all brain functions, including memory, movement, language, judgment, behavior, and abstract thinking, are eventually affected. Tangles are largely made up of a protein called tau which is part of a healthy nerve cell’s structural support and which is also responsible for delivering substances throughout the cell. In AD, tau is changed in a way that makes it collect into tangles, which causes the collapse of the neuron’s support and transport system.

Amyloid Plaques Found Outside the Cell

image: plaques outside the cell

Source: Courtesy of the Alzheimer’s Association. Used with permission.

Neurofibrillary Tangles Forming Within the Cell

image: amyloid plaques in the cell

Source: Courtesy of the Alzheimer’s Association. Used with permission.

In the earliest stages of Alzheimer’s disease, before symptoms can be detected, plaques and tangles form in the hippocampus, which is the area of the brain involved in learning new tasks, short-term memory, thinking, and planning. In the early stages of AD, patients typically experience memory impairment, lapses of judgment, and subtle changes in personality. As the disorder progresses, memory and language problems worsen and patients begin to have difficulty performing activities of daily living, such as balancing a checkbook or remembering to take medications. They also may have visual-spatial problems, such as difficulty navigating an unfamiliar route. They may become disoriented about places and times, may suffer delusions, and may become short-tempered and hostile.

In mild to moderate stages, plaques and tangles continue their spread from the hippocampus forward to the frontal lobes (shaded in blue, below). The frontal areas of the brain are involved with speaking and understanding speech, the sense of where your body is in space, and executive functions such as planning, ethical thinking, and judgment. Many people are first diagnosed with ADRD in this stage. Changes in personality and behavior occur and people begin to have trouble recognizing friends and family members.

Mild to Moderate Changes in the Brain Caused by AD

image: mild to moderate brain changes with AD

Source: Courtesy of the Alzheimer’s Association. Used with permission.

In advanced Alzheimer’s, the hippocampus is severely damaged as plaques and tangles (shaded in blue) spread throughout the cerebral cortex. Individuals lose their ability to communicate, to recognize family and loved ones, and to care for themselves. Note that the hippocampus (shaded in dark blue), which is the region of the brain responsible for the formation of new memories, is severely damaged.

Severe Changes in the Brain Caused by AD

image: severe brain changes with AD

Source: Courtesy of the Alzheimer’s Association. Used with permission.

Many people with advanced AD eventually develop symptoms such as aggression, agitation, depression, sleeplessness, or delusions. On average, patients with AD live for 8 to 10 years after they are diagnosed. However, some people live as long as 20 years. Patients with AD often die of aspiration pneumonia because they lose the ability to swallow late in the course of the disease.

Comparison of Healthy Brain and One Damaged by Alzheimer’s

image: brain comparison

A view of how nerve cell loss changes the whole brain in advanced Alzheimer’s disease. Left side: normal brain; right side, a brain damaged by advanced AD. Source: Courtesy of the Alzheimer’s Association. Used with permission.

Frontotemporal Dementia

Frontotemporal dementia (FTD), sometimes called frontal lobe dementia, describes a group of diseases characterized by degeneration of nerve cellsespecially those in the frontal and temporal lobes of the brain. In many people with FTD there is an abnormal form of tau protein in the brain, which accumulates into neurofibrillary tangles. This disrupts normal cell activities and may cause the cells to die.

Symptoms of FTD usually appear earlier that those seen with ADusually between the ages of 40 and 65. Rather than a loss of short-term memory, FTD is characterized by behaviors associated with damage to the frontal lobes of the brain, namely loss of moral reasoning, disinhibition, behavioral and personality changes, and declining judgment.

In many cases, people with FTD have a family history of dementia, suggesting a genetic factor in the disease. The duration of FTD varies, with some patients declining rapidly over 2 to 3 years and others showing only minimal changes for many years. People with FTD live with the disease for an average of 5 to 10 years after diagnosis.

Vascular Dementia

Vascular dementia is caused by damage associated with cerebrovascular or cardiovascular problemsusually strokes. It may also be caused by genetic diseases, endocarditis (infection of a heart valve), or amyloid angiopathy (a process in which amyloid protein builds up in the brain’s blood vessels, sometimes causing hemorrhagic or “bleeding” strokes). In many cases, it may coexist with AD. The incidence of vascular dementia increases with advancing age and its incidence is similar in men and women.

Other causes of vascular dementia include:

  • Vasculitis, an inflammation of the blood vessel system
  • Profound hypotension (low blood pressure)
  • Lesions caused by brain hemorrhage
  • Lupus erythematosus (an autoimmune disease)
  • Temporal arteritis, an inflammatory disease that can damage blood vessels in a way that leads to vascular dementia

Symptoms of vascular dementia often begin suddenlyusually after a stroke. Patients may have a history of high blood pressure, vascular disease, or previous strokes or heart attacks. Vascular dementia may or may not get worse with time, depending on whether the person has additional strokes. In some cases, symptoms may get better with time. When the disease does get worse, it often progresses in a stepwise manner, with sudden changes in ability.

Vascular dementia with brain damage to the mid-brain regions may cause a gradual, progressive cognitive impairment that resembles AD. Unlike people with AD, people with vascular dementia often maintain their personality and normal levels of emotional responsiveness until the later stages of the disease. People with vascular dementia may wander at night and often have other problems commonly found in people who have had a stroke, including depression and incontinence.

Lewy Body Dementia

Lewy body dementia (LBD) is one of the most common types of progressive dementia. It occurs sporadically, in people with no known family history of the disease, although rare familial cases have occasionally been reported. There is no cure for LBD, and treatments are aimed at controlling the parkinsonian and psychiatric symptoms of the disorder.

The symptoms of LBD overlap with AD in many ways, and may include memory impairment, poor judgment, and confusion. However, LBD typically also includes visual hallucinations, Parkinson-like symptoms such as a shuffling gait and flexed posture, and day-to-day fluctuations in the severity of symptoms. Patients with LBD live an average of 7 years after the onset of symptoms.

HIV-Associated Dementia

HIV-associated dementia (HAD) is caused by infection with the human immunodeficiency virus (HIV) that causes AIDS. HAD can cause widespread destruction of the brain’s white matter. This leads to a type of dementia that generally includes impaired memory, apathy, social withdrawal, and difficulty concentrating. People with HAD often develop movement problems as well. There is no specific treatment for HAD, but AIDS drugs can delay onset of the disease and may help to reduce symptoms.

Other Types of Dementia

Dementia Pugilistica

Dementia pugilistica, also called chronic traumatic encephalopathy or boxer’s syndrome, is caused by head trauma, such as that experienced by people who have been punched many times in the head during boxing. The most common symptoms of the condition are dementia and Parkinsonism, which can appear many years after the trauma ends. Affected individuals may also develop poor coordination and slurred speech.

Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, fatal brain disorder that affects about 1 in every million people per year worldwide. Symptoms usually begin after age 60 and most patients die within a year. CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become so filled with holes that they resemble sponges when viewed under a microscope. CJD is the most common of the known human TSEs.

Many researchers believe CJD is caused by the presence of an abnormal form of a protein called a prion. Most cases of CJD occur sporadicallythat is, in people who have no known risk factors for the disease. However, about 5% to 10% of cases of CJD in the United States are hereditary, caused by a mutation in the gene for the prion protein. In rare cases, CJD can also be acquired through exposure to diseased brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through the air or through casual contact with a CJD patient.

Patients with CJD may initially experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. Other symptoms may include insomnia and depression. As the illness progresses, mental impairment becomes severe. Patients often develop myoclonus (brief involuntary jerking) and they may go blind. They eventually lose the ability to move and speak, and go into a coma. Pneumonia and other infections often occur in these patients and can lead to death.

Secondary Dementias

Dementia may occur in patients who have other disorders that primarily affect movement or other functions. These cases are often referred to as secondary dementias. The relationship between these disorders and the primary dementias is not always clear. For instance, people with advanced Parkinson’s disease, which is primarily a movement disorder, sometimes develop symptoms of dementia. Many Parkinson’s patients also have amyloid plaques and neurofibrillary tangles like those found in AD. The two diseases may be linked in a yet-unknown way, or they may simply coexist in some people.

*Post mortem studies suggest that many people with dementia have mixed Alzheimer’s disease and vascular dementia pathology and that this “mixed dementia” is underdiagnosed. Source: Adapted with permission from Alzheimer’s Disease International, 2009.

Common Types of Dementia

Dementia subtype

Early, characteristic symptoms


Proportion of dementia cases

*Alzheimer’s disease (AD)

  • Impaired memory, apathy and depression
  • Gradual onset
  • Language and visuospatial deficits
  • Cortical amyloid plaques
  • Neurofibrillary tangles


*Vascular dementia


  • Similar to AD, but memory less affected, and mood fluctuations more prominent
  • Physical frailty
  • Stepwise onset
  • Patchy cognitive impairment
  • Often preventable
  • Cerebrovascular disease
  • Single infarcts in critical regions, or more diffuse multi-infarct disease
  • Group of syndromes



dementia (FTD)

  • Behavioral and personality changes
  • Mood changes
  • Disinhibition
  • Language difficulties
  • No single pathology: damage limited to frontal and temporal lobes
  • Early onset (45 to 60 yrs of age)


Dementia with Lewy

Bodies (DLB)

  • Marked fluctuation in cognitive ability
  • Visual hallucinations
  • Parkinsonism (tremor and rigidity)
  • Adverse reactions to antipsychotic medications

Cortical Lewy bodies



Dementia Pharmacotherapy

Medications used to treat the cognitive effects of dementia have only a modest effect. The most commonly prescribed drugs in this category are anti-cholinesterase inhibitors and NMDA receptor antagonists.

Treating the Cognitive Effects of Dementia

Certain medications can be prescribed for mild to moderate ADRD to control cognitive symptoms. Two classifications of medications are approved for this purpose: anticholinesterase inhibitors and NMDA (memantine) receptor antagonists. These medications have a very slight effect on a person’s ability to perform daily activities and sometimes dampen behavioral and psychological symptoms (although this is an off-label use).

Anticholinesterase inhibitors slow the breakdown of acetylcholine, allowing it to stay in the brain a little longer. Tacrine was the first anticholinesterase inhibitor approved by the Food and Drug Administration (FDA). Three better-tolerated anticholinesterase inhibitors have also been approved:

  • Aricept (donepezil)all stages of AD
  • Exelon (rivastigmine)mild to moderate AD
  • Razadyne (galantamine)mild to moderate AD

Memantine (NMDA, Namenda) is approved for use in moderate to severe dementia. Memantine is a receptor antagonist that works by decreasing abnormal activity in the brain. It can help people with AD think more clearly and perform daily activities more easily, but it is not a cure and does not stop the progression of the disease. It may help patients maintain certain daily functions a little longer than they would without the medication.

Clinical Trials

In May 2012 a five-year prevention trial, jointly funded by the National Institutes of Health, Banner Alzheimer’s Institute, and Genentech, became the first clinical trial to focus on people who are cognitively normal but at extremely high risk of developing Alzheimer’s disease. The effort is an international collaboration, working with a Colombian clan who share a genetic mutation known to cause observable signs of Alzheimer’s disease at around age 45.

The study approach reflects new thinkingthat testing therapies before signs of memory loss appear might be most effective in fighting Alzheimer’s disease. In this study, researchers will examine whether up to five years of an antibody treatment with crenezumab, which is designed to bind to and possibly clear away abnormal amounts of amyloid protein in the brains of people with Alzheimer’s, can prevent decline in cognitive function.

The study participantssome three hundred adult members of the Colombian clan that has a family history of early-onset Alzheimer’s, as well as a smaller number of U.S. participants age 30 and olderwill include both carriers and non-carriers of the gene. The study will use brain scans, fluid biomarkers, and cognitive testing to track amyloid levels, changes in brain structure and function, and cognitive performance.

The study aims to do more than look at the potential effectiveness of one therapy. It will be a test of how and to what extent biomarkers may predict disease progress or treatment success and will contribute vitally important information and samples to the study of Alzheimer’s disease.

Treating Behavioral and Psychological Symptoms of Dementia

Geriatrics specialists refer to the challenging behaviors seen in dementia as behavioral and psychological symptoms of dementia (BPSD). It is estimated that up to 90% of patients with Alzheimer’s disease exhibit at least one BPSD and about one-third have severe behavioral problems (Liperoti et al., 2008). Challenging behaviors also occur in other types of dementia, and some may differ depending on the type of dementia.

Pharmacotherapy has only a modest effect on BPSD, and many of the medications have potentially serious side effects. The most commonly used drugs for the treatment of BPSD are the antipsychotics.

Typical antipsychotics have been used since the 1950s for the treatment of psychosis in dementia, but they can cause irreversible physical symptoms such as Parkinsonism and tardive dyskinesia (extrapyramidal symptoms). These agents have also been systematically used for the treatment of other behavioral and psychological symptoms of dementia (besides psychosis) despite a substantial lack of scientific evidence to support their use (Liperoti et al., 2008).

Atypical antipsychotics were approved exclusively for the treatment of schizophrenia by the FDA in the 1990s. Soon after, these medications became the new standard of care for BPSD because of their reported advantages over conventional agents, particularly with respect to extrapyramidal symptoms (restlessness; muscles spasms of the neck, eyes, tongue, or jaw; resting tremor; involuntary movements; muscular rigidity; postural instability). In the late 1990s, atypical agents accounted for more than 80% of antipsychotic prescriptions used in dementia patients (Liperoti et al., 2008).

Over the last decade, the off-label use of atypical antipsychotics has been promoted by clinical practice guidelines although only a limited number of clinical trials suggest their efficacy in dementia. In 2008 the FDA issued a “drug alert” notifying prescribers that both typical and atypical antipsychotics are associated with an increased risk of mortality in elderly patients treated for dementia-related psychosis (FDA, 2009).

Because of safety considerations associated with antipsychotic medications, non-pharmacologic approaches are generally recognized as the first-line strategy for the treatment of BPSD. Antipsychotic medications are recommended only for short-term treatment (up to 3 months) and among those patients who manifest severe symptoms that may cause extreme distress and harm to themselves or others.

A prescriber may still choose to prescribe antipsychotic medications for BPSDand they may indeed be effective in some cases. The prescriber must, however, disclose to the patient or family that the medication is being used off-label* and obtain permission to use it for behavioral symptoms.

*Off-label use is the practice of prescribing pharmaceuticals for an unapproved indication, age group, dose, or form of administration.

Care of Those with Dementia

[The following section is taken largely from NINDS, 2011.]

Those with moderate or advanced dementia often need round-the-clock care and supervision and also may need assistance with daily activities such as eating, bathing, and dressing. Meeting these needs takes patience, understanding, and careful thought by the person’s caregivers.

A typical home environment presents many dangers and obstacles to a person with dementia, but simple changes can overcome many of these problems. For example, sharp knives, dangerous chemicals, tools, and other hazards should be removed or locked away. Other safety measures include installing bed and bathroom safety rails, removing locks from bedroom and bathroom doors, and lowering the hot water temperature to 120°F (48. 9°C) or less to reduce the risk of accidental scalding. People with dementia also should wear some form of identification at all times in case they wander away or become lost. Caregivers can help prevent unsupervised wandering by adding locks or alarms to outside doors.

People with dementia may develop behavior problems because of frustration with specific situations. Understanding and modifying or preventing the situations that trigger these behaviors may help to make life more pleasant for the person with dementia as well as the caregivers. For instance, the person may be confused or frustrated by the level of activity or noise in the surrounding environment. Reducing unnecessary activity and noise (such as limiting the number of visitors and turning off the television when it’s not in use) may make it easier for the person to understand requests and perform simple tasks. Confusion also may be reduced by simplifying home decorations, removing clutter, keeping familiar objects nearby, and following a predictable routine throughout the day. Calendars and clocks also may help patients orient themselves.

People with dementia should be encouraged to continue their normal leisure activities as long as they are safe and do not cause frustration. Activities such as crafts, games, and music can provide important mental stimulation and improve mood. Some studies have suggested that participating in exercise and intellectually stimulating activities may slow the decline of cognitive function in some.

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