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The Wien Center For Alzheimer’s Disease and Memory Disorders Mount Sinai Medical Center

INFORMATION PACKET •

Introduction…………………………………………………………………..….…2

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Dementia 101…………………………………………………………….……......3

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Alzheimer’s Disease: What We Know and What We Can Do……………......4

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Advances in the Diagnosis and Treatment of Alzheimer’s Disease………....9

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Mild Cognitive Impairment: An Intermediate Stage………………………......11

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What is Lewy Body Disease (LBD)? A Deeper Look Into LBD………..........13

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Becoming Familiar With Vascular Dementia………………………………….18

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Understanding Frontotemporal Dementia………………………………….... 20

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Reducing Risk for AD and VD among Unaffected Individuals……………...25

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Preventative Strategies: Lifestyle Changes and Alzheimer’s Disease........ 27

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Coping Strategies for Dementia Patients……………………………………..30

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Coping Strategies for Caregivers of Dementia Patients…………………….34

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Caregiver Do’s and Don’ts in the Management of Dementia patients…….37

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Revealing Diagnosis to the Patient……………………………………………45

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Telling Friends and Family: A Caregiver’s Guide……………………………48

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Nationwide and Community Resources for Patients and Caregivers……..51

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Sources and Other Helpful Websites………………………………………….60

 

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INTRODUCTION “The aging of the population is one of the major public health challenges of the 21st century. With more than 70 million baby boomers in the United States poised to join the ranks of those aged 65 or over, the prevention of diseases and injuries is one of the few tools available to reduce the expected growth of health care and long-term care costs” (This is a recent quotation from Dr Gerberding, Director of the Centers for Disease Control and Prevention, Atlanta). One hundred years ago, only 3 million people in the US were over the age of 65. Today, more than 33 million Americans are in this age group, and that number is expected to double over the next 25 years, as baby boomers age. In addition, the seniors of the future will be even more racially and ethnically diverse than today’s seniors. The aging of America is triggering a huge demand for health care and social services. Health-care expenditures for a 65-year-old are now four times those for a 40-year-old. Because the population will be older and greater in number, overall U.S. health care expenditures are projected to increase 25% by 2030. The best way to improve the quality of life of the elderly and to reduce their health care expenditure is to educate middle aged and elderly individuals regarding measures that can prevent or delay the onset of the most common chronic diseases that afflict the elderly community. These individuals can then spread the message and teach family members, friends and acquaintances about health practices that are likely to be successful in warding off chronic diseases and disability. Here at the Wien Center, we seek to not only treat but educate our patients on the history, progression, contributing factors, and ongoing research of dementia and other memory disorders. This information packet has been assembled in the hopes of providing an abundance of information to our patients regarding these diseases and

 

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also to aid our patients in making the necessary lifestyle changes in order to cope more effectively with their illness.

DEMENTIA 101 Dementia is a brain disorder that seriously affects a person’s ability to carry out daily activities. The most common form of dementia among older people is Alzheimer’s disease (AD), which initially involves the parts of the brain that control thought, memory, and language. Although scientists are learning more every day, right now they still do not know what causes AD, and there is no cure. Alzheimer’s Disease Alzheimer's disease is a progressive, degenerative disease of the brain, which causes thinking and memory to become seriously impaired. Lewy Body Dementia Lewy body dementia (LBD) is a progressive brain disease and the second leading cause of degenerative dementia in the elderly. Deficits in attention and executive function are typical. Prominent memory impairment may not be evident in the early stages. Symptoms often include fluctuating cognition with pronounced variations in attention and alertness, recurrent complex visual hallucinations (typically well formed and detailed) and spontaneous features of parkinsonism. Frontotemporal Dementia The development of behavioral or cognitive deficits manifested by either (a) early and progressive change in personality, characterized by difficulty in modulating behavior, often resulting in inappropriate responses or activities, or (b) early and progressive change in language, characterized by problems with expression of language or severe naming difficulty and problems with word meaning. Vascular Dementia Vascular Dementia is considered to be the second-most-common type of dementia. Impairment is caused by decreased blood flow to parts of the brain, often due to a series of small strokes that block arteries. Symptoms often overlap with those of Alzheimer’s, although memory may not be as seriously affected.

 

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Mild Cognitive Disorder Mild Cognitive Disorder (MCI) is a condition in which a person has problems with memory, language or another essential cognitive function that are severe enough to be noticeable to others and show up on tests, but not severe enough to interfere with daily life. Some people with mild cognitive impairment go on to develop dementia. For others, the symptoms of mild cognitive impairment do not progress to dementia, and some people who have mild cognitive impairment at one point in time later revert to normal cognitive status.

ALZHEIMER’S DISEASE: WHAT WE KNOW AND WHAT WE CAN DO Introduction Dementia is a brain disorder that seriously affects a person’s ability to carry out daily activities. The most common form of dementia among older people is Alzheimer’s disease (AD), which initially involves the parts of the brain that control thought, memory, and language. Although scientists are learning more every day, right now they still do not know what causes AD, and there is no cure. Scientists think that as many as 4.5 million Americans suffer from AD. The disease usually begins after age 60, and risk goes up with age. While younger people also may get AD, it is much less common. About 5 percent of men and women ages 65 to 74 have AD, and nearly half of those age 85 and older may have the disease. It is important to note, however, that AD is not a normal part of aging. AD is named after Dr. Alois Alzheimer, a German doctor. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. He found abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary tangles). Today, these plaques and tangles in the brain are considered signs of AD. Scientists also have found other brain changes in people with AD. Nerve cells die in areas of the brain that are vital to memory and other mental abilities, and connections between nerve cells are disrupted. There also are lower levels of some of the chemicals in the brain that carry messages back and forth between nerve cells. AD may impair thinking and memory by disrupting these messages. What Causes AD? Scientists do not yet fully understand what causes AD. There probably is not one single cause, but several factors that affect each person differently. Age is the most important known risk factor for AD. The number of people with the disease doubles every 5 years beyond age 65.

 

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Family history is another risk factor. Scientists believe that genetics may play a role in many AD cases. For example, early-onset familial AD, a rare form of AD that usually occurs between the ages of 30 and 60, is inherited. The more common form of AD is known as late-onset. It occurs later in life, and no obvious inheritance pattern is seen in most families. However, several risk factor genes may interact with each other and with non-genetic factors to cause the disease. The only risk factor gene identified so far for late-onset AD is a gene that makes one form of a protein called apolipoprotein E (ApoE). Everyone has ApoE, which helps carry cholesterol in the blood. Only about 15 percent of people have the form that increases the risk of AD. It is likely that other genes also may increase the risk of AD or protect against AD, but they remain to be discovered. Scientists still need to learn a lot more about what causes AD. In addition to genetics and ApoE, they are studying education, diet, and environment to learn what role they might play in the development of this disease. Scientists are finding increasing evidence that some of the risk factors for heart disease and stroke, such as high blood pressure, high cholesterol, and low levels of the vitamin folate, may also increase the risk of AD. Evidence for physical, mental, and social activities as protective factors against AD is also increasing. What Are the Symptoms of AD? AD begins slowly. At first, the only symptom may be mild forgetfulness, which can be confused with age-related memory change. Most people with mild forgetfulness do not have AD. In the early stage of AD, people may have trouble remembering recent events, activities, or the names of familiar people or things. They may not be able to solve simple math problems. Such difficulties may be a bother, but usually they are not serious enough to cause alarm. However, as the disease goes on, symptoms are more easily noticed and become serious enough to cause people with AD or their family members to seek medical help. Forgetfulness begins to interfere with daily activities. People in the middle stages of AD may forget how to do simple tasks like brushing their teeth or combing their hair. They can no longer think clearly. They can fail to recognize familiar people and places. They begin to have problems speaking, understanding, reading, or writing. Later on, people with AD may become anxious or aggressive, or wander away from home. Eventually, patients need total care. How is AD Diagnosed? An early, accurate diagnosis of AD helps patients and their families plan for the future. It gives them time to discuss care while the patient can still take part in making decisions. Early diagnosis will also offer the best chance to treat the symptoms of the disease. Today, the only definite way to diagnose AD is to find out whether there are plaques and tangles in brain tissue. To look at brain tissue, however, doctors usually must wait

 

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until they do an autopsy, which is an examination of the body done after a person dies. Therefore, doctors can only make a diagnosis of “possible” or “probable” AD while the person is still alive. At specialized centers, doctors can diagnose AD correctly up to 90 percent of the time. Doctors use several tools to diagnose “probable” AD, including: questions about the person’s general health, past medical problems, and ability to carry out daily activities, tests of memory, problem solving, attention, counting, and language, medical tests— such as tests of blood, urine, or spinal fluid, and brain scans. Sometimes these test results help the doctor find other possible causes of the person’s symptoms. For example, thyroid problems, drug reactions, depression, brain tumors, and blood vessel disease in the brain can cause AD-like symptoms. Some of these other conditions can be treated successfully. How is AD Treated? AD is a slow disease, starting with mild memory problems and ending with severe brain damage. The course the disease takes and how fast changes occur vary from person to person. On average, AD patients live from 8 to 10 years after they are diagnosed, though some people may live with AD for as many as 20 years. No treatment can stop AD. However, for some people in the early and middle stages of the disease, the drugs tacrine (Cognex, which is still available but no longer actively marketed by the manufacturer), donepezil (Aricept), rivastigmine (Exelon), or galantamine (Razadyne, previously known as Reminyl) may help prevent some symptoms from becoming worse for a limited time. Another drug, memantine (Namenda), has been approved to treat moderate to severe AD, although it also is limited in its effects. Also, some medicines may help control behavioral symptoms of AD such as sleeplessness, agitation, wandering, anxiety, and depression. Treating these symptoms often makes patients more comfortable and makes their care easier for caregivers. New Areas of Research The National Institute on Aging (NIA), part of the National Institutes of Health (NIH), is the lead Federal agency for AD research. NIA-supported scientists are testing a number of drugs to see if they prevent AD, slow the disease, or help reduce symptoms. Researchers undertake clinical trials to learn whether treatments that appear promising in observational and animal studies actually are safe and effective in people. Some ideas that seem promising turn out to have little or no benefit when they are carefully studied in a clinical trial. Neuroimaging. Scientists are finding that damage to parts of the brain involved in memory, such as the hippocampus, can sometimes be seen on brain scans before symptoms of the disease occur. An NIA public-private partnership—the AD

 

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Neuroimaging Initiative (ADNI)—is a large study that will determine whether magnetic resonance imaging (MRI) and positron emission tomography (PET) scans, or other imaging or biological markers, can see early AD changes or measure disease progression. The project is designed to help speed clinical trials and find new ways to determine the effectiveness of treatments. For more information on ADNI, call the NIA’s Alzheimer’s Disease Education and Referral (ADEAR) Center at 1-800-438-4380, or visit www.alzheimers.nia.nih.gov. AD Genetics. The NIA is sponsoring the AD Genetics Study to learn more about risk factor genes for late onset AD. To participate in this study, families with two or more living siblings diagnosed with AD should contact the National Cell Repository for AD tollfree at 1-800-526-2839. Information may also be requested through the study’s website: http://ncrad.iu.edu. Mild Cognitive Impairment. During the past several years, scientists have focused on a type of memory change called mild cognitive impairment (MCI), which is different from both AD and normal age-related memory change. People with MCI have ongoing memory problems, but they do not have other losses such as confusion, attention problems, and difficulty with language. The NIA-funded Memory Impairment Study compared donepezil, vitamin E, or placebo in participants with MCI to see whether the drugs might delay or prevent progression to AD. The study found that the group with MCI taking donepezil were at reduced risk of progressing to AD for the first 18 months of a 3-year study, when compared with their counterparts on placebo. The reduced risk of progressing from MCI to a diagnosis of AD among participants on donepezil disappeared after 18 months, and by the end of the study, the probability of progressing to AD was the same in the two groups. Vitamin E had no effect at any time point in the study when compared with placebo. Inflammation. There is evidence that inflammation in the brain may contribute to AD damage. Some studies have suggested that drugs such as nonsteroidal antiinflammatory drugs (NSAIDs) might help slow the progression of AD, but clinical trials thus far have not demonstrated a benefit from these drugs. A clinical trial studying two of these drugs, rofecoxib (Vioxx) and naproxen (Aleve) showed that they did not delay the progression of AD in people who already have the disease. Another trial, testing whether the NSAIDs celecoxib (Celebrex) and naproxen could prevent AD in healthy older people at risk of the disease was suspended due to concerns over possible cardiovascular risk. Researchers are continuing to look for ways to test how other antiinflammatory drugs might affect the development or progression of AD. Antioxidants. Several years ago, a clinical trial showed that vitamin E slowed the progress of some consequences of AD by about 7 months. Additional studies are investigating whether antioxidants—vitamins E and C—can slow AD. Another clinical trial is examining whether vitamin E and/or selenium supplements can prevent AD or cognitive decline, and additional studies on other antioxidants are ongoing or being planned, including a study of the antioxidant treatments—vitamins E, C, alpha-lipoic acid, and coenzyme Q—in patients with mild to moderate AD.

 

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Ginkgo biloba. Early studies suggested that extracts from the leaves of the ginkgo biloba tree may be of some help in treating AD symptoms. There is no evidence yet that ginkgo biloba will cure or prevent AD, but scientists now are trying to find out in a clinical trial whether ginkgo biloba can delay cognitive decline or prevent dementia in older people. Estrogen. Some studies have suggested that estrogen used by women to treat the symptoms of menopause also protects the brain. Experts also wondered whether using estrogen could reduce the risk of AD or slow the disease. Clinical trials to test estrogen, however, have not shown that estrogen can slow the progression of already diagnosed AD. And one study found that women over the age of 65 who used estrogen with a progestin were at greater risk of dementia, including AD, and that older women using only estrogen could also increase their chance of developing dementia. Scientists believe that more research is needed to find out if estrogen may play some role in AD. They would like to know whether starting estrogen therapy around the time of menopause, rather than at age 65 or older, will protect memory or prevent AD. Participating in Clinical Trials People with AD, those with MCI, or those with a family history of AD, who want to help scientists test possible treatments may be able to take part in clinical trials. Healthy people also can help scientists learn more about the brain and AD. The NIA maintains the AD Clinical Trials Database, which lists AD clinical trials sponsored by the Federal government and private companies. To find out more about these studies, contact the NIA’s ADEAR Center at 1-800-438-4380 or visit the ADEAR Center website at www.nia.nih.gov/Alzheimers/ResearchInformation/ClinicalTrials. You also can sign up for e-mail alerts on new clinical trials as they are added to the database. Additional clinical trials information is available at www.clinicaltrials.gov. Many of these studies are being done at NIA-supported Alzheimer’s Disease Centers located throughout the United States. These centers carry out a wide range of research, including studies of the causes, diagnosis, treatment, and management of AD. To get a list of these centers, contact the ADEAR Center. Advancing Our Understanding Scientists have come a long way in their understanding of AD. Findings from years of research have begun to clarify differences between normal age-related memory changes, MCI, and AD. Scientists also have made great progress in defining the changes that take place in the AD brain, which allows them to pinpoint possible targets for treatment. These advances are the foundation for the NIH Alzheimer’s Disease Prevention Initiative, which is designed to: understand why AD occurs and who is at greatest risk of developing it, improve the accuracy of diagnosis and the ability to identify those at risk, discover, develop, and test new treatments, and discover treatments for behavioral problems in patients with AD.

 

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Advances in the Treatment and Diagnosis of Alzheimer’s Disease By:

Ranjan Duara, MD, FAAN Alzheimer’s disease was first identified more than 100 years ago and currently affects

over 5.4 million people. However, it’s been the past 30 years that have been instrumental in generating research findings that can help unlock this debilitating disease. Advances in our knowledge of the biology of Alzheimer’s disease have provided important insights about preventive measures, the earliest possible stages of diagnosis and the best approaches available for treatment. This is why The Wien Center for Alzheimer’s Disease and Memory Disorders at Mount Sinai Medical Center remains committed to the advancement and development of new diagnostic tools and treatment options for Alzheimer’s disease through active participation in clinical research trials. When Alzheimer’s disease progresses to the point where symptoms manifest, areas of the brain become affected resulting in impairment of language, sensory perception, judgment, manual skills and emotional control. However, improvements in clinical assessment and brain imaging have enabled clinicians to diagnose Alzheimer’s more reliably and at an earlier stage which can result in immediate medical intervention. The earliest abnormality in the brain in Alzheimer’s disease is the abnormal deposition of a protein called beta-amyloid, whose amounts tend to increase with age, but especially in those who will ultimately develop Alzheimer’s disease. Very recently it has become possible to detect the presence and amount of amyloid in the brain, using a new type of PET scan. Shrinkage or atrophy of the hippocampus and neighboring brain structures, which are intimately involved with learning and memory, are also visible and measurable on MRI scans of the brain. Atrophy of these brain regions are associated with impairment of memory, which can now also be detected at a very early stage with specific cognitive tests. As a result, these tests are now being used to diagnose Alzheimer’s, even before there are any symptoms, especially among those with major genetic or other risk factors for the disease.

 

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begin to treat the disease early. Such therapies are likely to be more effective when there is less pathology and secondary problems. Many disease-modifying approaches to treating Alzheimer’s disease are currently under intense investigation, especially those targeting the overproduction of amyloid, its removal from the brain (by vaccines) or prevention of its toxic effects. Non-amyloid treatments targeting other proteins involved in Alzheimer’s, such as tauprotein, are also being devised and tested. Not all individuals with these early markers of the disease will actually develop the typical symptoms and progression of Alzheimer’s disease. However, genetic and medical risk factors such as uncontrolled high blood pressure, high cholesterol, stroke, diabetes, cigarette smoking, chronic infections and inflammations can increase the likelihood of development. Managing of these risk factors coupled with regular physical and mental exercise, a healthy diet, stress reduction and frequent social interactions can provide individuals with a window of opportunity, of as much as two decades, to prevent or substantially delay the onset of Alzheimer’s disease. With an annual patient load of approximately 500 new patients, 2,000 follow-up patients and over 20 active clinical trials and research projects, The Wien Center is undoubtedly one of the most active centers, nationally, devoted to the diagnosis and care of patients with memory disorders. The Wien Center utilizes the most advanced cognitive and diagnostic tests, and disease-modifying agents available in an effort to treat Alzheimer’s disease at the earliest stage possible. In addition, The Wien Center provides free memory screenings to anyone over the age of 50 in an effort to help diagnose the earliest possible stages of Alzheimer’s. Mount Sinai’s free memory screening is a non-invasive, oral and written test available anytime throughout the year by simply making an appointment. The Wien Center also hosts the annual Mild Cognitive Impairment Symposium - an international forum that attracts top doctors from all over the world to discuss the latest in diagnosis and treatment of the earliest forms of Alzheimer’s. The Wien Center has also managed and operated The State of Florida Brain Bank since its inception in 1985. By focusing on research and advancements in technology, we aim to improve memory and mental responsiveness in Alzheimer’s patients, educate the community on healthy aging, delay the onset of Alzheimer’s disease and, ultimately, find a cure.

 

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Dr. Ranjan Duara is the Medical Director for The Wien Center for Alzheimer’s Disease and Memory Disorders at Mount Sinai Medical Center. The Wien Center is currently recruiting participants who believe they may be at risk of developing Alzheimer’s disease for various clinical research trials. Clinical research trials provide patients with access to innovative treatments and medications, at no cost, that are not yet available to the public. For more information about Alzheimer’s disease, The Mount Sinai Wien Center, information on clinical research trials or to schedule a free memory screening, call 305-674-2543 or visit www.msmc.com.

MILD COGNITIVE IMPAIREMENT: AN INTERMEDIATE STAGE www.mayoclinic.org Mild cognitive impairment (MCI) is an intermediate stage between the expected cognitive decline of normal aging and the more pronounced decline of dementia. It involves problems with memory, language, thinking and judgment that are greater than typical age-related changes. If you have mild cognitive impairment, you may be aware that your memory or mental function has "slipped." And your family and close friends may also notice a change. But generally these changes aren't severe enough to interfere with your day-to-day life and usual activities. Mild cognitive impairment increases your risk of later developing dementia, including Alzheimer's disease, especially when your main difficulty is with memory. But some people with mild cognitive impairment never get worse, and a few eventually get better. SYMPTOMS Your brain changes as you grow older just like the rest of your body. Many people notice gradually increasing forgetfulness as they age. It may take longer to think of a word or to recall a person's name. But consistent or increasing concern about your mental performance may suggest MCI. Cognitive issues may go beyond what's expected and indicate possible MCI if you experience any or all of the following: * You forget things more often. * You forget important events such as appointments or social engagements. * You lose your train of thought or the thread of conversations, books or movies. * You feel increasingly overwhelmed by making decisions, planning steps to accomplish a task or interpreting instructions. * You start to have trouble finding your way around familiar environments. * You become more impulsive or show increasingly poor judgment. * Your family and friends notice any of these changes. If you have MCI, you may also experience: * Depression

 

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* Irritability and aggression * Anxiety * Apathy RISK FACTORS The strongest risk factors for MCI are: * Increasing age * Having a specific form of a gene known as APOE-e4, also linked to Alzheimer's disease — though having the gene doesn't guarantee that you'll experience cognitive decline Other medical conditions and lifestyle factors have been linked to an increased risk of cognitive change, but the evidence for these risk factors is less clear-cut. These risk factors include: * Diabetes * Current smoking * Depression * High blood pressure * Elevated cholesterol * Lack of physical exercise * Infrequent participation in mentally or socially stimulating activities TREATMENT AND DRUGS Currently, no MCI drugs or other treatments are specifically approved by the Food and Drug Administration (FDA). But MCI is an active area of research. Clinical studies are under way to shed more light on the disorder and find treatments that may improve symptoms or prevent or delay progression to dementia. Doctors sometimes prescribe cholinesterase inhibitors, a type of drug approved for Alzheimer's disease, for people with MCI when the main symptom is memory loss. However, cholinesterase inhibitors aren't recommended for routine use in MCI because they don't appear to provide lasting benefit. Other common conditions besides MCI can make you feel forgetful or less mentally sharp than usual. Treating these conditions can help improve your memory and overall mental function. Conditions that can affect memory include: * High blood pressure. People with MCI tend to be more likely to have problems with the blood vessels inside their brains. High blood pressure can worsen these problems and cause memory difficulties. Your doctor will monitor your blood pressure and recommend steps to lower it if it's too high.

 

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* Depression. When you're depressed, you often feel forgetful and mentally "foggy." Depression is common in people with MCI. Treating depression may help improve memory, while making it easier to cope with the changes in your life. * Sleep apnea. In this condition, your breathing repeatedly stops and starts while you're asleep, making it impossible to get a good night's rest. Sleep apnea can make you feel excessively tired during the day, forgetful and unable to concentrate. Treatment can improve these symptoms and restore alertness.

WHAT IS LEWY BODY DEMENTIA (LBD)?: A DEEPER LOOK INTO LBD Introduction Lewy body dementia (LBD) is a progressive brain disease and the second leading cause of degenerative dementia in the elderly. The clinical name, “dementia with Lewy bodies” (DLB), accounts for up to 20% of all dementia cases, or 800,000 patients in the US. Over 50% of Parkinson’s disease patients develop “Parkinson’s disease dementia” (PDD), which accounts for at least 750,000 patients. (PDD is also a Lewy body dementia.) Other names for the Lewy body dementias are: Lewy body disease (LBD); Diffuse lewy body disease (DLBD); Cortical Lewy body disease (CLBD); Lewy body Variant of Alzheimer's (LBVA); Parkinson's disease with dementia (PDD). In the early 1900’s, while researching Parkinson's disease, the scientist Friederich H. Lewy discovered abnormal protein deposits that disrupt the brain's normal functioning. These Lewy body proteins are found in an area of the brain stem where they deplete the neurotransmitter dopamine, causing Parkinsonian symptoms. In Lewy body dementia, these abnormal proteins are diffuse throughout other areas of the brain, including the cerebral cortex. The brain chemical acetylcholine is depleted, causing disruption of perception, thinking, and behavior. Lewy body dementia exists either in pure form, or in conjunction with other brain changes, including those typically seen in Alzheimer's disease and Parkinson's disease. Lewy body dementia diagnostic criteria and symptoms Diagnosis Every person with LBD is different and will manifest different degrees of the following symptoms. Some will show no signs of certain features, especially in the early stages of the disease. Symptoms may fluctuate as often as moment-to-moment, hour-to-hour or

 

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day-to-day. NOTE: Some patients meet the criteria for LBD yet score in the normal range of some cognitive assessment tools. The Mini-Mental State Examination (MMSE), for example, cannot be relied upon to distinguish LBD from other common syndromes. The latest clinical diagnostic criteria for LBD groups symptoms into three types: Core features: • • •

Fluctuating cognition with pronounced variations in attention and alertness. Recurrent complex visual hallucinations, typically well formed and detailed. Spontaneous features of parkinsonism.

Suggestive features: • • •

REM sleep behavior disorder (RBD), which can appear years before the onset of dementia and parkinsonism. Severe sensitivity to neuroleptics occurs in up to 50% of LBD patients who take them. Low dopamine transporter uptake in the brain's basal ganglia as seen on SPECT and PET imaging scans. (These scans are not yet available outside of research settings.)

Supportive features: • • • • • •

Repeated falls and syncope (fainting). Transient, unexplained loss of consciousness. Autonomic dysfunction. Hallucinations of other modalities. Visuospatial abnormalities. Other psychiatric disturbances.

A clinical diagnosis of LBD can be probable or possible based on different symptom combinations. A probable LBD diagnosis requires either: • •

Dementia plus two or more core features, or Dementia plus one core feature and one or more suggestive features.

A possible LBD diagnosis requires: • • •

Dementia plus one core feature, or Dementia plus one or more suggestive features. An experienced clinician within the medical community should perform a diagnostic evaluation. If one is not available, the neurology department of the nearest medical university should be able to recommend appropriate resources

 

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or may even provide an experienced diagnostic team skilled in Lewy body dementia. A thorough dementia diagnostic evaluation includes physical and neurological examinations, patient and family interviews (including a detailed lifestyle and medical history), and neuro-psychological and mental status tests. The patient’s functional ability, attention, language, visuospatial skills, memory and executive functioning are assessed. In addition, brain imaging (CT or MRI scans), blood tests and other laboratory studies may be performed. The evaluation will provide a clinical diagnosis. Currently, a conclusive diagnosis of LBD can be obtained only from a postmortem autopsy for which arrangements should be made in advance. Some research studies may offer brain autopsies as part of their protocols. Participating in research studies is a good way to benefit others with Lewy body dementia. Symptoms In this section we'll discuss each of the symptoms, starting with the key word: dementia. Dementia is a process whereby the person becomes progressively confused. The earliest signs are usually memory problems, changes in their way of speaking, such as forgetting words, and personality problems. Cognitive symptoms of dementia include poor problem solving, difficulty with learning new skills and impaired decision making. Other causes of dementia should be ruled out first, such as alcoholism, overuse of medication, thyroid or metabolic problems. Strokes can also cause dementia. If these reasons are ruled out then the person is said to have a degenerative dementia. Lewy Body Dementia is second only to Alzheimer's disease as the most common form of dementia. Fluctuations in cognition will be noticeable to those who are close to the person with LBD, such as their partner. At times the person will be alert and then suddenly have acute episodes of confusion. These may last hours or days. Because of these fluctuations, it is not uncommon for it to be thought that the person is "faking". This fluctuation is not related to the well-known "sundowning" of Alzheimer's. In other words, there is no specific time of day when confusion can be seen to occur. Hallucinations are usually, but not always, visual and often are more pronounced when the person is most confused. They are not necessarily frightening to the person. Other modalities of hallucinations include sound, taste, smell, and touch. Parkinsonism or Parkinson's Disease symptoms, take the form of changes in gait; the person may shuffle or walk stiffly. There may also be frequent falls. Body stiffness in the arms or legs, or tremors may also occur. Parkinson's mask (blank stare, emotionless look on face), stooped posture, drooling and runny nose may be present. REM Sleep Behavior Disorder (RBD) is often noted in persons with Lewy Body Dementia. During periods of REM sleep, the person will move, gesture and/or speak.

 

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There may be more pronounced confusion between the dream and waking reality when the person awakens. RBD may actually be the earliest symptom of LBD in some patients, and is now considered a significant risk factor for developing LBD. (One recent study found that nearly two-thirds of patients diagnosed with RBD developed degenerative brain diseases, including Lewy body dementia, Parkinson’s disease, and multiple system atrophy, after an average of 11 years of receiving an RBD diagnosis. All three diseases are called synucleinopathies, due to the presence of a mis-folded protein in the brain called alpha-synuclein.) Sensitivity to neuroleptic (anti-psychotic) drugs is another significant symptom that may occur. These medications can worsen the Parkinsonism and/or decrease the cognition and/or increase the hallucinations. Neuroleptic Malignancy Syndrome, a life-threatening illness, has been reported in persons with Lewy Body Dementia. For this reason, it is very important that the proper diagnosis is made and that healthcare providers are educated about the disease. Visuospatial difficulties, including depth perception, object orientation, directional sense and illusions may occur. Autonomic dysfunction, including blood pressure fluctuations (e.g. postural/orthostatic hypotension) heart rate variability (HRV), sexual disturbances/impotence, constipation, urinary problems, hyperhidrosis (excessive sweating), decreased sweating/heat intolerance, syncope (fainting), dry eyes/mouth, and difficulty swallowing which may lead to aspiration pneumonia. Other psychiatric disturbances may include systematized delusions, aggression and depression. The onset of aggression in LBD may have a variety of causes, including infections (e.g., UTI), medications, misinterpretation of the environment or personal interactions, and the natural progression of the disease. Medications Medications are one of the most controversial subjects in dealing with LBD. A medication that doesn't work for one person may work for another person. Prescribing should only be done by a physician who is thoroughly knowledgeable about LBD. With new medications and even “over-the-counter,” the patient should be closely monitored. At the first sign of an adverse reaction, consult with the patient's physician. Consider joining the online caregiver support groups to see what others have observed with prescription and over-the-counter medicines. Risk Factors Advanced age is considered to be the greatest risk factor for Lewy body dementia, with onset typically, but not always, between the ages of 50 and 85. Some cases have been reported much earlier. It appears to affect slightly more men than women. Having a

 

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family member with Lewy body dementia may increase a person’s risk. Observational studies suggest that adopting a healthy lifestyle (exercise, mental stimulation, nutrition) might delay age-associated dementias. Clinical Trials The recruitment of LBD patients for participation in clinical trials for studies on LBD, other dementias and Parkinsonian studies is now steadily increasing. Prognosis and Stages No cure or definitive treatment for Lewy body dementia has been discovered as yet. The disease has an average duration of 5 to 7 years. It is possible, though, for the time span to be anywhere from 2 to 20 years, depending on several factors, including the person’s overall health, age and severity of symptoms. Defining the stages of disease progression for LBD is difficult. The symptoms, medicine management and duration of LBD vary greatly from person to person. To further complicate the stages assessment, LBD has a progressive but vacillating clinical course. It is typical to observe a significance progression, followed by regression back to a higher functioning level. Downward fluctuations are often caused by medications, infections or other compromises to the immune system, but may also be due to the natural course of the disease. Awareness and Education LBDA Pamphlet LBDA is pleased to offer you our free pamphlet about Lewy Body Dementia. This is a must-read publication for LBD families, and all medical and caring professionals as well. You can download a copy (PDF) or if you need larger quantities, please send your name, address and quantity to [email protected]. Fact Sheet The LBDA is pleased to share its fact sheet about Lewy Body Dementia. You can download a copy or if you need a larger quantity, please email your name, address and quantity to [email protected] LBDA Newsletter: The Thistle The LBDA’s quarterly newsletter is a rich resource for caregivers and the general public on all matters pertaining to LBD. LBDA Web Site Filled with information on LBD, caregiving, and the latest news in LBD research, the Web site is a comprehensive tool for both families and medical professionals.

 

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Medical Conferences The LBDA attends and exhibits at national medical conferences, reaching a wide variety of physicians and scientists. Caregiving Conferences The LBDA attends and exhibits at national conferences for professional caregivers, like nurses, social workers, and long term care professionals. Volunteers also exhibit at local health fairs for the general public.

BECOMING FAMILIAR WITH VASCULAR DEMENTIA www.mayoclinic.org Vascular dementia is a general term describing problems with reasoning, planning, judgment, memory and other thought processes caused by brain damage from impaired blood flow to your brain. You can develop vascular dementia after a stroke blocks an artery in your brain, but strokes don't always cause vascular dementia. Whether a stroke affects your thinking and reasoning depends on your stroke's severity and location. Vascular dementia also can result from other conditions that damage blood vessels and reduce circulation, depriving your brain of vital oxygen and nutrients. Factors that increase your risk of heart disease and stroke — including high blood pressure, high cholesterol and smoking — also raise your vascular dementia risk. Controlling these factors can help lower your chances of developing vascular dementia. SYMPTOMS Vascular dementia symptoms vary, depending on the part of your brain where blood flow is impaired. Symptoms often overlap with those of other types of dementia, especially Alzheimer's disease. Vascular dementia symptoms may be most clear-cut when they occur suddenly following a stroke. When changes in your thinking and reasoning seem clearly linked to a stroke, this condition is sometimes called "poststroke dementia." Another characteristic pattern of vascular dementia symptoms sometimes follows a series of strokes or mini strokes. In this pattern, changes in your thought processes occur in noticeable "steps" downward from your previous level of function, unlike the gradual, steady decline that typically occurs in Alzheimer's disease. But vascular dementia can also develop very gradually, just like Alzheimer's disease. What's more, vascular dementia and Alzheimer's often occur together. Studies show that people with dementia symptoms usually have brain changes typical of more than one type. Some doctors call this condition "mixed dementia."

Vascular dementia symptoms include:

 

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* Confusion * Trouble paying attention and concentrating * Reduced ability to organize thoughts or actions * Decline in ability to analyze a situation, develop an effective plan, and communicate plan to others * Difficulty deciding what to do next * Problems with memory * Restlessness and agitation * Unsteady gait * Sudden or frequent urge to urinate, or inability to control passing urine * Wandering at night * Depression RISK FACTORS In general, the risk factors for vascular dementia are the same as those for heart disease and stroke. Risk factors for vascular dementia include: * Increasing age. Your risk for vascular dementia rises as you grow older. The disorder is rare before age 65, and risk rises substantially as you reach your 80s and 90s. * History of heart attack, strokes or mini strokes. If you've had a heart attack, you may be at increased risk of having blood vessel problems in your brain. The brain damage that occurs with a stroke or a mini stroke (transient ischemic attack) may increase your risk of developing dementia. * Atherosclerosis. This condition occurs when deposits of cholesterol and other substances (plaques) build up in your arteries and narrow your blood vessels. Atherosclerosis can increase your risk of vascular dementia — and possibly your risk of Alzheimer's disease — by reducing the flow of blood that nourishes your brain. * High cholesterol. Elevated levels of low-density lipoprotein (LDL), the so-called "bad" cholesterol, are associated with an increased risk of vascular dementia, and possibly with a higher risk of Alzheimer's disease. * High blood pressure. When your blood pressure's too high, it puts extra stress on blood vessels everywhere in your body, including your brain. This increases the risk of vascular problems in the brain.

 

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* Diabetes. High glucose levels damage blood vessels throughout your body. Damage in brain blood vessels can increase your risk of stroke and vascular dementia. * Smoking. Smoking directly damages your blood vessels, increasing your risk of atherosclerosis and other circulatory diseases, including vascular dementia. * Atrial fibrillation. In this abnormal heart rhythm, the upper chambers of your heart begin to beat rapidly and irregularly, out of coordination with your heart's lower chambers. Atrial fibrillation increases your risk of stroke by leading to poor blood flow to your brain and elsewhere in your body. TREATMENT AND DRUGS Controlling underlying conditions and risk factors Controlling conditions that affect the underlying health of your heart and blood vessels can sometimes slow the rate at which vascular dementia gets worse, and may also sometimes prevent further decline. Depending on your individual situation, your doctor may prescribe medications to: * Lower your blood pressure * Reduce your cholesterol level * Prevent your blood from clotting and keep your arteries clear * Help control your blood sugar if you have diabetes Alzheimer's medications The Food and Drug Administration (FDA) has not approved any drugs specifically to treat changes in judgment, planning, memory and other thought processes caused by vascular dementia. However, certain medications approved by the FDA to treat these symptoms in Alzheimer's disease may also help people with vascular dementia to the same modest extent they help those with Alzheimer's. Doctors may prescribe one or both types of the following Alzheimer's drugs:

* Cholinesterase inhibitors — including donepezil (Aricept), galantamine (Razadyne) and rivastigmine (Exelon) — work by boosting levels of a brain cell chemical messenger involved in memory and judgment. Side effects can include nausea, vomiting, muscle cramps and diarrhea. * Memantine (Namenda) regulates another brain cell chemical messenger important for information processing, storage and retrieval. Side effects can include headache, constipation, confusion and dizziness.

 

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UNDERSTANDING FRONTOTEMPORAL DEMENTIA By: Peter Doskoch Given the overlap in cognitive and behavioral symptoms, diagnosing the various non-Alzheimer’s disease dementias can be a difficult process. This is certainly true for frontotemporal dementia (FTD), although the challenge of identifying FTD is perhaps exceeded by the challenge of keeping track of the ever-shifting changes in terminology and diagnostic criteria. In the past eight years, at least three different sets of criteria, each featuring a somewhat different taxonomy, have been published. (Part of the problem is that FTD is a clinical syndrome rather than a single disease with a unitary pathology.) Nonetheless, navigating through the potential confusion to obtain a correct diagnosis is important, as the course, presentation, and treatment of FTD differs from that of other dementias. At the annual meeting of the American Neuropsychiatric Association, Tiffany Chow, MD, an Assistant Professor of Clinical Neurology at the University of Southern California in Los Angeles, described the key manifestations of FTD and suggested tips that can aid diagnosis. She also offered advice on how to treat the behavioral and cognitive components of the syndrome. FTD IN A NUTSHELL As the name suggests, patients with FTD have dysfunction of the brain’s prefrontal regions, temporal lobes, or both. In many cases, there may be significant atrophyæeasily visible with magnetic resonance imagingæspecific to the affected regions; in other instances, the abnormalities may be functional rather than structural. Mild ischemic white matter changes consistent with normal aging may be present as well. Although some patients have Pick bodies, most do not. It is controversial whether those with semantic deficits have atrophy of the anterior hippocampus to the degree seen in Alzheimer’s disease, Dr. Chow noted. The frontal-subcortical circuits affected by FTD are important in self-monitoring (orbitofrontal areas), motivation (the anterior cingulate), and executive functions (the dorsolateral prefrontal cortex); many patients have impairment to some degree in all three of these areas. Patients with a predominantly behavioral clinical presentation may have subjective and/or objective memory disturbances but do not have an amnestic syndrome, and they generally remain oriented to time and place. When only one temporal lobe is involved, the presentation depends on which hemisphere is affected. Patients with primarily left temporal lobe dysfunction typically behave in a socially appropriate manner but present with aphasia and decreased facial expressiveness; these patients are often diagnosed as having semantic dementia. These are the FTD syndrome patients who are most like Alzheimer’s disease patients, because they can also suffer short-term memory loss. Those with predominantly right temporal abnormalities are more likely to exhibit antisocial behavior, bizarre dress,

 

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apathy, and hyperorality (patients may routinely put inedible items in their mouths, much as young children do). EVOLVING CRITERIA Given the wide range of behaviors mediated by the frontal and temporal lobes, it is not surprising that the process of determining the core diagnostic features of FTD has been an ongoing endeavor. The Lund-Manchester criteria, published in 1994,1 required the presence of at least two of the following features: loss of personal awareness, strange eating habits, perseveration, and mood change. In addition, patients had to have one or more of the following: frontal executive dysfunction, reduced speech, and preserved visuospatial ability. (In contrast, patients with Alzheimer’s disease generally develop impaired visuospatial ability as memory declines.) Finally, the authors of the criteria cited several important supporting features, including onset before age 65, a family history of FTD, early urinary incontinence, motor neuron disease, and (in the late stages) akinesia, rigidity, and tremor. The criteria published by Neary and colleagues four years later2 incorporated most of the above features and added some others. However, the authors subdivided patients into three separate clinical presentations: frontotemporal dementia (characterized primarily by personality change and disordered social conduct), progressive nonfluent aphasia (in which patients have difficulty with initiation but not comprehension of speech), and semantic aphasia (distinguished by impaired understanding of word meaning and/or object identity). The general term frontotemporal lobar degeneration was used to refer to any of the three syndromes. Although both the Neary and Lund-Manchester criteria emerged from consensus meetings, their purpose was more to establish a common set of standards for researchers than to aid clinical diagnosis. Thus, a third set of criteria, developed by the Work Group on Frontotemporal Dementia and Pick’s Disease, was published last year with the specific aim of helping clinicians diagnose FTD.3 The criteria, listed in the box at right, are considerably simpler than the Neary criteria and lump together all patients under the umbrella of FTD, although the authors did note that patients will have either a “behavioral presentation” or a “language presentation.” (Detailed descriptions of these “core clinical phenotypes” were not included in the formal criteria but appeared elsewhere in the paper.) The work group summarized the diverse pathological abnormalities that have been observed in FTD but opted not to incorporate these findings into the descriptions for the two phenotypes because neuropathology and clinical features do not always correlate. In summary, Dr. Chow said, clinicians should consider any of the following to be a “red flag” for possible FTD in a patient with dementia: • onset in the sixth decade (the mean age of onset among Dr. Chow’s patients is 56); • onset of disinhibited or criminal behavior;

 

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• loss of social awareness. This, Dr. Chow said, “is the [symptom] that your receptionist will tell you about”—the patient who, for example, might come up to the receptionist’s window and not leave; • compulsive behavior; • distractibility or impulsivity (these are also seen in Alzheimer’s but are more characteristic of FTD); • disordered mood (usually depression but sometimes euphoria); • stereotyped speech. Moreover, Dr. Chow added, patients tend to be “environmentally dependent”—during an office visit “they can’t leave the stuff on your desk alone.” TREATMENT STRATEGIES Several biochemical abnormalities have been identified in patients with FTD. These include loss of serotonin receptors in the frontal and temporal cortices and the brainstem, and low cerebrospinal fluid levels of the homovanillic acid. Similar abnormalities are also seen in Alzheimer’s disease. Compared with Alzheimer’s, however, FTD results in higher levels of 4-hydroxy-3-methoxy-phenylglycol, and there are no cholinergic deficits. Given the present lack of disease-modifying interventions, the treatment of FTD is necessarily symptomatic. Unfortunately, not all of the behavioral and cognitive problems respond equally well to pharmacotherapy. For example, because FTD patients with executive dysfunction in some ways resemble individuals with attention-deficit/hyperactivity disorder (ADHD)—both groups have difficulty with attention and concentration—some investigators have hypothesized that alpha-2 agonists, which are helpful in ADHD, might be effective in treating FTD. However, findings from a recent open-label guanfacine study did not reveal impressive benefits. The 11 participants, all with moderate to advanced FTD, received 1 mg qam for most of the four-month trial; the dose was lower for the first two weeks of the study (0.5 mg qam) and higher for the final month (1 mg bid). The results, presented by Dr. Chow in a poster at the neuropsychiatry meeting, failed to show objective benefits on any cognitive measure, though she noted that “there were some subjective reports of improvement that are encouraging.” The next step, she added, “is to try higher doses, to use different instruments to monitor efficacy, and to get other centers involved in placebo-controlled crossover trials.” Because patients with frontotemporal dementia do not have cholinergic abnormalities, medications targeting this neurotransmitter system, such as cholinesterase inhibitors, are not effective. Patients with deficits in expressive language (ie, those classified by

 

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the Neary criteria as having non-fluent primary progressive aphasia) who are treated with amantadine show subjective increases in fluency for three to six months, although the improvement on objective measures has not been compelling. Some patients may respond to bromocriptine, Dr. Chow suggested, but she noted that the drug has not been evaluated in a double-blind trial and that patients generally do not tolerate it as well as they do amantadine. Depression can be common in patients with primary progressive aphasia, perhaps in part because patients continue to retain a good degree of self-awareness; this insight may foster reactive mood changes. Unfortunately, Dr. Chow said that she has had little success in treating this problem with selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants. Nearly all patients with FTD will exhibit obsessive-compulsive behavior at some point during their illness, and these behaviors are much more responsive to treatment. Dr. Chow has found the SSRIs to be very useful for reducing obsessive-compulsive symptoms; she particularly favors paroxetine, starting at 10 mg/d and increasing the dosage if necessary to 20 or 40 mg/d. Sertraline and citalopram are reasonable alternatives. SSRIs may also be helpful for reducing anxiety and sexual disinhibition. For agitation or psychosis, Dr. Chow advises against the use of typical neuroleptics, which can worsen motor symptoms. She said she has found the atypical antipsychotics to be useful, particularly quetiapine, which she starts at 25 mg/d and increases as needed up to 50 mg/d. Risperidone is also an option, but dosages higher than 1 mg/d may produce parkinsonism, Dr. Chow noted. Valproic acid can be a useful adjunct to the atypicals; trazodone is worth considering if sundowning is a problem. Agitation and confusion may be worsened by benzodiazepines. For agitation or psychosis, Dr. Chow advises against the use of typical neuroleptics, which can worsen motor symptoms. She said she has found the atypical antipsychotics to be useful, particularly quetiapine, which she starts at 25 mg/d and increases as needed up to 50 mg/d. Risperidone is also an option, but dosages higher than 1 mg/d may produce parkinsonism, Dr. Chow noted. Valproic acid can be a useful adjunct to the atypicals; trazodone is worth considering if sundowning is a problem. Agitation and confusion may be worsened by benzodiazepines. Insomnia is often refractory in patients with FTD and may be related to the involvement of serotonergic neurons in REM sleep. The effects of zolpidem and zaleplon in this population are transient at best, according to Dr. Chow, but trazodone is sometimes helpful. If the patient is receiving an atypical antipsychotic for agitation or other reasons, a bedtime dose may provide a “bonus” of improved sleep. The motoric disturbances that tend to appear in the later stages of FTD respond to levodopa/carbidopa in some cases; dopamine agonists can be helpful but the clinician should be alert for the possibility of psychosis.

 

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Finally, behavioral interventions may be helpful for patients who are compliant and have good cognitive function, though any benefits will likely be lost as the disease progresses. One investigator has reported success using behavioral interventions to reduce obsessive-compulsive symptoms, and patients with aphasia may benefit from learning Amerind sign language. Dr. Chow’s review of the diagnosis and treatment of FTD will be published in an upcoming issue of the Journal of Neuropsychiatry and Clinical Neurosciences.

Measures That May Reduce Risk for Alzheimer’s Disease and Vascular Dementia among Unaffected Individuals (these measures may also slow down the progression of AD and vascular dementia).  

1. Diet: A low fat and carbohydrate diet that maintains your weight in the ideal range for you build. Although it is well recognized, by many people now, that high fat intake increases risk for vascular disease, it is generally not recognized that high carbohydrate intake (especially, refined rice, white bread, sugar, desserts) are equally, if not more responsible for such diseases. Certain ethnic/racial groups are particularly likely to consume a high carbohydrate diet in addition to a high fat diet. These groups include Hispanics and African Americans, who thus increase their risk for vascular and degenerative disease. On the other hand a high intake of natural anti-oxidants, such as fruits, vegetables and nuts and regular intake of wine up to two glasses a day), can reduce risk for these diseases. Oxygen Free Radicals, i.e., reactive oxygen molecules that cause damage to tissues and to the DNA within the cells, are known to play an important role in causing or aggravating many chronic diseases. These free radicals are released as a part of normal metabolism in the body, but the ability to counteract their effects declines with increasing age. Tobacco smoke, ultraviolet light, excessive alcohol intake and even stress all stimulate excess formation of free radicals. Antioxidants have the capacity to "mop up" or quench free radicals and prevent them from causing harm. Even the aging process may be slowed down by quenching these free radicals. The pigments that give many fruits their color are called anthocyanins, carotenoids and flavinoids. They are made of compounds that have antioxidant capacity, some with more capacity than others. Food scientists have shown that fruits and vegetables that have the highest pigmentations - darker, richer colors - have the highest levels of antioxidants, which seems to reduce risk of heart disease, cancer and degenerative diseases..

 

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Anthocyanins and flavinoid content in the pigments of blue and red berries, strawberries, blackberries, plums and red grapes are very high, giving these foods a high antioxidant capacity. Similarly, vegetables with high pigment content, such as red and yellow peppers, various types of lettuce, spinach, brussel sprouts, beets, broccoli and red onions have high antioxidant content. Black tea, olive oils, wine or apple vinegars, various spices including garlic, cumin, curcumin and fresh ginger also make very significant contribution to antioxidant capacity of the diet. 2. Activities: Regular and aerobic forms of exercises (45 minutes of physical activities, seven days of the week would be ideal). Physical exercise that results in weight reduction is of especially great benefit. Regular and enjoyable social interactions reduce risk for a variety of chronic diseases(dancing includes physical and social activites, may be particularly beneficial). Regular and stimulating activities that challenge the intellect and/or include active involvement of manual skills and dexterity are beneficial. Engaging in hobbies, such as playing bridge or other card games, learning a new language or skill, such as using a computer or a specific computer program “exercise” the brain, help in the formation of new connections (synapses) between nerve cells, increase the reserve capacity of the brain, release growth factors that sustain nerve cells and protect individuals from the effects of chronic diseases. 3. General Health: There is considerable evidence that conditions such as diabetes, obesity, hypertension and cardiovascular disease increase risk for degenerative and vascular diseases of the brain. This increased risk to the brain may be due to secondary effects of diseases in other parts of the body and to a direct affect of these conditions on the brain. Awareness of and careful control (with appropriate medications, when necessary) of certain medical conditions, such as: Hypertension, Elevated Cholesterol and Lipids, Diabetes Mellitus, and Vascular Disease, in general, and obesity may considerably reduce risk for vascular disease and degenerative disease of the brain. (Note: There is some evidence that the “Statin” group of drugs, used to treat elevated cholesterol, may independently reduce risk for Alzheimer’s disease). 4. Supplements: Regular use of antioxidant supplements and vitamins may be helpful (though evidence suggests that if antioxidants are taken in the diet they are more effective). Recommendations include: Vitamin C at about 500 mg daily, Vitamin E at about 400 IU daily, and Folic Acid at about 2 mg daily. Use of anti-inflammatory drugs, especially Ibuprofen at about 200 to 400 mg daily, may reduce risk for Alzheimer’s disease. (Note: Ibuprofen and other over-the-counter drugs anti-inflammatory drugs may have substantial side effects, especially on the gastrointestinal tract, in susceptible individuals – consult your physician before deciding to take this group of medication). 5. Avoidance of contact sports or other activities that may predispose towards repetitive head injuries may be important to reduce risk of Alzheimer’s disease. For example,

 

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boxers are known to have a substantially higher risk for developing dementia/Alzheimer’s disease. Similarly, soccer players who head the ball, may sustain frequent minor head trauma that could heighten their risk for these conditions.

PREVENTATIVE STRATEGIES: LIFESTYLE CHANGES AND ALZHEIMER’S DISEASE Lifestyle and the Development of AD: Relevant lifestyle changes include dietary changes to emphasize a low intake of carbohydrate and fats , a high intake of proteins, vegetable, fruit, spices and nuts (especially those that provide high antioxidant and antiinflammatory benefit), moderate alcohol and caffeine consumption, and elimination of smoking of cigarettes. Other lifestyle changes include emphasizing regular aerobic exercises (about 45 min every day, seven days a week, including going to the gym, walking, bicycling, jogging and dancing), stress free social interactions, hobbies (such as gardening, painting, reading for pleasure, listening to music) and mental stimulation in cultural and intellectual activities. Relevant medical conditions that should be detected as early as possible and managed optimally include hypertension, diabetes mellitus, coronary artery disease and arrhythmias, elevated cholesterol and lipids, peripheral vascular disease, carotid artery disease, sleep apnoea and chronic lung diseases, chronic renal disease, medication, drug and alcohol abuse. Specific medications that may be reduce risk for future cognitive impairment, even in the absence of the medical conditions for which they are usually prescribed, are antiinflammatory drugs, such as ibuprofen (Advil or Motrin), statin group of drugs (such as Lipitor, Zocor) and possibly the ACE-inhibitor group of drugs (such as Accupril, Lisinopril). Medical Factors and Cognitive Decline: The rate of cognitive decline in longitudinal studies is well known to be associated positively with the systolic and diastolic blood pressure, as well as to elevated serum cholesterol levels. Those with either hypertension or hypercholesterolemia were found to have a two fold increased risk of developing AD after a mean follow up of 21 years, whereas those with the combination of hypertension, hypercholesterolemia and another vascular risk factor, such as smoking, had a four fold increased risk for AD. Treatment of hypertension appeared to reduce or eliminate the excess rates of cognitive decline attributed to it. Among 4129 participants in the Cardiovascular Health Study (CHS), a high risk for stroke was associated with lower cognitive function and increased risk for incident cognitive decline. In a follow-up study in this cohort, the prevalence of scores