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Dementia is a term used to describe a group of symptoms affecting memory, thinking and social abilities. In people who have dementia, the symptoms interfere with their daily lives. Dementia isn't one specific disease. Several diseases can cause dementia.

Dementia generally involves memory loss. It's often one of the early symptoms of the condition. But having memory loss alone doesn't mean you have dementia. Memory loss can have different causes.

Alzheimer's disease is the most common cause of dementia in older adults, but there are other causes of dementia. Depending on the cause, some dementia symptoms might be reversible.

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Dementia symptoms vary depending on the cause. Common symptoms include:

Cognitive changes

• Memory loss, which is usually noticed by someone else.
• Problems communicating or finding words.
• Trouble with visual and spatial abilities, such as getting lost while driving.
• Problems with reasoning or problem-solving.
• Trouble performing complex tasks.
• Trouble with planning and organizing.
• Poor coordination and control of movements.
• Confusion and disorientation.

Psychological changes

• Personality changes.
• Depression.
• Inappropriate behavior.
• Being suspicious, known as paranoia.
• Seeing things that aren't there, known as hallucinations.

When to see a doctor

See a health care professional if you or a loved one has memory problems or other dementia symptoms. It's important to determine the cause. Some medical conditions that cause dementia symptoms can be treated.

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Dementia is caused by damage to or loss of nerve cells and their connections in the brain. The symptoms depend on the area of the brain that's damaged. Dementia can affect people differently.

Dementias are often grouped by what they have in common. They may be grouped by the protein or proteins deposited in the brain or by the part of the brain that's affected. Also, some diseases have symptoms like those of dementia. And some medicines can cause a reaction that includes dementia symptoms. Not getting enough of certain vitamins or minerals also can cause dementia symptoms. When this occurs, dementia symptoms may improve with treatment.

Progressive dementias

Dementias that are progressive get worse over time. Types of dementias that worsen and aren't reversible include:

Alzheimer's disease. This is the most common cause of dementia.

Although not all causes of Alzheimer's disease are known, experts do know that a small percentage are related to changes in three genes. These gene changes can be passed down from parent to child. While several genes are probably involved in Alzheimer's disease, one important gene that increases risk is apolipoprotein E4 ( APOE ).

People with Alzheimer's disease have plaques and tangles in their brains. Plaques are clumps of a protein called beta-amyloid. Tangles are fibrous masses made up of tau protein. It's thought that these clumps damage healthy brain cells and the fibers connecting them.

Vascular dementia. This type of dementia is caused by damage to the vessels that supply blood to the brain. Blood vessel problems can cause stroke or affect the brain in other ways, such as by damaging the fibers in the white matter of the brain.

The most common symptoms of vascular dementia include problems with problem-solving, slowed thinking, and loss of focus and organization. These tend to be more noticeable than memory loss.

Lewy body dementia. Lewy bodies are balloonlike clumps of protein. They have been found in the brains of people with Lewy body dementia, Alzheimer's disease and Parkinson's disease. Lewy body dementia is one of the more common types of dementia.

Common symptoms include acting out dreams in sleep and seeing things that aren't there, known as visual hallucinations. Symptoms also include problems with focus and attention. Other signs include uncoordinated or slow movement, tremors, and stiffness, known as parkinsonism.

• Frontotemporal dementia. This is a group of diseases characterized by the breakdown of nerve cells and their connections in the frontal and temporal lobes of the brain. These areas are associated with personality, behavior and language. Common symptoms affect behavior, personality, thinking, judgment, language and movement.
• Mixed dementia. Autopsy studies of the brains of people age 80 and older who had dementia indicate that many had a combination of several causes. People with mixed dementia can have Alzheimer's disease, vascular dementia and Lewy body dementia. Studies are ongoing to determine how having mixed dementia affects symptoms and treatments.

Other disorders linked to dementia

• Huntington's disease. Huntington's disease is caused by a genetic change. The disease causes certain nerve cells in the brain and spinal cord to waste away. Symptoms include a decline in thinking skills, known as cognitive skills. Symptoms usually appear around age 30 or 40.

Traumatic brain injury (TBI). This condition is most often caused by repetitive head trauma. Boxers, football players or soldiers might develop TBI .

Dementia symptoms depend on the part of the brain that's injured. TBI can cause depression, explosiveness, memory loss and impaired speech. TBI also may cause slow movement, tremors and stiffness. Symptoms might not appear until years after the trauma.

Creutzfeldt-Jakob disease. This rare brain disorder usually occurs in people without known risk factors. This condition might be due to deposits of infectious proteins called prions. Symptoms of this fatal condition usually appear after age 60.

Creutzfeldt-Jakob disease usually has no known cause but it can be passed down from a parent. It also may be caused by exposure to diseased brain or nervous system tissue, such as from a cornea transplant.

• Parkinson's disease. Many people with Parkinson's disease eventually develop dementia symptoms. When this happens, it's known as Parkinson's disease dementia.

Dementia-like conditions that can be reversed

Some causes of dementia-like symptoms can be reversed with treatment. They include:

• Infections and immune disorders. Dementia-like symptoms can result from a fever or other side effects of the body's attempt to fight off an infection. Multiple sclerosis and other conditions caused by the body's immune system attacking nerve cells also can cause dementia.
• Metabolic or endocrine problems. People with thyroid problems and low blood sugar can develop dementia-like symptoms or other personality changes. This also is true for people who have too little or too much sodium or calcium, or problems absorbing vitamin B-12.
• Low levels of certain nutrients. Not getting enough of certain vitamins or minerals in your diet can cause dementia symptoms. This includes not getting enough thiamin, also known as vitamin B-1, which is common in people with alcohol use disorder. It also includes not getting enough vitamin B-6, vitamin B-12, copper or vitamin E. Not drinking enough liquids, leading to dehydration, also can cause dementia symptoms.
• Medicine side effects. Side effects of medicines, a reaction to a medicine or an interaction of several medicines can cause dementia-like symptoms.
• Subdural bleeding. Bleeding between the surface of the brain and the covering over the brain can be common in older adults after a fall. Subdural bleeding can cause symptoms similar to those of dementia.
• Brain tumors. Rarely, dementia can result from damage caused by a brain tumor.
• Normal-pressure hydrocephalus. This condition is a buildup of fluid in the cavities in the brain known as ventricles. It can result in walking problems, loss of bladder control and memory loss.

Risk factors

Many factors can eventually contribute to dementia. Some factors, such as age, can't be changed. You can address other factors to reduce your risk.

Risk factors that can't be changed

• Age. The risk of dementia rises as you age, especially after age 65. However, dementia isn't a typical part of aging. Dementia also can occur in younger people.
• Family history. Having a family history of dementia puts you at greater risk of developing the condition. However, many people with a family history never develop symptoms, and many people without a family history do. There are tests to determine whether you have certain genetic changes that may increase your risk.
• Down syndrome. By middle age, many people with Down syndrome develop early-onset Alzheimer's disease.

Risk factors you can change

You might be able to control the following risk factors for dementia.

• Diet and exercise. Research has found that people at higher risk of dementia who followed a healthy lifestyle lowered their risk of cognitive decline. They ate a diet that included fish, fruits, vegetables and oils. They also exercised, had cognitive training and participated in social activities. While no specific diet is known to reduce dementia risk, research indicates that those who follow a Mediterranean style diet rich in produce, whole grains, nuts and seeds have better cognitive function.
• Drinking too much alcohol. Drinking large amounts of alcohol has long been known to cause brain changes. Several large studies and reviews found that alcohol use disorders were linked to an increased risk of dementia, particularly early-onset dementia.
• Cardiovascular risk factors. These include obesity, high blood pressure, high cholesterol, and the buildup of fats in the artery walls, known as atherosclerosis. Diabetes and smoking also are cardiovascular risk factors. Having diabetes can increase the risk of dementia, especially if it's poorly controlled. Smoking might increase the risk of developing dementia and blood vessel disease.
• Depression. Although not yet well understood, late-life depression might indicate the development of dementia.
• Air pollution. Studies in animals have indicated that air pollution particulates can speed degeneration of the nervous system. And human studies have found that air pollution exposure — particularly from traffic exhaust and burning wood — is associated with greater dementia risk.
• Head trauma. People who've had a severe head trauma have a greater risk of Alzheimer's disease. Several large studies found that in people age 50 years or older who had a traumatic brain injury (TBI), the risk of dementia and Alzheimer's disease increased. The risk increases in people with more-severe and multiple TBIs . Some studies indicate that the risk may be greatest within the first six months to two years after the TBI .
• Sleep problems. People who have sleep apnea and other sleep disturbances might be at higher risk of developing dementia.
• Low levels of certain vitamins and nutrients. Low levels of vitamin D, vitamin B-6, vitamin B-12 and folate can increase the risk of dementia.

Medicines that can worsen memory. These include sleep aids that contain diphenhydramine (Benadryl) and medicines to treat urinary urgency such as oxybutynin (Ditropan XL).

Also limit sedatives and sleeping tablets. Talk to a health care professional about whether any of the medicines you take might make your memory worse.

Complications

Dementia can affect many body systems and, therefore, the ability to function. Dementia can lead to:

• Poor nutrition. Many people with dementia eventually reduce or stop eating, affecting their nutrient intake. Ultimately, they may be unable to chew and swallow.
• Pneumonia. Trouble swallowing increases the risk of choking. And food or liquids can enter the lungs, known as aspiration. This can block breathing and cause pneumonia.
• Inability to perform self-care tasks. As dementia gets worse, people have a hard time bathing, dressing, and brushing their hair or teeth. They need help using the toilet and taking medicines as directed.
• Personal safety challenges. Some day-to-day situations can present safety issues for people with dementia. These include driving, cooking, and walking and living alone.
• Death. Coma and death can occur in late-stage dementia. This often happens because of an infection.

There's no sure way to prevent dementia, but there are steps you can take that might help. More research is needed, but it might be beneficial to do the following:

• Keep your mind active. Mentally stimulating activities might delay the onset of dementia and decrease its effects. Spend time reading, solving puzzles and playing word games.
• Be physically and socially active. Physical activity and social interaction might delay the onset of dementia and reduce its symptoms. Aim for 150 minutes of exercise a week.
• Quit smoking. Some studies have shown that smoking in middle age and beyond might increase the risk of dementia and blood vessel conditions. Quitting smoking might reduce the risk and improve health.

Get enough vitamins. Some research suggests that people with low levels of vitamin D in their blood are more likely to develop Alzheimer's disease and other forms of dementia. You can increase your vitamin D levels with certain foods, supplements and sun exposure.

More study is needed before an increase in vitamin D intake is recommended for preventing dementia. But it's a good idea to make sure you get adequate vitamin D. Taking a daily B-complex vitamin and vitamin C also might help.

Manage cardiovascular risk factors. Treat high blood pressure, high cholesterol and diabetes. Lose weight if you're overweight.

High blood pressure might lead to a higher risk of some types of dementia. More research is needed to determine whether treating high blood pressure may reduce the risk of dementia.

• Treat health conditions. See your doctor for treatment of depression or anxiety.
• Maintain a healthy diet. A diet such as the Mediterranean diet might promote health and lower the risk of developing dementia. A Mediterranean diet is rich in fruits, vegetables, whole grains and omega-3 fatty acids, which are commonly found in certain fish and nuts. This type of diet also improves cardiovascular health, which also may help lower dementia risk.
• Get good-quality sleep. Practice good sleep hygiene. Talk to a health care professional if you snore loudly or have periods where you stop breathing or gasp during sleep.
• Treat hearing problems. People with hearing loss have a greater chance of developing problems with thinking, known as cognitive decline. Early treatment of hearing loss, such as use of hearing aids, might help decrease the risk.

Dementia care at Mayo Clinic

• What is dementia? Alzheimer's Association. https://www.alz.org/alzheimers-dementia/what-is-dementia. Accessed April 24, 2023.
• Dementias. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Hope-Through-Research/Dementia-Hope-Through-Research. Accessed April 24, 2023.
• Larson EB. Evaluation of cognitive impairment and dementia. https://www.uptodate.com/contents/search. Accessed April 24, 2023.
• Rao RV, et al. Rationale for multi-factorial approach for the reversal of cognitive decline in Alzheimer's disease and MCI: A review. International Journal of Molecular Sciences. 2023; doi:10.3390/ijms24021659.
• Press D, et al. Management of the patient with dementia. https://www.uptodate.com/contents/search. Accessed April 24, 2023.
• Livingston G, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet. 2020; doi:10.1016/S0140-6736(20)30367-6.
• Luo G, et al. Effectiveness of non-pharmacological therapies on cognitive function in patients with dementia — A network meta-analysis of randomized controlled trials. Frontiers in Aging: Neuroscience. 2023; doi:10.3389/fnagi.2023.1131744.
• Creutzfeldt-Jakob disease, classic (CJD): Occurrence and transmission. Centers for Disease Control and Prevention. https://www.cdc.gov/prions/cjd/occurrence-transmission.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fprions%2Fcjd%2Foccurance-transmisison.html. Accessed April 24, 2023.
• Palimariciuc M, et al. The quest for neurodegenerative disease treatment — Focusing on Alzheimer's disease personalised diets. Current Issues in Molecular Biology. 2023; doi:10.3390/cimb45020098.
• Dementia. Merck Manual Professional Version. https://www.merckmanuals.com/professional/neurologic-disorders/delirium-and-dementia/dementia. Accessed April 24, 2023.
• Press D, et al. Prevention of dementia. https://www.uptodate.com/contents/search. Accessed April 24, 2023.
• Sleep issues and sundowning. Alzheimer's Association. https://www.alz.org/help-support/caregiving/stages-behaviors/sleep-issues-sundowning. Accessed May 2, 2023.
• Medications for memory. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/treatments/medications-for-memory. Accessed April 24, 2023.
• How to communicate with a person with dementia. Alzheimer's Society. https://www.alzheimers.org.uk/about-dementia/symptoms-and-diagnosis/symptoms/tips-for-communicating-dementia. Accessed April 24, 2023.
• Press D, et al. Management of neuropsychiatric symptoms of dementia. https://www.uptodate.com/search/contents. Accessed May 2, 2023.
• Leqembi (approval letter). Biologic License Application 761269. U.S. Food and Drug Administration. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=761269. Accessed July 7, 2023.
• Lecanemab approved for treatment of early Alzheimer's disease. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/treatments/lecanemab-leqembi. Accessed May 4, 2023.
• Van Dyck CH, et al. Lecanemab in early Alzheimer's disease. New England Journal of Medicine. 2023; doi:10.1056/NEJMoa2212948.
• Shi M, et al. Impact of anti-amyloid-β monoclonal antibodies on the pathology and clinical profile of Alzheimer's disease: A focus on aducanumab and lecanemab. Frontiers in Aging and Neuroscience. 2022; doi:10.3389/fnagi.2022.870517.
• Cummings J, et al. Alzheimer's disease drug development pipeline: 2022. Alzheimer's and Dementia. 2022; doi:10.1002/trc2.12295.
• Oxybutynin oral. Facts & Comparisons eAnswers. https://fco.factsandcomparisons.com. Accessed April 28, 2023.
• Diphenhydramine oral. Facts & Comparisons eAnswers. https://fco.factsandcomparisons.com. Accessed April 28, 2023.
• Rashad A, et al. Donanemab for Alzheimer's disease: A systematic review of clinical trials. Healthcare. 2022; doi:10.3390/healthcare11010032.
• Budson AE, et al. Cholinesterase inhibitors. In: Memory Loss, Alzheimer's Disease, and Dementia. 3rd ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed May 4, 2023.
• Leqembi (prescribing information). Eisai; 2023. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&varApplNo=761269. Accessed July 10, 2023.
• Mintun MA, et al. Donanemab in early Alzheimer's disease. New England Journal of Medicine. 2021; doi:10.1056/NEJMoa2100708.
• Graff-Radford J (expert opinion). Mayo Clinic. May 15, 2023.
• Ami TR. Allscripts EPSi. Mayo Clinic. May 17, 2023.
• Kisunla (approval letter). Biologic License Application 761248. U.S. Food and Drug Administration. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=BasicSearch.process. Accessed July 9, 2024.
• Sims JR, et al. Donanemab in early symptomatic Alzheimer disease: The TRAILBLAZER-ALZ 2 randomized clinical trial. JAMA. 2023; doi:10.1001/jama.2023.13239.
• Kisunla (prescribing information). Eli Lilly and Company; 2024. https://www.lilly.com/. Accessed July 3, 2024.
• Limbic-predominant age-related TDP-43 encephalopathy (LATE)

Associated Procedures

• Complete blood count (CBC)
• EEG (electroencephalogram)

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Dementia: The Basics

Mar 15, 2019

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Dementia: The Basics. What is dementia? What are the types of dementia? What are the stages? Treatment?. Normal Aging…or Symptoms of Mental Illness …or an Age-Related Disease Process?. There are widespread misconceptions about what happens to us cognitively as we age.

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Presentation Transcript

Dementia: The Basics What is dementia? What are the types of dementia? What are the stages? Treatment?

Normal Aging…or Symptoms of Mental Illness …or anAge-Related Disease Process? • There are widespread misconceptions about what happens to us cognitively as we age. • We have all heard that forgetfulness is an inevitable consequence of aging –but the facts do not support this, and this myth exerts a powerful bias on the views of lay people as well as those of us in health care. • Memory function as measured by delayed recall of newly learned information is not substantially decreased for most people as they age. Older persons do experience a decline in processing speed and rote memory. However, in regard to information that they are allowed sufficient time to acquire, older persons experience no more memory loss over time of newly learned material than do young people. Numerous studies document that aging in and of itself does not degrade memory; disease does.

Normal Aging…or Symptoms of Mental Illness …or anAge-Related Disease Process? • It is true that memory function fails in everyone, of every age, every day. Because memory failures are so common, it is easy for observers to overlook genuine memory lapses in developing dementia. • Conversely normal memory failures can mislead persons with normal brain function into thinking that they are developing a dementia such as Alzheimer ’s disease. • Additionally, other problems such as depression and anxiety which are common in elders can also cause memory and other cognitive deficits mimicking dementia, and often incorrectly diagnosed as Alzheimer’s dementia.

Dementia vsDelirium vsDepressionvsMild Cognitive Impairment • Other problems such as depression and anxiety which are common in elders can also cause memory and other cognitive deficits mimicking dementia, and often incorrectly diagnosed as Alzheimer’s dementia. • Physical changes, acute medical illness such as urinary infection can result in cognitive changes that mimic dementia but may be better understood and need to be evaluated for delirium. • Mild cognitive impairments are sometimes present and do not necessarily indicate presence of dementia process.

Dementia Defined • Dementia is a permanent and progressive loss in the ability to make new memories and general cognitive decline ultimately resulting in death. There are many types of dementia with varying causes such as Alzheimer’s disease, HIV, cardio-vascular disease, Parkinson’s disease, to name just a few. • Diagnosis of Dementia requires: a significant memory impairmentand a significant impairment in another cognitive domain. Cognitive Domains : • Inability to learn, retain, and retrieve newly acquired information (memory) • Inability to comprehend and express verbal information (language) • Inability to manipulate and synthesize nonverbal, geographic, or graphic information / or inability to carry out motor activities despite intact motor functioning (psycho-motor functioning) • Inability to perform abstract reasoning, solve problems, plan for future events, mentally manipulate more than one idea at a time, maintain mental focus in the face of distraction, or shift mental effort easily (executive functioning)

Delirium • Delirium is an acute decline in mental status that can be resolved and is primarily a disturbance of consciousness, with change in cognition (memory deficit, disorientation, language disturbance) or perceptual disturbance that is the direct physiological consequence of a medical condition. Delirium should be considered any time there is an acute change in mental status. • Abrupt onset (hours to days) • Fluctuating level of consciousness (altered sleep/wake cycle) • Perceptual disturbances (hallucinations, sensory misinterpretations) • Disordered thoughts • Disorientation, memory impairment, inattention, decreased concentration and attention • Changes in psychomotor activity

Delirium continued… • Delirium is a medical emergency which may indicate a serious medical illness. • Treatment of delirium consists of correcting the underlying cause and treatment of symptoms. Risk factors for delirium include: increasing age, pre-existing cognitive impairment and polypharmacy (especially Rx with a high anti-cholinergic load). • Suspect delirium if psychosis is suddenly present in a resident who previously did not have psychotic symptoms.

Mild Cognitive Impairment • MCI is a decline in at least 1 cognitive domain that is noticeable, but not significant enough to warrant a diagnosis of dementia. • People with MCI typically function independently in their daily affairs. • The most frequently encountered MCI is the amnesic type defined as subjective and objective memory impairment with the other cognitive functions and activities of daily living preserved. • While in many instances people with MCI demonstrate progressive decline ultimately being diagnosed with dementia, many do not progress to such severity.

Depression (Pseudo-Dementia) • Pseudo-dementia is not a discreet diagnostic category; rather it represents a constellation of symptoms that mimic the cognitive impairment normally associated with dementia (especially memory and executive functioning deficits). • Some reports suggest that as many as 20%-50% of elderly patients are misdiagnosed with degenerative dementia when they are instead experiencing cognitive decline associate with another psychiatric disorder usually depression. • The highest rates of depression are found among nursing home populations. Symptoms of depression can be found in 44%-68% of nursing home residents. Rate of Major Depression among nursing home residents is 9%-38%. Depressed patients have higher risks of morbidity and mortality.

Types of Dementia • Alzheimer’s Dementia: Alzheimer's disease is the underlying cause of -- of all dementia cases. Research indicates that the disease is associated with plaques and tangles in the brain. Alzheimer’s dementia tends to be slow and is always progressive, although some cases are more aggressive. • Vascular Dementia: The second most common form of dementia, vascular dementia is caused by poor blood flow to the brain, which deprives brain cells of the nutrients and oxygen they need to function normally. One of the ten dementia types, vascular dementia can result from any number of conditions which narrow the blood vessels, including stroke, diabetes and hypertension. • Mixed Dementia: Sometimes dementia is caused by more than one medical condition. This is called mixed dementia. The most common form of mixed dementia is caused by both Alzheimer's and vascular disease.

Types of Dementia continued… • Dementia with Lewy Bodies: Parkinson’s Disease can lead to is one type of dementia with Lewy Body involvement. Sometimes referred to as Lewy Body Disease, this type of dementia is characterized by abnormal protein deposits called Lewy bodies, which appear in nerve cells in the brain stem. These deposits disrupt the brain's normal functioning, impairing cognition and behavior and can also cause tremors. • Frontotemporal Dementia: Pick’s Disease is one type of frontal lobe dementia., it is a rare disorder which causes damage to brain cells in the frontal and temporal lobes. Pick's disease affects the individual's personality significantly, usually resulting in a decline in social skills, coupled with emotional apathy. Unlike other types of dementia, Pick's disease typically results in behavior and personality changes manifesting before memory loss and speech problems. • Creutzfeldt-Jacob Dementia: CJD is a degenerative neurological disorder, which is also known as mad cow disease. The incidence is very low, occurring in about one in one million people. There is no cure. Caused by viruses that interfere with the brain's normal functioning, dementia due to CJD progresses rapidly, usually over a period of several months. Symptoms include memory loss, speech impairment, confusion, muscle stiffness and twitching, and general lack of coordination, making the individual susceptible to falls. Occasionally, blurred vision and hallucinations are also associated with the condition.

Types of Dementia continued… • Wernicke-Korsakoff Syndrome: Wernicke-Korsakoff syndrome is caused by a deficiency in thiamine (Vitamin B1) and often occurs in alcoholics, although it can also result from malnutrition, cancer which have spread in the body, abnormally high thyroid hormone levels, long-term dialysis and long-term diuretic therapy (used to treat congestive heart failure). The symptoms of dementia caused by Wernicke-Korsakoff syndrome include confusion, permanent gaps in memory, and impaired short-term memory. Hallucinations may also occur. • Huntington's Disease: Huntington's disease is an inherited progressive dementia that affects the individual's cognition, behavior and movement. The cognitive and behavioral symptoms of dementia due to Huntington's include memory problems, impaired judgment, mood swings, depression and speech problems (especially slurred speech). Delusions and hallucinations may occur. In addition, the individual may experience difficulty ambulating, and uncontrollable jerking movements of the face and body. • Others: There are other types of dementia but those noted above are some of the most well known. Comprehensive evaluation is often needed for proper differential diagnosis of cognitive decline.

Course & Progression • The various types of dementia have varying rates of progression and course. For example, the rate of progression for vascular dementia is highly variable depending on re-occurring cerebral-vascular events, and the progression is step-wise. • Alzheimer’s type dementia tends to have a slow and progressive course and the stages tend to be demarcated by a regular constellations of symptoms. However, even though the stages in Alzheimer’s dementia tend to follow a fairly regular course the effect on each individual is idiosyncratic and while many patients with Alzheimer’s will show significant problems with mental calculations by the middle stages, many will not especially if math was always a strength for them. Thus, testing is required for accurate differential diagnosis.

Stages of Alzheimer’s Dementia Early Stages: mild cognitive decline • The person may feel as if he or she is having memory lapses such as forgetting familiar words or the location of everyday objects. Alternatively, they may have no awareness of changes, but friends, family or co-workers begin to notice difficulties. During a detailed medical interview, doctors may be able to detect problems in memory or concentration. • Common difficulties include: • Noticeable problems coming up with the right word or name • Trouble remembering names when introduced to new people • Having noticeably greater difficulty performing tasks in social or work settings Forgetting material that one has just read • Losing or misplacing a valuable object • Increasing trouble with planning or organizing • May demonstrate some spatial disorientation

Stages of Alzheimer’s Dementia Middle Stages: moderate cognitive decline • At this point, cognitive changes are more overt., and at times personality changes may also become evident. Individuals in the middle stages will begin needing help with activities of daily living. • Common difficulties include: • Impaired ability to perform challenging mental arithmetic — for example, counting backward from 100 by 7s • Greater difficulty performing complex tasks, such as planning dinner for guests, paying bills or managing finances • Memory impairments become more obvious, and some forgetfulness about one's own personal history may be observed • Becoming moody or withdrawn, especially in socially or mentally challenging situations • Confusion about where they are or what day it is • Hygiene and personal grooming may decline • Important autobiographical memories are generally still intact. Need help handling details of toileting (for example, flushing the toilet, wiping or disposing of tissue properly)

Stages of Alzheimer’s Dementia Late Stages: severe cognitive decline • Memory continues to worsen, personality changes may take place or worsen, individuals need extensive help with daily activities. • Difficulties Include: • Lose awareness of recent experiences as well as of their surroundings • Remember their own name, but have difficulty remembering their personal history • Distinguish familiar and unfamiliar faces but have trouble remembering the name of a spouse or caregiver • Need help dressing properly and may, without supervision, make mistakes such as putting pajamas over daytime clothes or shoes on the wrong feet • Experience major changes in sleep patterns — sleeping during the day and becoming restless at night • Have increasingly frequent trouble controlling their bladder or bowels • Experience major personality and behavioral changes, including suspiciousness and delusions (such as believing that their caregiver is an impostor)or compulsive, repetitive behavior like hand-wringing or tissue shredding

Stages of Alzheimer’s Dementia • In the final stage of this disease, individuals lose the ability to respond to their environment, to carry on a conversation and, eventually, to control movement. They may still say words or phrases. At this stage, individuals need help with much of their daily personal care, including eating or using the toilet. They may also lose the ability to smile, to sit without support and to hold their heads up. Reflexes become abnormal. Muscles grow rigid. Swallowing can be impaired.

Treatment • Effective treatment for dementia, regardless of the type, is dependent on proper diagnosis, good understanding of cognitive and adaptive functioning, and management of physical health. • Research is clear that the best treatment for patients with dementia includes a combination of psychotherapy, medical management, occupational and physical therapy, and recreation. • The specific type of psychotherapy should be determined by idiosyncratic needs and functioning of each patient but can include, talk therapy, cognitive-behavioral treatment, behavioral treatment aimed at assessing and managing environmental factors, narrative therapy, supportive treatment, and family therapy. • Medical management includes managing physical and health related issues as well as psychopharmacological management of psychiatric symptoms associated with dementia.

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• Understanding Alzheimer's Disease

Understanding Alzheimer's Disease

What is Alzheimer's disease?

Alzheimer's disease is a brain disease that slowly destroys memory and thinking skills. It is a progressive disease, which means it gets worse over time.

Alzheimer's disease is irreversible. People with Alzheimer's eventually lose the ability to carry out the simplest of tasks.

Alzheimer's is the most common cause of dementia among people aged 65 and older. Dementia is loss of the ability to think and remember things that is severe enough that a person has trouble doing day-to-day activities.

About 5.8 million people in the United States have Alzheimer's disease.

Rarely, people younger than 65 can have Alzheimer's. This is called early-onset Alzheimer's disease . Around one of every 20 people with Alzheimer's have early-onset Alzheimer's disease.

You're more likely to get Alzheimer's if one or more of your close family members – parents, brothers, or sisters – has it.

Common early symptoms of Alzheimer's disease

The most common early symptom of Alzheimer's disease is trouble remembering recent events.

Other early symptoms may include

• Having trouble completing daily tasks, and
• Getting lost when driving on a route the person used to know well

These symptoms are not the same as normal forgetfulness, which can happen to all of us as we get older. For example, if you sometimes forget about an appointment, forget a person's name, or misplace your keys, it doesn't mean you have Alzheimer's.

Symptoms of mild Alzheimer's disease

A person with mild Alzheimer's disease may

• Need help with usual tasks (like managing finances, planning meals, and keeping appointments)
• Have trouble sleeping, and
• Become anxious or depressed.

Symptoms of moderate Alzheimer's disease – When Alzheimer's disease worsens

As symptoms of Alzheimer's disease get worse, a person may

• Have some trouble recognizing family members and friends.
• Need help with daily activities like getting dressed.
• Become fearful or suspicious of other people.
• Believe they are seeing or hearing things that aren't real.

Symptoms of severe Alzheimer's disease – When Alzheimer's disease becomes severe

When Alzheimer's disease becomes severe , a person loses much of their ability to communicate and needs full-time help to take care of themselves.

What causes Alzheimer's disease?

Doctors don't fully understand what causes Alzheimer's disease in most people.

Most people with Alzheimer's disease are older, but just getting older doesn't cause the disease. Many people live well into their 90s without getting Alzheimer's disease.

What causes Alzheimer's disease? – Genes associated with Alzheimer's disease

Carrying a variant of a gene known as APOE increases a person's risk for Alzheimer's disease, especially the late-onset form of the disease. But not everyone who has this gene gets the disease, and people who don't have the gene can still get the disease.  

Early-onset Alzheimer's disease can also be caused by an inherited change in one of three other genes, yet these genes are very uncommon.

What causes Alzheimer's disease? – Conditions that may increase risk for Alzheimer's disease

Other conditions that may increase risk for Alzheimer's disease include

• High blood pressure
• An unhealthy diet

What happens in the brain in Alzheimer's disease?

Doctors now know that changes begin happening in the brain 10-20 years or more before a person with Alzheimer's disease shows any symptoms.

Neurons are brain cells that send and receive signals to and from the brain. Everything we do as living beings – walking, thinking, forming memories – happens because of these signals. A healthy adult brain contains about 100 billion neurons.

When a person has Alzheimer's disease, tiny pieces of a protein called beta amyloid build up in between neurons, forming clusters, or plaques .

Another protein, called tau , builds up inside neurons, forming dense, thread-like tangles .

Together, these plaques and tangles block neurons from sending and receiving signals .

Because of these and other abnormal changes in the brain, neurons start to die. The first place this happens is in the parts of the brain where memories are formed.

As more neurons die, the brain starts to shrink. As Alzheimer's gets worse over time, the brain may shrink to about a third of its normal size.

What is mixed dementia?

Mixed dementia is dementia that's caused by brain changes due to Alzheimer's disease and one or more other brain diseases.

For example, a person may have dementia that's caused by both Alzheimer's disease and Parkinson's disease.

What is vascular dementia?

A person may also have both Alzheimer's disease and vascular dementia . This type of dementia occurs when the brain gets less blood than it needs. This can happen after a person has had a series of small strokes.

Can Alzheimer's disease be prevented?

Studies show there are steps you can take to reduce your risk for Alzheimer's disease.

• Don't smoke.
• Keep your body and your mind active.
• Stay in touch with family and friends.
• Eat a healthy diet.
• Maintain a healthy weight.
• Control high blood pressure.
• Drink alcohol in moderation.
• Drink coffee in moderation.

Recent studies suggest that getting vaccinated against pneumonia and the flu can also help lower your risk for Alzheimer's disease.

• National Institute on Aging. Alzheimer's Disease Fact Sheet. https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet. Reviewed 5/22/2019.
• National Institute of Neurological Disorders and Stroke. Alzheimer's Disease Information Page. Definition. https://www.ninds.nih.gov/Disorders/All-Disorders/Alzheimers-Disease-Information-Page. Last modified 3/27/2019.
• Alzheimer's Association. 2020 Alzheimer's Disease Facts and Figures. https://www.alz.org/media/Documents/alzheimers-facts-and-figures.pdf.
• Zhu XC, Tan L, Wang HF, et al. Rate of early onset Alzheimer's disease: a systematic review and meta-analysis. Ann Transl Med 2015;3:38.
• National Institute on Aging. Alzheimer's and Hallucinations, Delusions, and Paranoia. https://www.nia.nih.gov/health/alzheimers-and-hallucinations-delusions-and-paranoia. Reviewed 5/17/2017.
• National Institute on Aging. Alzheimer's Disease Genetics Fact Sheet. https://www.nia.nih.gov/health/alzheimers-disease-genetics-fact-sheet. Reviewed 12/24/2019.
• Dementia Care Central. Normal Brain vs. Alzheimer's. https://www.dementiacarecentral.com/video/video-brain-changes/.
• National Institute on Aging. What Do We Know About Diet and Prevention of Alzheimer's Disease? https://www.nia.nih.gov/health/what-do-we-know-about-diet-and-prevention-alzheimers-disease. Reviewed 11/27/2019.
• Livingston G, Sommerlad A, Orgeta V, et al. Dementia prevention, intervention, and care. Lancet. 2017;390(10113):2673-2734. doi:10.1016/S0140-6736(17)31363-6
• The SPRINT MIND Investigators for the SPRINT Research Group. Effect of Intensive vs Standard Blood Pressure Control on Probable Dementia: A Randomized Clinical Trial. JAMA. 2019;321(6):553–561. doi:10.1001/jama.2018.21442
• Neafsey EJ, Collins MA. Moderate alcohol consumption and cognitive risk. Neuropsychiatr Dis Treat. 2011;7:465-484. doi:10.2147/NDT.S23159
• Driscoll I, Shumaker SA, Snively BM, et al. Relationships Between Caffeine Intake and Risk for Probable Dementia or Global Cognitive Impairment: The Women's Health Initiative Memory Study. J Gerontol A Biol Sci Med Sci. 2016;71(12):1596-1602. doi:10.1093/gerona/glw078
• Alzheimer's Association. Flu, Pneumonia Vaccinations Tied to Lower Risk of Alzheimer's Dementia [press release]. 2020 July 27. https://www.alz.org/aaic/releases_2020/vaccines-dementia-risk.asp

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Diagnosis and Management of Dementia: A Review

Zoe arvanitakis.

1 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL.

2 Dept of Neurological Sciences, Rush University Medical Center, Chicago, IL.

Raj C. Shah

3 Dept of Family Medicine, Rush University Medical Center, Chicago, IL.

David A. Bennett

Collection, management, analysis, and interpretation of the data: Dr. Arvanitakis.

Preparation, review, or approval of the manuscript: Drs. Arvanitakis, Shah, and Bennett.

Decision to submit the manuscript for publication: Drs. Arvanitakis and Bennett.

Associated Data

Worldwide, 47 million people live with dementia and, by 2050, the number is expected to increase to 131 million.

Observations

Dementia is an acquired loss of cognition in multiple cognitive domains sufficiently severe to affect social or occupational function. In the US, Alzheimer’s disease (AD) affects 5.8 million people. However, dementia is commonly associated with more than one neuropathology, usually AD with cerebrovascular pathology. Diagnosing dementia requires a history evaluating for cognitive decline and impairment in daily activities, with corroboration from a close friend or family member, in addition to a moderately extended mental status examination by a clinician to delineate impairments in memory, language, attention, visuospatial cognition such as spatial orientation, executive function, and mood. Brief cognitive impairment screening questionnaires can assist in initiating and organizing the cognitive assessment. However, if the assessment is inconclusive (e.g., symptoms present, but normal examination), neuropsychological testing can help with a diagnosis. Physical examination may help identify the etiology of dementia. For example, focal neurologic abnormalities suggest stroke. Brain neuroimaging may demonstrate structural changes including, but not limited to, focal atrophy, infarcts, and tumor, that may not be identified on physical examination. Additional evaluation with cerebrospinal fluid assays or genetic testing should be considered in atypical dementia cases, such as age of onset under 65 years, rapid symptom onset, and/or impairment in multiple cognitive domains but not episodic memory. For treatment, patients benefit from non-pharmacologic approaches, including cognitively engaging activities such as reading, physical exercise such as walking, and socialization such as family gatherings. Pharmacologic approaches can provide modest symptomatic relief. For AD, this includes an acetylcholinesterase inhibitor such as donepezil for mild-to-severe dementia, and memantine (used alone or as an add-on therapy) for moderate-to-severe dementia. Rivastigmine is approved for the symptomatic treatment of Parkinson’s disease dementia.

Conclusions and Relevance

AD currently affects 5.8 million persons in the US, and is a common cause of dementia which is usually accompanied by other neuropathology. Causes of dementia can be diagnosed by medical history, cognitive and physical examination, laboratory testing, and brain imaging. Management should include both non-pharmacologic and pharmacologic approaches.

INTRODUCTION

Dementia is a common public health problem. 1 Worldwide, approximately 47 million people have dementia and this number is expected to increase to 131 million by 2050. 1 Reductions in age-adjusted incidence of dementia have occurred in the United States (US) and other developed countries over the last 20 years, perhaps associated with increasing formal educational attainment. However, without improved treatments or preventive therapy, the adverse consequences of dementia will continue to increase. 2

In the US, the prevalence of dementia is 15% in people older than 68 years. 3 Dementia is most commonly attributed to Alzheimer’s disease (AD), with over five million people currently affected by AD, and 13.8 million are projected to be affected by the year 2050. 4 AD is the 6 th leading cause of death, and the 5 th leading cause among persons older than 65 years. 5 , 6 This review summarizes diagnosis and management of dementia, defined as significant cognitive impairment in two or more cognitive domains.

We conducted a literature search in PubMed, using the search terms “dementia and (diagnosis or management)” in the title field. The following inclusion criteria were applied: a publication date from November 19, 2013 to June 29, 2019; English language; female or male sex; and “aged, 65 + years” (to exclude studies about less common causes of dementia). Original research studies with sample sizes less than 100 persons were excluded.

OBSERVATIONS

The search yielded 200 articles published in the past five and a half years. We excluded 37 studies with fewer than 100 persons, 52 on topics not relevant to this review, 41 about non-US public policy or practice, 20 about caregivers, 7 about pathology, 5 about medical record documentation or coding, and 11 that were not original research. The remaining 27 articles of original research, including 22 observational studies and 5 randomized clinical trials, informed this review.

Risk factors and Neuropathology

Aging is an important risk factor for all-cause dementia. AD affects 5–10% of people older than 65 years, and 50% of those 85 years old. 7 Non-modifiable risk factors for AD include female sex, Black race, Hispanic ethnicity, and genetic factors such as the apolipoprotein E ( APOE) gene. 8 – 13 Modifiable risk factors for all-cause dementia include hypertension and diabetes, diet, and limited cognitive, physical, and social activities. 14 – 18 Pathologically, “mixed dementia” is the most common form of dementia, found in 46% of persons with clinically diagnosed AD, and most commonly consisting of AD neurodegeneration and cerebrovascular disease. 19 Other neurodegenerative pathologies such as Lewy body disease (pathologically confirmed in 17% of cases) and frontotemporal lobar degeneration (in <5% of cases) are less frequent. 19 – 25

Definition and Characterization

Dementia is defined by chronic, acquired loss of two or more cognitive abilities caused by brain disease or injury ( Box 1 ). This definition has been used in clinical practice for decades, although recent changes in the Diagnostic Statistical Manual, 5 th Edition, have moved away from using the term dementia and have recognized that dementia can be present with impairment in a single domain (i.e. by this definition, a patient with a severe expressive aphasia could be classified as having dementia). 26 , 27 Memory requires the recording, storage, and retrieval of information. The most common clinical presentation of AD is a slow onset and gradually progressive loss of memory, typically with inability to learn new information and particularly autobiographical information, such as recent events in ones’ life. This is because AD preferentially affects brain networks involved in episodic memory. Examples of episodic memory loss include forgetting appointments, to pay bills or to take medication. Typically, a person with AD repeats questions and conversations. The memory loss is often accompanied by subjective memory complaints. Difficulty recalling names which are recalled later, is common in aging but is not a typical early sign of dementia. Mild cognitive impairment (MCI) is defined by performance that is lower than normal on objective neuropsychological testing of cognition, but with maintained daily functions (e.g., maintained abilities to function within society such as for daily activities at work, home, and in social settings, and maintained activities of daily living such as for personal care) and therefore not consistent with dementia ( Box 1 ). 28 MCI can be categorized into “amnestic” MCI, in which reduced performance on memory is the key finding, versus “non-amnestic” MCI, in which reduced cognitive performance is in a non-memory domain such as language. MCI can also be characterized into “single domain” versus “multi-domain” MCI, in which multiple cognitive performance measures are impaired. MCI does not always progress to dementia, and a patient’s cognitive status may become normal or fluctuate between MCI, normal cognition, and dementia. Fluctuations in cognition are also present in some conditions including neurodegenerative diseases (such as in early stages of Lewy body disease), cerebrovascular disease (e.g., intermittent small strokes), and psychiatric conditions (e.g., depression, anxiety), and with medications affecting cognition (e.g., opioids), and variability in cognitive test results.

Dementia is a clinical syndrome with variable manifestations ( Table 1 ), which help attribute the cause of dementia and guide management. While research studies have defined a “preclinical” AD, 27 , 29 in clinical care, AD is not diagnosed before symptom onset. Differentiating AD from other causes of dementia is easiest in the early stage of illness, as dementias in the late stage look similar ( Table 2 ). 30 – 34

Manifestations of dementia *

Clinical and pathologic characteristics differentiating select causes of dementia

Because mixed dementia is common, the evaluation focuses on identifying conditions likely to contribute to dementia ( Box 1 and Table 2 ). Cerebrovascular disease is the most frequent co-morbid condition with AD, and evidence of cerebrovascular disease does not reduce the likelihood of AD. However, approximately five percent of people with dementia show evidence of only cerebrovascular disease. After AD, the most common neurodegenerative dementias are Lewy body disease, characterized by chronic REM behavior disorder with early visuospatial impairment and parkinsonism, 21 , 22 , 32 , 33 and frontotemporal dementia, characterized by a behavioral variant (the most common presentation is disinhibition) or less often, a language impairment variant (such as a semantic dementia, in which the meaning of the patient’s speech is unclear; Table 2 ). 23 , 34

Diagnosis and Management

Clinical evaluations, differential diagnosis, and management of dementia most commonly occur in the primary care setting, with appropriate specialist input as needed.

Clinical Evaluation for Diagnosis

The 2014 US Preventive Services Task Force indicated that there was insufficient evidence to evaluate the balance of benefits and harms for universal screening for cognitive impairment using formal screening instruments in community-dwelling adults age 65 years and older. 35 While the Task Force concluded that adequate evidence existed for some screening tools that have sufficiently high sensitivity and specificity for identifying dementia, there is no published evidence of the effect of screening on decision making or planning by patients, clinicians, or caregivers. 35 However, report of memory complaints 36 – 38 or rapidly-progressive cognitive problems over several months may indicate an underlying medical condition that warrants further evaluation with cognitive, laboratory, and other tests. 39 – 40

Evaluation of possible dementia requires a brief medical history and a cognitive and neurologic examination ( Box 2 ). The history remains the most important diagnostic tool and should be obtained from both the patient and a close family member or friend. While some patients complain of forgetfulness, others are unable to recall details of their history and in some instances have anosognosia (i.e., lack of insight into one’s disease). One clue that a patient has a memory problem occurs when the person accompanying them provides the medical history. The history should characterize the nature, magnitude, and course of cognitive changes. The nature refers to the cognitive domains affected. Is there loss of episodic memory (e.g., what the patient did that morning, yesterday, and last week), or language abilities (e.g., word finding difficulties with circumlocutions)? The magnitude refers to the severity: does the cognitive loss affect daily functions, such as the patient’s ability to manage her own affairs (e.g., does she get lost while driving, not pay her bills, forget to take medications)? Is the course with an insidious onset and a slow progression (as in neurodegeneration) or a rapid onset and fluctuating and stepwise progression (as in cerebrovascular disease)? The history should focus on medical conditions that could affect cognition including vascular disease risk factors (such as hypertension and diabetes), existing brain conditions (such as stroke, Parkinson’s Disease, head trauma), and use of medications that can impair cognition (e.g., sleep aids and anxiolytics such as benzodiazepines; analgesics such as codeine containing agents; anticholinergics such as tricyclic antidepressants and bladder antimuscarinics). 41 , 42 A family history might identify young-onset dementia (onset in persons younger than 65 years) in first-degree relatives, suggesting one of the rare inherited genetic forms of dementia.

The cognitive examination identifies the presence, severity, and nature of cognitive impairment (e.g., memory versus language), and should consider cultural, linguistic, educational, and other factors such as anxiety and sleep deprivation. One commonly used screening tool is the Montreal Cognitive Assessment (MoCA; range 0–30, follow-up evaluation to screening recommended if score <24/30). The MoCA requires about 10 minutes to administer and is useful in early detection of cognitive impairment, including MCI with executive dysfunction. 43 The Mini-Mental State Exam was developed more than 4 decades ago. It is less sensitive to the presence of MCI and less thoroughly evaluates the domains of executive function, higher-level language skills, and complex visuospatial processing. 43 – 47

The neurologic examination evaluates for objective evidence of neurocognitive problems such as aphasia, apraxia, and agnosia. Unusual behaviors, such as disinhibition with hyperorality or hypersexuality, suggest a frontotemporal dementia, which comprises a group of uncommon conditions associated with neuronal loss beginning in the frontal and/or temporal regions of the brain while other areas are relatively spared. The examination may demonstrate focal neurologic signs or parkinsonism (e.g., as typically seen in the early stages of Lewy body disease). The routine evaluation also includes physical examination to identify systemic vascular disease and systemic signs which may be pertinent to rarer causes of dementia (e.g., golden-brown eye discoloration [Kayser-Fleischer rings] of Wilson’s disease).

The routine work-up typically includes a limited number of blood tests (e.g., B12 and TSH) and neuroimaging to identify cortical and hippocampal atrophy (as seen in AD), or neuropathology including potentially treatable causes of dementia (e.g., resectable tumor, or normal pressure hydrocephalus which may be shunted), using brain imaging with either MRI or CT ( Box 2 ). 48 – 53 Additional evaluation is sometimes warranted. For example, in highly-educated and highly-functioning individuals, a compelling history of cognitive decline (e.g., no longer able to perform a complex task which could easily be done a year ago, such as filling a tax return or working at a cognitively demanding job such as doctor or lawyer), can suggest dementia despite the presence of “normal” function on a brief, screening cognitive test. In this instance, referral for detailed neuropsychological testing should be considered to assess a broader range of cognitive abilities (e.g., memory, executive function, language, attention, visuospatial abilities) with increased levels of difficulty. 54

If the etiology of dementia is unclear after a brief history and examination, additional history and examination, and select blood, neurologic and medical tests should be considered ( Box 2 ).

Recent biomedical advances have led to additional tests that may be helpful in the differential diagnosis of dementia, in particular disease biomarkers which are still commonly used in research. 55 For a patient whose presentation is not consistent with AD (commonly called “atypical dementia”; see Supplemental Materials , eTable 1 ) and for patients in whom diagnostic certainty is low, clinicians may consider specialist referral and additional testing. Functional neuroimaging 56 such as positron emission tomography (PET) 57 can show changes suggestive of AD, usually asymmetric, bilateral temporal-parietal hypometabolism with routine tracers such as fluorodeoxyglucose (FDG) which has a sensitivity of 91% and a specificity of 85% for AD. 58 – 59 FDG PET, covered by health insurance for suspected frontotemporal dementia, may differentiate this etiology from AD, facilitating diagnosis of this less common cause of dementia. For patients with frontotemporal dementia, FDG PET typically shows decreased, asymmetric frontal lobe hypometabolism in the behavioral variant, and anterior temporal lobe hypometabolism in the language (semantic) variant. 60 Amyloid PET can also be used in patients with cognitive impairment who are evaluated for AD or other causes of cognitive decline. 58 – 59 , 61 In a recent observational, multisite, longitudinal study of Medicare beneficiaries, amyloid PET results were associated with change in management plans in more than 60% of patients, compared to pre-PET scan. Change in management plans consisted of change in AD medication or other medication therapy, and changes in counseling about safety and future planning. 62 However, there is no evidence that PET scan changes clinical outcomes. Functional neuroimaging with tau radioligands are only appropriate for research purposes. 63

Cerebrospinal fluid (CSF) testing may be considered to obtain evidence of AD (low amyloid and high tau levels), other neurodegenerative disease (e.g., elevated protein 14–3-3 for Creutzfeldt-Jakob disease) or other etiologies (e.g., positive cultures in infection, oligoclonal bands in demyelination; improved gait after high volume CSF removal in normal pressure hydrocephalus). 64 – 68 Genetic testing may be reasonable, usually for young patients with a history of first-degree relatives with young-onset dementia (e.g., parents or siblings with dementia in their fourth or fifth decade of life). Rare autosomal dominant forms of dementia (e.g., presenilin gene mutations) warrant genetic counseling to determine whether other family members need to be screened. 69 Assessment for the APOE genotype is not recommended for routine evaluation of AD because most people with AD dementia do not have either the protective ε2 allele or the ε4 allele (associated with increased risk) and, more importantly, because currently, medical management would not be altered by the test results. 8 Additional neurologic work-up, such as for amyotrophic lateral sclerosis and medical work-up, such as for cardiac, metabolic, and other etiologies, may be considered with particular attention to ruling out reversible causes of cognitive impairment such as psychiatric disorders (depression) and thyroid dysfunction (see Supplemental Materials , eTable 2 ). 70

The overall goals are to reduce suffering caused by the cognitive and accompanying symptoms (e.g., in mood and behavior), while delaying progressive cognitive decline. Both non-pharmacologic and pharmacologic approaches are used to achieve the overall goals.

Non-pharmacologic management

For complex manifestations of dementia, referrals to specialists, such as clinician managers (e.g., geriatric nurse practitioners), social workers, occupational or speech therapists, and others may be helpful. Evidence primarily from observational studies and a few randomized controlled trials suggest potential benefits of select non-pharmacologic approaches in dementia ( Box 3 ). Although data demonstrating benefit are limited, they are inexpensive and generally safe. Cognitive training and activities such as reading and playing cognitively engaging games (e.g., chess, bridge) may help maintain cognition and function, as shown in randomized trials. 71 – 73 However, frustration and stress from challenging tasks should be avoided. Music or art therapy, and other experiential approaches, may help maintain cognition or improve quality of life. 74 Because old memories of childhood are preserved the longest, reminiscence therapy, consisting of psychotherapy using the personal history of an individuals’ early-life stories and events, may improve psychological well-being. 75

Physical exercise, both aerobic (e.g., walking, swimming) and non-aerobic/conditioning (e.g., weights), improves cardiovascular health through benefits on blood pressure and stroke risk, and randomized trials suggest these interventions may positively affect cognitive and physical function. 76 – 78 But, not all randomized trials have shown benefits from exercise for cognition. 79 – 80 In a randomized clinical trial, a comprehensive sleep education training program reduced night-time awakenings, total time awake at night, and depressive symptoms over 6 months. 81 Social activities may be beneficial, including participating in birthday parties, holidays, support groups with cognitively impaired individuals, and interacting with trained pets (e.g., dog therapy). Eating a brain-healthy diet (e.g., nuts, berries, leafy greens, fish) or a Mediterranean diet is also suggested. 82 – 85 A randomized clinical trial found that a combined diet, exercise, cognitive training, and vascular risk monitoring intervention improved cognition in people at-risk for cognitive decline. 86 However, patients with moderate-to-severe dementia have difficulty participating in cognitive, physical, and social activities, and activities should be limited when patients can no longer participate safely and productively.

Day care centers and assisted living facilities may also be helpful for either the patient or caregiver, but may not delay nursing home admission. 87 A randomized trial of staff and persons in residential care facilities showed that a clinical protocol for behavioral and psychological symptoms of dementia used by staff, improved patients’ behavioral symptoms and staff stress. 86 In the terminal phase of dementia, palliative care may be helpful.

Clinical attention for the caregiver, often a close relative, is important. While efforts continue to effectively deliver primary care for dementia, 88 caregiver education and interventions may improve outcomes for patients with dementia, and inexpensive and useful information is available (See Supplemental Materials , eTable 3 ). Safety, including for the patient’s mental, physical, and financial well-being, should be monitored by the caregiver, with attention to home safety, such as risk of kitchen fires which may be associated with patient burns. 89 Other home safety measures include controlling medication intake, limiting access to firearms and other weapons, and monitoring for elder abuse. Safety outside the home includes at work, where the caregiver may facilitate the patient cutting back or stopping work, for instance if managing machinery or making decisions regarding a company’s finances. Also, driving may need to be modified, including limiting driving to neighborhood and daytime driving to prevent getting lost. While no single test is associated with better driving safety, driving ability should be re-assessed periodically and cessation recommended based on dementia severity, to prevent accidents and injuries. 90 The caregiver can assist in planning for health care and finances as soon as possible in the course of the illness, to determine advanced directives before late-stage dementia. 91 Educating the family on effective communication with a person with dementia, who eventually develop aphasia, is important. Similarly, family should be educated on promoting psychological health and socially adaptive behaviors (e.g., simple and clear instructions to encourage cooperation with activities to address physical and mental health needs, without inciting agitation or aggression).

Behavioral problems, such as physical aggression, are a main cause of emergency room visits and institutionalization, and are associated with poor outcomes for patients (e.g., psychological and medical complications) and families. 92 , 93 Caregiver interventions may prevent patient institutionalization. For example, the family can learn to recognize fear, frustration, and anger (e.g., yelling, lashing out), and address signs of aggression (e.g., by redirecting the patients’ attention to something they enjoy), potentially preventing negative outcomes. 94

An important consideration for families with a member who has dementia, is the high burden of caregiving. 95 This burden may be physical/medical (e.g., neglect of caregiver’s own health, with potential medical complications), emotional and psychological (stress, burnout, depression), and/or financial. Prevention, early recognition, and treatment of these issues (e.g., referrals to social work for additional support), are integral to an effective management plan. A randomized trial demonstrated that delivering caregiver assistance in-person versus by telephone only, both improved care quality and without differences in effectiveness. 96

Pharmacologic management

Table 3 shows the Food and Drug Administration (FDA) approved drugs for AD dementia. Five drugs, four of which are currently available for prescription, yield modest symptomatic benefit for cognitive symptoms. Acetylcholinesterase inhibitors were the first drugs approved in the US for AD. These drugs inhibit the brain acetylcholinesterase enzyme, thereby promoting relative increases in acetylcholine abundance at the synaptic cleft for cholinergic neurotransmission. In a meta-analysis review of 10 randomized, double blind, placebo controlled trials each with a six month duration of drug exposure, acetylcholinesterase inhibitors were associated with 2.4 points slower decline (95%CI −2.7 to −2.0; p<0.00001) in a research measure of cognition spanning 70 points. 97 This is equivalent to about 6 months of decline from natural history studies of AD dementia, but the magnitude of the clinically relevant benefit is uncertain. 35 Also, modest improvements were observed in activities of daily living and behaviors. The efficacy of anticholinesterase inhibitors is similar among the individual drugs (donepezil, rivastigmine, galantamine). 96 Given the modest benefits and known risks, clinicians should engage in shared decision making regarding the initiation of an acetylcholinesterase inhibitor for the symptomatic treatment of AD dementia. 90

Approved * pharmacologic treatments for dementia attributed to AD

Each drug shown in Table 3 is available for use orally, and one is also available for transdermal use (rivastigmine). A slow titration dosing regimen over 4–8 weeks is recommended to reach the target dose and minimize adverse effects for all of the drugs. Some drugs are used at different maintenance doses depending on effects/adverse effects. For example, donepezil maintenance can be at 5 mg (e.g., if higher dose is associated with poor tolerability), 10mg (typical target), or 23 mg (rarely used), once daily. Despite a slow titration, adverse effects, such as gastrointestinal (e.g., nausea, vomiting, and diarrhea; in about 5 percent of users) may occur ( Table 3 ). Adverse effects may be higher than previously recognized. 98 If encountered, dosage may be lowered (e.g., from 10 mg of donepezil to 5 mg), either temporarily (e.g., days to weeks) before re-escalating more slowly and monitoring for recurrence of adverse effects (family instructed to call clinician if adverse effects). Alternatively, the drug can be discontinued and a different drug can be prescribed even in the same class (another acetylcholinesterase inhibitor), given that adverse effects vary among same-class drugs. 99 Approximately 5 percent of patients discontinue the drug due to adverse effects. If tolerated, annual brief assessments using the history (e.g., progression of cognitive problems, new cognitive problems, functional status) and a brief cognitive test can be used in the absence of new problems. Often, clinicians cannot appreciate a benefit and must rely on caregiver reports. A good response to a drug would result in the caregiver noticing a slight improvement in day-to-day life (e.g., improved ability to function at home). Routine cognitive tests such as the MoCA, 43 can be used to monitor disease course on treatment, and to identify unexpected trends such as rapid decline which would prompt consideration for a medical evaluation (e.g., for systemic infection). However, benefits are typically not seen on such routine tests. Monitoring requires periodic re-evaluation of cognition, function, neuropsychiatric and behavioral symptoms, and medication reconciliation. 100 – 103

As neurodegeneration in AD progresses, further cognitive and functional decline invariably occur, and consideration should be given in the moderate-to-severe stages of dementia for adding memantine ( Table 3 ). Memantine can also be used as a first-line drug, for instance when a patient with moderate dementia presents for a first evaluation but is not taking any medication for cognition. Another use is for patients who cannot tolerate an acetylcholinesterase inhibitor. Adverse effects of memantine include headaches and constipation.

Aside from AD, few other dementia etiologies have approved pharmacologic treatments for cognitive symptoms, and no disease specific treatments exist for Lewy body disease or frontotemporal dementia. In addition to AD, rivastigmine has also received approval for Parkinson disease dementia. There are currently no FDA-approved drugs for MCI, 104 and studies of acetylcholinesterase inhibitors failed to show benefit in this population. 105 At this time, more than 100 drugs are being investigated for dementia and cognition, and include potential disease modifying agents. 106 – 107

Medical management should address common causes of cognitive impairment and dementia, including polypharmacy which affects a third of persons older than 60 years. 108 – 109 Special considerations may be appropriate for patients with medical comorbidities (e.g., kidney dysfunction). Another approach in dementia management is reducing brain ischemia and stroke risk by treating vascular risk factors (hypertension, diabetes, hyperlipidemia) and consideration of the risk-benefit ratio for anti-thrombotics and anticoagulants (if prior stroke or atrial fibrillation are present). A recent randomized clinical trial of dementia prevention showed that intensive blood pressure lowering in persons with hypertension (comparing a target systolic blood pressure below 120mmHg, to a pressure between 120–140mmHg) did not reduce risk of dementia, but did reduce the combined rate of MCI or probable dementia in a post-hoc analysis. 110

Dementia is often accompanied by neuropsychiatric and behavioral problems. About 95% of patients have at least mild symptoms, most commonly apathy (83%) and depression (63%). 111 Approved treatments do not exist for these non-cognitive manifestations in the setting of dementia. For depression, a low dose antidepressant can be tried such as with a selective serotonin-reuptake inhibitor (e.g., escitalopram). Management of agitation and aggression can be challenging. Conventional antipsychotics such as haloperidol, should be avoided. 112 Newer generation “atypical” antipsychotics such as risperidone and quetiapine fumarate, should be avoided if possible, given their association with serious risks, especially in older patients. 113 Specifically, death, cardiac effects such as heart failure, and stroke, have resulted in a black box warning. Therefore, antipsychotics should only be used in controlled environments (e.g., under close medical supervision) and for a limited time only (e.g., a few weeks) when all other non-pharmacologic approaches have failed or the patient’s behavior poses a substantial threat to themselves or others. 112

CONCLUSIONS

AD currently affects 5.8 million persons in the US, and is a common cause of dementia which is usually accompanied by other neuropathology. The cause of dementia can be diagnosed by medical history, cognitive and physical examination, laboratory testing, and brain imaging. Management should include both non-pharmacologic approaches with cognitive, physical, and social activities, and pharmacologic approaches such as with an acetylcholinesterase inhibitor for AD, although efficacy of treatments remains limited.

Supplementary Material

Supplemental material, acknowledgements.

This study was supported by the National Institutes of Health, grant numbers P30 AG010161, R01 AG040039, R01 NS084965, and RF1 AG059621; the Health Resources and Services Administration for HRSA-15-057; and the Illinois Department of Public Health. The study funders had no role in the design or conduct of the study; collection, management, analysis, or interpretation of the data; preparation, review, or approval of the manuscript, or decision to submit the manuscript for publication.

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