6.16: Dementia

Dementia is a broad category of diseases, all of which involve a serious decline in memory accompanied by a major decline in at least one other mental function. Three other criteria must be met before a person can be said to have dementia. First, the person must be affected to such an extent that he or she has significant difficulty carrying out normal activities and interacting with other people. Second, these difficulties must be present on a continuing and long‑term basis rather than sporadically. Third, they must be caused by an identifiable physical abnormality or at least must not be caused by an identifiable mental illness such as depression. Functions that are often reduced in patients with dementia include abstract thinking; speaking, reading, and writing; making judgments; solving problems; identifying common objects; and performing simple voluntary tasks.

The number and rate of cases of dementia are increasing because the number of older people and the proportion of the population made up of older people are growing. In addition, since better diagnostic tests are being developed and the social stigma attached to the diagnosis of dementia is declining, more cases are being identified and reported. However, incidence rates and death rates are only estimates because of difficulty with diagnosis, and other diseases can mask the presence of dementia. Also, dementias contribute to other causes of death, leaving cases of dementia unreported as the cause of death.

The incidence of dementia increases with the age of a population. The incidence rate rises exponentially, meaning the greater the age, the faster the rate of incidence rises. Very few cases occur in people below age 60, and less than 2 percent of all people between the ages of 60 and 65 have dementia. The percentages approximately double for every five years above age 65, so that more than 30 percent of those over age 85 suffer from dementia to some degree. Overall, between 16 and 24 percent of the population over age 65 suffer from mild dementia and up to 8 percent of those over age 65 have severe dementia. Among those over age 65, the number of people with dementia is greater than the number who have strokes. For adults, the death rate from dementias approximately doubles with each decade of life until age 90, when the death rate begins to plateau.

There are more than 60 different types of dementia. Some forms are reversible, including dementia caused by medications; drugs; alcohol; anemia; malnutrition; CNS infection; malfunction of the thyroid gland or adrenal glands; and malfunction of organs such as the liver and kidneys. Some forms of dementia are irreversible, including the forms associated with Alzheimer's disease and Parkinson's disease and those caused by strokes, heart failure, repeated head injury, AIDS, and Huntington’s disease.

Some individuals have more than one type of dementia. Others have dementia along with nervous system disorders such as delirium and depression. As a result, a definitive diagnosis of dementia is quite difficult to obtain. At present, cases can be diagnosed with about 90 percent accuracies.

The many causes of dementia occur as follows: 10 percent to 20 percent from atherosclerosis or, occasionally, another circulatory system disease: at least 55 percent from Alzheimer's disease; 8 percent from Parkinson's disease; 4 percent from head trauma; 12 percent from a mixture of these causes; and 6 percent from other causes. Approximately 70 percent of cases after age 60 are caused by Alzheimer's disease.

Multi‑Infarct Dementia

Dementia caused by circulatory disease is often called multi‑infarct dementia because it results from having many areas of the brain die from inadequate blood flow. Free radicals also cause damage. The amount of infarction usually increases over an extended period because the victim has one stroke after another or because arteries remain nearly completely blocked. Therefore, multi‑infarct dementia becomes progressively worse. Sometimes one large stroke will leave the patient with dementia. Since almost all cases of multi‑infarct dementia result from atherosclerosis, taking steps to prevent atherosclerosis reduces the risk of multi‑infarct dementia.

Alzheimer's Disease

Alzheimer's disease (AD) is named for Alois Alzheimer, who first described the disease in 1907. The rate of occurrence of Alzheimer's disease doubles every five years after age 60 up to age 90. The earliest cases occur at about age 40. However, less than 1 percent of those under age 65 have AD, compared with up to 20 percent of those over age 80. Overall, 10 percent to 15 percent of people over age 64 have Alzheimer's disease, and it affects approximately 50 percent of those over age 84. Alzheimer's disease occurs more frequently in women compared with men.

There are now four million people with AD. The number is expected to reach nine million by AD. 2040. Alzheimer's disease is now the fourth leading cause of death in the U.S., causing 100,000 deaths per year. AD is becoming more important, as death rates from cardiovascular disease and strokes continue to decline, the elder population continues to increase, and the proportion of very elderly people increases. Older statistical tables do not list AD as a major cause of death among older people because widespread and accurate diagnosis of AD has occurred only in recent years. By AD. 2020, costs from AD are expected to exceed costs from heart disease and cancer. Costs come from physicians, health care providers, social workers and in-home care givers; diagnostic procedures and medications; hospitalizations and nursing homes; special apparatus, diets, and living accommodations; and loss of income and productivity. These costs bear on families, insurance companies, and society as a whole. Non-economic costs include social costs (e.g., disrupted family life, isolation, increased conflicts) and personal costs (e.g., stress, fatigue, psychological detriments such as depression and anger, reduced quality of life). These costs increase synergistically as the disease progresses and as other disorders develop.

Types

Alzheimer's disease can be subdivided into two types. One type is early onset AD or familial AD (FAD). Onset occurs before age 65, usually during the sixth decade of life. The second is late onset AD or senile dementia of the Alzheimer's type (SDAT), with onset usually after age 60. SDAT, also called sporadic Alzheimer's disease, is the most common form of AD.

Though the causes of most AD cases are not known, as many as 50 percent are probably caused by genetic abnormalities since AD tends to run in families. Other factors must be involved because when one identical twin develops AD, the other may not develop the disease (see Genetics of AD, below). A main difficulty in finding causes of AD is that no animals are known to develop AD or conditions very similar to AD. Therefore, research is limited.

Some scientists propose that AD is not a disease but is part of normal aging. They point out that all aging brains develop the same physical changes found in brains from AD victims, though to a lesser degree. Perhaps like other age changes, AD develops in everyone, though at different rates. They suggest that if people lived long enough, everyone might eventually develop AD.

Though the causes of some forms of AD remain unknown, risk factors have been identified. The greatest risk factor is increasing age. Other risk factors include having relatives with AD; suffering head trauma (e.g., boxing); being exposed to aluminum; having high blood cholesterol; having low education; and for women, being postmenopausal. Factors that seem to reduce the risk for AD include education; taking anti-inflammatory medications (e.g., steroids, ibuprofen) or folic acid supplements; smoking; and for postmenopausal women, taking estrogen supplements.

Effects

The effects of Alzheimer's disease develop in a steady and fairly predictable sequence. At first there is a decrease in short‑term memory. Because the change is gradual and resembles the normal decrease, it is not uncommon for normal individuals to fear that they have Alzheimer's disease when the ability to remember begins to decline. Conversely, individuals with Alzheimer's disease may attribute their memory impairment to aging.

With AD, however, memory function declines to such an extent that affected individuals have considerable difficulty performing ordinary daily activities such as preparing food, dressing, and shopping. Patients with AD become disoriented with respect to location and have trouble learning new information. Early in the disease some patients begin to have trouble with language skills such as speaking. Perhaps because of fear of some of these changes or because of the disease itself, personality changes such as irritability, hostility, and agitation may appear. Often affected individuals tend to withdraw from social contact.

As AD progresses, loss of short‑term memory becomes severe enough to dramatically decrease the ability to learn information or new skills, solve problems, and perform the ordinary tasks of daily living or working. Abstract thinking and making judgments become increasingly impaired. Language functions such as speaking, reading, and writing decline. Affected individuals become easily disoriented not only in terms of where they are but also with regard to time and date. Confusion occurs easily and frequently. Many patients wander away from home and become lost. Long‑term memory, including recognizing familiar people, may also diminish.

Major personality changes that commonly accompany these more advanced effects of Alzheimer's disease may include high levels of agitation, paranoia, hostility, and aggressiveness. These patients may have verbal and physical outbursts of anger or other emotions. They may strike out violently. These changes make cooperation and acceptable interactions with others difficult. For many people, social withdrawal becomes more intense.

By this stage affected individuals require a great deal of care. They need to be bathed, dressed, and fed. Their behavior must be monitored so that they do not engage in destructive actions or wander off. Eventually the care must extend for 24 hours a day. The changes in personality and behavioral traits caused by AD make providing such care emotionally draining on family members. Families that cannot provide adequate care are faced with the financial burden of paying others to provide it. All these problems intensify as the disease progresses.

In the most advanced stages of Alzheimer's disease patients lose essentially all memory and intelligence capabilities. Performing any task and talking with others become impossible. Apparently, there is a complete loss of awareness of one's surroundings. Bladder and bowel incontinence develop. The nervous system seems to forget how to stimulate muscles so that walking, eating, and other voluntary motions dwindle and finally cease. Curiously, long‑lasting muscle spasms may occur. The victim becomes bedridden and paralyzed. The final result of Alzheimer's disease is death, which is caused by complications from immobilization. The complications may include infections of the skin and respiratory systems, thrombus and embolus formation, malnutrition, and respiratory failure.

Though this sequence of events occurs in most patients with Alzheimer's disease, individual cases vary considerably. For example, changes in personality may be the first noticeable indication that something is wrong. In other cases, problems with speaking may occur early in the disease or not until most of the other effects have developed.

There is also much variation in the time that passes from the diagnosis of AD until death occurs; this period may range from 2 to 20 years. The average length of time from diagnosis to death is eight years. More rapidly progressing and serious cases are correlated with an earlier age of onset. Alzheimer's disease almost always progresses at a steady rate. There is never a period of improvement.

Diagnosis

Diagnosing Alzheimer's disease by observing changes in behavior is difficult until the disease has progressed into more advanced stages because at first these changes seem to be normal fluctuations. Only specific tests can detect early abnormalities in mental status. Repeating tests every few years to detect changes associated with AD may help detect AD at earlier stages.

Making a definitive diagnosis of Alzheimer's disease remains difficult even after the recognition of abnormal behaviors because similar behavioral changes can be caused by many other factors (e.g., medications, depression, altered social situations) and by other diseases of the nervous system or other systems. Furthermore, the simultaneous presence of other types of dementia can mask the presence of AD. Researchers continue developing other diagnostic procedures including tests at the chemical, genetic, and cellular through system levels. Being able to detect and diagnose AD earlier could lead to developing effective treatments.

Eventually, after all other possible causes of the behavioral signs and symptoms have been ruled out, a clinical diagnosis of Alzheimer's disease can be made with an accuracy of over 90 percent. Only an autopsy examination of the brain can determine conclusively that a person had Alzheimer's disease.

Changes in the brain

A brain from an Alzheimer's patient can be identified because it has two characteristics: an excessive number of senile plaques and neurofibrillar tangles (Figure 6.12). A third important finding is a low level of the neurotransmitter acetylcholine. These features are especially prevalent in brain areas involved in memory. The functioning of synapses in these areas may be hampered because the neurons produce inadequate neurotransmitter, the tangles may prevent enough neurotransmitters from reaching the ends of the axons; and the plaques may block transmission at synapses.

Plaques and tangles

Figure 6.11 Alzheimer’s disease (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

Figure 6.12 Plaques and tangles in Alzheimer’s disease (Sources of images and videos below. Used with permission.)

Senile plaques (SPs) are round microscopic masses having various mixtures and densities of materials. They are at or near synapses. SPs usually contain a protein called beta-amyloid (β-A), dead neurons and neuroglia cells, pieces of synapses, and fibrous material called neurofibrillar tangles (NTs) (Figure 6.12). Neurofibrillar tangles are composed of one or two protein fibers twisted into a helix. Much of the protein is tau protein (τ-protein). NTs also contain other materials including enzymes, inflammatory molecules, β-A, a lipoprotein called apolipoprotein E (APOE), and carbohydrate/protein complexes. NTs also form in neuron cell bodies, axons, and dendrites.

SPs and NTs appear first in the hippocampus region, which is near the center and bottom of the cerebral hemispheres. The hippocampus has a major role in memory functions. Later, SPs and NTs appear in wider areas near the bottom of the hemispheres. Later still they appear in upper regions of the cerebral cortex. Eventually, all regions of the cerebral cortex develop SPs and NTs. Neuron connections to the nucleus of Meynert also develop many SPs and NTs, and SPs form in the cerebellum. The final distribution of SPs and NTs in brain areas corresponds to the sequence in which they appear. Areas showing SPs and NTs first developing the highest densities of them.

As SPs and NTS form, neurons are damaged and die, and synapses are destroyed. Scientists do not know if SPs and NTs form and then cause damage to neurons or if neurons damage occurs first, causing SPs and NTs to develop. Neurons that interconnect other neurons (i.e., association neurons) are affected much more than sensory neurons and motor neurons.

As AD progresses, brain vessels also change. Small vessels accumulate much β-A in their middle layer. Vessels become twisted, shrunken and broken, which reduces blood flow in the brain. The cerebral hemispheres shrink dramatically (Figure 6.11). Some scientists believe that reduction in blood flow causes the SPs, NTs, and other neuronal and synaptic changes in the AD brain.

Beta-amyloid

Many cells in the body produce amyloid protein. There are more than 10 types of amyloid protein. The type called β-amyloid (β-A) is found in AD. Its function is unknown. Beta-amyloid may be produced by neurons and by blood vessels. It is produced when an enzyme breaks a protein called amyloid precursor protein (APP), which extends across cell membranes. Breaking normal APP produces a small amount of soluble short β-A. In AD, APP is abnormal. When it is broken by enzymes, much abnormal long β-A is produced and released from the cell membrane.

The abnormal "sticky" β-A binds easily to APOE and to τ-protein, forming many SPs quickly. The abnormal β-A increases free radicals, inflammation, cell membrane damage, and neuron apoptosis. Excess glycation of proteins also occurs. All these processes seem to promote each other synergistically. Finally, APP itself binds to τ-protein and to APOE, suggesting that it can contribute to the formation of NTs and SPs.

The causes, method of formation, sources of β-A and NTs, and sequence in which these materials are deposited are unknown.

Tau protein

Brain cells produce other proteins called tau proteins (τ-proteins). Their functions are unknown, though they seem to promote microtubule formation. The brain contains at least six types of τ-protein, and their proportions vary from childhood through adulthood. Abnormal modifications of τ-proteins (e.g., glycation, adding phosphate groups) cause τ-proteins to help form NTs.

APOE

Many cells produce apolipoprotein E (e.g., brain, liver, adrenals). Most brain APOE comes from neuroglia cells and macrophages. Though neurons do not produce APOE, it enters them. APOE helps move cholesterol and other lipoproteins from cell to cell and through cell membranes. APOE also seems to help in neuron development and repair.

Brain APOE has different forms including APOE-ε3 and APOE-ε4. APOE-ε4 seems to promote the formation of SPs and NTs. The mechanisms are not clear, but they may involve disruption of neuron membranes; formation of free radicals; excess accumulation of β-A; and the formation of abnormal microtubules in neurons. Interactions between the β-A and the abnormal microtubules seem to result in SPs and NTs.

Presenilins

The last groups of brain proteins to mention are the presenilins. Two important forms of presenilin in the brain are presenilin-1 (PS-1) and presenilin-2 (PS-2), which are membrane proteins. Their functions are unknown.

In summary, AD may be caused by or promoted by abnormal protein formation; chronic inflammation; inadequate blood flow; free radical damage from brain proteins, metal ions, damaged endothelium, or neurotransmitters; decreased *FR defenses; mitochondrial malfunctioning; reduced insulin sensitivity; immune responses; or abnormal apoptosis of neurons. Regardless of the causes or mechanisms, the results are the same; too many SPs, too many NTs, too much neuron death, and too much loss of synapses.

Genetics of AD

There are several genes that promote different types of AD. Though these genes are in different chromosomal locations, have effects at different ages, and may act by different mechanisms, they all produce the same outcomes in the brain and the same manifestations of AD. Some genes that promote or modify AD have not been identified. One or more of these genes may contribute to a form of AD that begins after age 70. These latter genes may be on chromosomes 12 or 3.

Three genes for one type of familial Alzheimer's disease (FAD) are on chromosomes 21. The mutated forms of the genes cause the production of abnormal "sticky" ß-amyloid, resulting in 7 percent of AD cases and 25 percent of FAD cases. Age of onset is between ages 45 and 65, with most cases developing before age 60. The mutations are present in approximately 19 families. An individual with only one copy of one of the mutated genes has a 100 percent chance of developing AD because each mutated gene is a dominant gene.

Certain forms of a gene on chromosome 19 promote SDAT. The gene has three forms (i.e., three alleles), each of which contains the genetic information for producing APOE-ε. One form codes for APOE-ε4, one form for APOE-ε3, and one for APOE-ε2. Since a person has two copies of chromosome 19, each person has two of these genes. The pair of genes may be in any combination (i.e., ε4:ε4, ε4:ε3, ε4:ε2, ε3:ε3, ε3:ε2, ε2:ε2). In the general population, the genes are found in the proportion ε4:ε3:ε2::14:78:8.

The genes are codominant, meaning that each produces its form of APOE-ε regardless of which other forms of the gene are present. Having two ε4 genes provides the highest risk from APOE genes and makes the AD occur at earlier ages. The risk for developing AD is eight times higher in people with two ε4 genes than in people with two ε2 genes. However, people with two ε4 genes do not always get AD.

The different combinations of APOE-ε genes provide decreasing risk of getting AD and increasing average age of onset in the order ε4:ε4 (age 68), ε4:ε3 (age 71), ε3:ε3 (age 74). Still, age of onset shows great variability with any of these combinations. Very few people with even one ε2 gene develop AD.

The APOE-ε gene influences other problems. Having an ε4 gene increases the age-related decline in cognitive functions even if AD does not develop. The ε4 gene also promotes amyloid formation in blood vessels, so people with the ε4 gene are at higher risk for developing atherosclerosis. Having an ε2 gene reduces the risk of atherosclerosis.

Chromosome 14 has the gene for PS-1, and chromosome 1 has the gene for PS-2. Nearly 50 percent of FAD cases are associated either with mutations in the APP gene on chromosome 21 or a presenilin gene. Nearly 70 percent of cases of FAD are associated with mutations in the PS genes. Mutations in either presenilin gene increase the risk of developing AD, apparently because abnormal PS-1 and abnormal PS-2 increase the production of "sticky" β-A.

The PS-1 mutation is known to occur in nearly 50 families. The PS-2 mutation is known to occur in descendants from certain German families (i.e., Volga Germans). For people with the PS-1 mutation, average age of onset is in the fifth decade, but cases develop as early as age 30. The PS-1 mutation also promotes late onset SDAT. For people with the PS-2 mutation, the average age of onset is higher than with the PS-1 mutation, but onset may occur before age 30.

Treatments

There are no effective treatments to slow, stop, or reverse the effects of Alzheimer's disease. Therapies being investigated include antioxidant supplements; anti-inflammatory drugs; medications that increase brain acetylcholine (e.g., tacrine); medications that slow atherosclerosis or reduce blood clotting; and for women, estrogen supplements. Until effective treatments are found, all that can be done is reduce the signs and symptoms and maintain as much functioning as possible. In the early stages of the disease memory aids such as notes and verbal reminders help. Various medications can alleviate the behavioral and psychological problems. Maintaining social contacts and providing emotional support for the patient and his or her families are important components in a complete treatment program.

As the disease progresses, outside help from support groups and social agencies is usually required. Day care centers can relieve the burden of full‑time care by family members. Attention must be paid to preventing complications such as malnutrition and infections. Finally, full‑time institutionalization may be necessary.

Parkinson's Disease

Though the incidence of Parkinson's disease is less than half that of strokes or Alzheimer's disease, it remains a leading disease of the nervous system among older Americans. Its rate of occurrence is extremely low before age 50, but the rate increases gradually after that until about age 75; after that age it diminishes steadily. About 2 percent of those over age 50 will develop Parkinson's disease. This disease occurs with equal frequency in men and in women and among people of different races. (Suggestion 146.01.03)

Causes

The cause of true, or primary, Parkinson's disease is unknown, and it does not tend to run in families. Scientists suspect the involvement of free radicals and reduced blood flow. Many cases of what appear to be Parkinson's disease actually result from abnormalities such as CNS infections, atherosclerosis, brain tumors or other brain diseases, head injury, toxins, and medications. These cases are called secondary parkinsonism.

Effects

The development of Parkinson’s disease is shown primarily by changes in the control of muscle contractions. These changes usually occur in the same sequence. At first, ongoing movements of the fingers and hands occur. The movements of the fingers give the appearance that the victim is rolling pills between the fingers. (Suggestion: Chap 06 - 146-1-3)

Tremors of the hand, arm, and leg muscles often develop next. The movements are rhythmic, with alternating contractions between muscles that bend the joints and muscles that straighten them. Four to eight contractions occur each second. The tremors are greatest when the person is awake but resting. They diminish during voluntary movements and stop when the patient falls asleep.

Further progress of the disease causes muscle stiffness and difficulty moving rapidly and smoothly. As control of muscle contraction diminishes further, the patient may find it impossible to complete a motion once it has been started. For example, a person who is walking may suddenly stop in the middle of taking a step. Ordinary motions occur ever more slowly. Performing ordinary tasks and job‑related activities becomes difficult or impossible.

As normal contractions of muscles continue to diminish, facial expressions disappear. The voice becomes soft and loses inflection. Weaker, slower, and fewer contractions of leg, trunk, and arm muscles cause walking to occur more slowly and with shuffling of the feet, a stooped posture, and little swinging of the arms. Muscle contractions for swallowing and breathing also weaken and slow.

Declining muscle control and muscle activity causes drooling. Constipation is not uncommon because patients are less active and have weaker contraction of the abdominal muscles that normally help with bowel movements.

Gradually, coordination of muscles declines to such an extent that the person has trouble with balance. Not only do these patients tend to fall more frequently, they make little or no effort to slow or stop themselves as they are falling.

Parkinson's disease often produces effects other than those involving control of muscles. During the night, patients tend to wake up and have difficulty going back to sleep. They become restless and begin to wander about. Because of declining muscle coordination and balance, they are at great risk of physical injury from falls. The interrupted sleep also causes these patients to be sleepy during the day.

Psychological changes may begin at any stage in the disease. Many patients experience depression, loss of interest in activities, and other mood changes. These psychological alterations seem to be caused partly by the disease itself and partly by the awareness of its effects. Reductions in very short-term memory are common. Parkinson's disease causes dementia in over 15 percent of patients.

While the sequence of changes caused by Parkinson's disease is fairly regular and progresses steadily, the rate of change varies greatly from one person to another. A few cases reach extreme conditions in as few as five years, although most cases progress more slowly, so that severe disability is delayed for many years.

Nervous System Changes

The mechanism by which Parkinson's disease affects muscle control is fairly clear. Recall that impulses controlling voluntary movements are modified as they descend through the somatic motor pathway. Some areas of modification are in the basal ganglia inside the cerebral hemispheres (Figure 6.13). The normal impulse modifications occurring in the basal ganglia actually result from the interplay among several neurotransmitters in the basal ganglia. Acetylcholine tends to increase the impulses and thus increases muscle contractions. Dopamine (DOPA) and another neurotransmitter (gamma‑aminobutyric acid) tend to dampen the impulses and the movements they cause.

Figure 6.13 Basal ganglia (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

In Parkinson's disease a major decline in the amount of DOPA in the basal ganglia creates an imbalance among the antagonistic transmitters. This imbalance causes impulses and the muscle contractions they produce to become excessive and uncontrolled. Hence, muscle contractions occur. Neurotransmitter imbalances also cause the other effects of this disease.

Diagnosis

Parkinson's disease is accompanied by a decrease in certain CNS chemicals that are used by the brain to manufacture dopamine. Dopamine is a neurotransmitter that is present in inadequate amounts in patients with Parkinson's disease. Because this and the other effects of the disease are somewhat different from those of other diseases and the effects develop in a fairly regular sequence, Parkinson's disease can be diagnosed accurately.

Treatments

There is no cure for Parkinson's disease and no way to slow its progress. However, its effects can be greatly diminished by administering levodopa because this chemical boosts brain production of DOPA. Dosages must be carefully monitored and adjusted during the disease to minimize adverse side effects such as increased uncontrolled movements. Since increasing the level of DOPA seems to be so important, attempts have been made to implant into the brains of Parkinson's disease patients’ tissues that produce DOPA. Pieces of adrenal medulla and pieces of brain regions from aborted human fetuses have been used. Transplants of adrenal medulla have not yet produced satisfactory results. However, experiments using fetal brain tissue have resulted in dramatic and long‑term improvements in muscle control in individuals having severe cases of Parkinson's disease. As the controversial and experimental techniques employing fetal brain tissue improve and become more standardized, they may gain widespread acceptance and use.

Other medications can relieve certain signs and symptoms sometimes. However, the specific types and amounts of substances used to treat Parkinson's disease vary from case to case because individuals have such varied responses to these medications and because their responses change as the disease progresses.

Besides medications, treatment of Parkinson's disease should include physical therapy to help sustain the movements used in ordinary tasks and in the patient's occupation. Speech therapy and psychological support are also important components of a treatment plan.

Dementia with Lewy Bodies

Dementia with Lewy bodies is a newly classified type of age-related dementia. It has been identified in nearly 20 percent of the brains from people who died after developing any dementia. Lewy bodies are round masses of clumped microfilaments in neurons. They occur in all areas of the brain. (Figure 6.14) This type of dementia also shows amyloid deposits.

Figure 6.14 Microscopic views of Lewy bodies (Source of image below. Used with permission.)