FAQs – Alzheimer’s & Dementia

Alzheimer’s disease is a degenerative brain disease and the most common form of dementia. Dementia is not a specific disease. It’s an overall term that describes a group of symptoms.

Vascular dementia often arises as a result of a stroke when blood supply is cut off from the brain, which can kill brain cells. This type of dementia is different from Alzheimer’s disease in that it is caused by brain damage due to compromised blood flow, where Alzheimer’s has a mostly unknown cause. Anyone with a history of vascular complications, including blood clots and strokes, is at risk for vascular dementia, and the risk compounds with each vascular episode.

Lewy Body Dementia (LBD) is a type of progressive dementia that leads to a decline in thinking, reasoning, and independent function because of abnormal microscopic deposits that damage brain

No, dementia is not a single disease; it’s an overall term — like heart disease — that covers a wide range of specific medical conditions, including Alzheimer’s disease. Disorders grouped under the general term “dementia” are caused by abnormal brain changes. These changes trigger a decline in thinking skills, also known as cognitive abilities, severe enough to impair daily life and independent function. They also affect behavior, feelings, and relationships.

Alzheimer’s disease accounts for 60-80% of cases. Vascular dementia, which occurs because of microscopic bleeding and blood vessel blockage in the brain, is the second most common cause of dementia. Those who experience brain changes of multiple types of dementia simultaneously have mixed dementia. There are many other conditions that can cause symptoms of dementia, including some that are reversible, such as thyroid problems and vitamin deficiencies.

Dementia is often incorrectly referred to as “senility” or “senile dementia,” which reflects the formerly widespread but incorrect belief that serious mental decline is a normal part of aging.

1. Memory loss that disrupts daily life:
   forgetting events, repeating yourself, or relying on more aids to help you remember (like sticky notes or reminders).
2. Challenges in planning or solving problems:
   having trouble paying bills or cooking recipes you have used for years.
3. Difficulty completing familiar tasks at home, at work, or at leisure:
   having problems with cooking, driving places, using a cell phone, or shopping.
4. Confusion with time or place:
   having trouble understanding an event that is happening later, or losing track of dates.
5. Trouble understanding visual images and spatial relations:
   having more difficulty with balance or judging distance, tripping over things at home, or spilling or dropping things more often.
6. New problems with words in speaking or writing:
   having trouble following or joining a conversation or struggling to find a word you are looking for (saying “that thing on your wrist that tells time” instead of “watch”).
7. Misplacing things and losing the ability to retrace steps:
   placing car keys in the washer or dryer or not being able to retrace steps to find something.
8. Decreased or poor judgment:
   being a victim of a scam, not managing money well, paying less attention to hygiene, or having trouble taking care of a pet.
9. Withdrawal from work or social activities:
   not wanting to go to church or other activities as you usually do, not being able to follow football games or keep up with what’s happening.
10. Changes in mood and personality:
    getting easily upset in common situations or being fearful or suspicious.

If you notice one or more signs in yourself or another person, it can be difficult to know what to do. It’s natural to feel uncertain or nervous about discussing these changes with others. Voicing worries about your own health might make them seem more “real.” Or, you may fear upsetting someone by sharing observations about changes in his or her abilities or behavior. However, these are significant health concerns that should be evaluated by a doctor, and it’s important to take action to figure out what’s going on.

• Learn more about diagnosing Alzheimer’s
• Doctor’s appointment checklist (PDF)
• 10 warning signs worksheet (PDF)
• Know the 10 Signs: Early Detection Matters (free online course)
• 10 steps to approach memory concerns (PDF)
• Why get checked

s a type of progressive dementia that leads to a decline in thinking, reasoning, and independent function because of abnormal microscopic deposits that damage brain

Most experts estimate that Lewy body dementia may be the third most common cause of dementia after Alzheimer’s disease and vascular dementia, accounting for 5 to 10 percent of cases.

The hallmark brain abnormalities linked to Lewy body dementia are named after Frederich H. Lewy, M.D., the neurologist who discovered them while working in Dr. Alois Alzheimer’s laboratory during the early 1900s. Alpha-synuclein protein, the chief component of Lewy bodies, is found widely in the brain, but its normal function isn’t yet known.

Lewy bodies are also found in other brain disorders, including Alzheimer’s disease and Parkinson’s disease dementia. Many people with Parkinson’s eventually develop problems with thinking and reasoning, and many people with Lewy body dementia experience movement symptoms, such as hunched posture, rigid muscles, a shuffling walk, and trouble initiating movement.

This overlap in symptoms and other evidence suggests that Lewy body dementia, Parkinson’s disease, and Parkinson’s disease dementia may be linked to the same underlying abnormalities in how the brain processes the protein alpha-synuclein. Many people with both Lewy body dementia and Parkinson’s dementia also have plaques and tangles — hallmark brain changes linked to Alzheimer’s disease.

• Changes in thinking and reasoning.
• Confusion and alertness that varies significantly from one time of day to another or from one day to the next.
• Slowness, gait imbalance, and other parkinsonian movement features.
• Well-formed visual hallucinations.
• Delusions.
• Trouble interpreting visual information.
• Sleep disturbances.
• Malfunctions of the “automatic” (autonomic) nervous system.
• Memory loss that may be significant, but less prominent than in Alzheimer’s.

As with other types of dementia, there is no single test that can conclusively diagnose Lewy body dementia. Today, Lewy body dementia is a “clinical” diagnosis, which means it represents a doctor’s best professional judgment about the reason for a person’s symptoms. As with many forms of dementia, the only way to conclusively diagnose Lewy body dementia is through a postmortem autopsy.

• Memory loss tends to be a more prominent symptom in early Alzheimer’s than in early Lewy body dementia, although advanced Lewy body dementia may cause memory problems in addition to its more typical effects on judgment, planning, and visual perception.
• Movement symptoms are more likely to be an important cause of disability early in Lewy body dementia than in Alzheimer’s, although Alzheimer’s can cause problems with walking, balance, and getting around as it progresses to moderate and severe stages.
• Hallucinations, delusions, and misidentification of familiar people are significantly more frequent in early-stage Lewy body dementia than in Alzheimer’s.
• REM sleep disorder is more common in early Lewy body dementia than in Alzheimer’s.
• Disruption of the autonomic nervous system, causing a blood pressure drop on standing, dizziness, falls and urinary incontinence, is much more common in early Lewy body dementia than in Alzheimer’s.

Since Lewy bodies tend to coexist with Alzheimer’s brain changes, it may sometimes be hard to distinguish Lewy body dementia from Alzheimer’s disease, especially in the early stages.

As with other types of dementia, there is no single test that can conclusively diagnose Lewy body dementia. Today, Lewy body dementia is a “clinical” diagnosis, which means it represents a doctor’s best professional judgment about the reason for a person’s symptoms. As with many forms of dementia, the only way to conclusively diagnose Lewy body dementia is through a postmortem autopsy.

The diagnosis is Lewy Body dementia when:

• Dementia symptoms consistent with Lewy body dementia develop first.
• When both dementia symptoms and movement symptoms are present at the time of diagnosis.
• When dementia symptoms appear within one year after movement symptoms.

The diagnosis is Parkinson’s disease dementia when a person is originally diagnosed with Parkinson’s based on movement symptoms, and dementia symptoms don’t appear until a year or more later.

Many experts now believe that Lewy body dementia and Parkinson’s disease dementia are two different expressions of the same underlying problems with brain processing of the protein alpha-synuclein. But most experts recommend continuing to diagnose Lewy body dementia and Parkinson’s dementia as separate disorders.

Vascular dementia often arises as a result of a stroke when blood supply is cut off from the brain, which can kill brain cells. This type of dementia is different from Alzheimer’s disease in that it is caused by brain damage due to compromised blood flow, where Alzheimer’s has a mostly unknown cause. Anyone with a history of vascular complications, including blood clots and strokes, is at risk for vascular dementia, and the risk compounds with each vascular episode.

Vascular contributions to cognitive impairment and dementia (VCID) are conditions arising from stroke and other vascular brain injuries that cause significant changes to memory, thinking, and behavior. Cognition and brain function can be significantly affected by the size, location, and the number of brain injuries.

Two forms of VCID—vascular dementia and vascular cognitive impairment (VCI)—arise as a result of risk factors that similarly increase the risk for cerebrovascular disease (stroke), including atrial fibrillation (a problem with the rhythm of the heartbeat), high blood pressure, diabetes, and high cholesterol.

Multiple small strokes may cause more gradual changes in thinking and behavior, as with each stroke smaller vessels are damaged that eventually lead to an increasing number of damaging blockages to the brain. Memory loss is inevitably the biggest warning sign of vascular dementia, and after experiencing a vascular event like a stroke or blood clot, it is important to keep track of and work to maintain your cognition.

Symptoms that are specific to vascular dementia tend to be more dramatic directly after a stroke, and include:

• Disorientation, confusion, and inability to concentrate
• Trouble with speech, such as being unable to find the right words or pronounce them
• Vision loss and changes in senses like smell and taste
• Classic stroke symptoms like a droopy face, body numbness, or paralysis
• Uncontrollable emotional behavior like laughing or crying
• Uncontrollable body movements like hand grabbing or hitting

Much like Alzheimer’s disease and other dementias, these symptoms can be confused with other problems and need to be discussed with a healthcare professional in order to diagnose. Using blood tests, heart scans, and brain scans, your doctor will be able to help you determine the cause of your memory loss and other symptoms of dementia.

Symptoms of Vascular Cognitive Impairment and Dementia (VCID) can begin suddenly and progress or subside during one’s lifetime. VCID can occur along with Alzheimer’s disease. People with VCID almost always have abnormalities in the brain on magnetic resonance imaging scans. These abnormalities include evidence of prior strokes, often small and asymptomatic, as well as diffuse changes in the brain’s “white matter”—the connecting “wires” of the brain that are critical for relaying messages between brain regions. Microscopic brain examination shows thickening of blood vessel walls called arteriosclerosis and thinning or loss of components of the white matter.

Vascular dementia refers to the progressive loss of memory and other cognitive functions caused by vascular injury or disease within the brain. Symptoms of vascular dementia may sometimes be difficult to distinguish from Alzheimer’s disease. Problems with organization, attention, slowed thinking, and problem-solving are all more prominent in VCID, while memory loss is more prominent in Alzheimer’s.

Vascular cognitive impairment involves changes with language, attention, and the ability to think, reason, and remember that are noticeable but are not significant enough to greatly impact daily life. These changes, caused by vascular injury or disease within the brain, progress slowly over time.

Post-stroke dementia can develop months after a major stroke. Not everyone who has had a major stroke will develop vascular dementia, but the risk for dementia is significantly higher in someone who has had a stroke.

Multi-infarct dementia is the result of many small strokes (infarcts) and mini-strokes. Language or other functions may be impaired, depending on the region of the brain that is affected. The risk for dementia is significantly higher in someone who has had a stroke. Dementia is more likely when strokes affect both sides of the brain. Even strokes that don’t show any noticeable symptoms can increase the risk of dementia.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an extremely rare inherited disorder caused by a thickening of the walls of small- and medium-sized blood vessels, which reduces the flow of blood to the brain. CADASIL is associated with multi-infarct dementia, stroke, and other disorders. The first symptoms can appear in people between ages 20 and 40. CADASIL may have symptoms that can be confused with multiple sclerosis. Many people with CADASIL are undiagnosed.

Subcortical vascular dementia, previously called Binswanger’s disease, involves extensive microscopic damage to the small blood vessels and nerve fibers that make up white matter in the brain. Cognitive changes include problems with short-term memory, organization, attention, decision making, and behavior. Symptoms tend to begin after age 60, and they progress in a stepwise manner. People with subcortical vascular disease often have high blood pressure, a history of stroke, or evidence of disease of the large blood vessels in the neck or heart valves.

Cerebral amyloid angiopathy is a buildup of amyloid plaques in the walls of blood vessels in the brain. It is generally diagnosed when multiple tiny bleeds in the brain are discovered using magnetic resonance imaging.

Vascular dementia is thought to affect in the same way as other forms of dementia. For this reason, AChE inhibitors are among the most common ways to treat dementia symptoms associated with this disorder. To prevent further damage, people at risk of strokes that lead to vascular dementia are often prescribed blood pressure management regimes.

How is VCID Treated?

Vascular contributions to cognitive impairment and dementia (VCID) are often managed with drugs to prevent strokes or reduce the risk of additional brain damage. Some studies suggest that drugs that improve memory in Alzheimer’s might benefit people with early vascular dementia. Treating the modifiable risk factors, such as high blood pressure, can help prevent additional stroke.

For more information about vascular dementia and VCI, see NIA’s list of resources.

Read about this topic in Spanish. Lea sobre este tema en español.

It is common for people with dementia to have mixed dementia—a combination of two or more types of dementia. A number of combinations are possible. For example, some people have both Alzheimer’s disease and vascular dementia.

Some studies indicate that mixed dementia is the most common cause of dementia in the elderly. For example, autopsy studies looking at the brains of people who had dementia indicate that most people age 80 and older probably had mixed dementia caused by a combination of brain changes related to Alzheimer’s disease, vascular disease-related processes, or another neurodegenerative condition. Some studies suggest that mixed vascular-degenerative dementia is the most common cause of dementia in older adults.

In a person with mixed dementia, it may not be clear exactly how many of a person’s symptoms are due to Alzheimer’s or another disease. In one study, researchers who examined older adults’ brains after death found that 78 percent had two or more pathologies (disease characteristics in the brain) related to neurodegeneration or vascular damage. Alzheimer’s was the most common pathology but rarely occurred alone.

Researchers are trying to better understand how underlying disease processes in mixed dementia influence each other. In the study described above, the researchers found that the degree to which Alzheimer’s pathology contributed to cognitive decline varied greatly from person to person. In other words, the impact of any given brain pathology differed dramatically depending on which other pathologies were present.

For more information visit the National Institute of Health’s website

• “What Is Mixed Dementia? Causes and Diagnosis“
• “Vascular Contributions to Cognitive Impairment and Dementia“

Behavioral Symptoms of Frontotemporal Disorders

• Problems with executive functioning—Problems with planning and sequencing (thinking through which steps come first, second, third, and so on), prioritizing (doing more important activities first and less important activities last), multitasking (shifting from one activity to another as needed), and self-monitoring and correcting behavior.
• Perseveration—A tendency to repeat the same activity or to say the same word over and over, even when it no longer makes sense.
• Social disinhibition—Acting impulsively without considering how others perceive the behavior. For example, a person might hum at a business meeting or laugh at a funeral.
• Compulsive eating—Gorging on food, especially starchy foods like bread and cookies, or taking food from other people’s plates.
• Utilization behavior—Difficulty resisting impulses to use or touch objects that one can see and reach. For example, a person picks up the phone while walking past it when the phone is not ringing and the person does not intend to place a call.

Language Symptoms of Frontotemporal Disorders

• Aphasia—A language disorder in which the ability to use or understand words is impaired but the physical ability to speak properly is normal.
• Dysarthria—A language disorder in which the physical ability to speak properly is impaired (e.g., slurring) but the message is normal.

People with PPA may have only problems using and understanding words or also problems with the physical ability to speak. People with both kinds of problems have trouble speaking and writing. They may become mute, or unable to speak. Language problems usually get worse, while other thinking and social skills may remain normal longer before deteriorating.

Emotional Symptoms of Frontotemporal Disorders

• Apathy—A lack of interest, drive, or initiative. Apathy is often confused with depression, but people with apathy may not be sad. They often have trouble starting activities but can participate if others do the planning.
• Emotional changes—Emotions are flat, exaggerated, or improper. Emotions may seem completely disconnected from a situation or are expressed at the wrong times or in the wrong circumstances. For example, a person may laugh at sad news. Pseudobulbar affect, a condition of sudden, frequent outbursts of crying or laughing that cannot be controlled, may occur and is treatable.
• Social-interpersonal changes—Difficulty “reading” social signals, such as facial expressions, and understanding personal relationships. People may lack empathy—the ability to understand how others are feeling—making them seem indifferent, uncaring, or selfish. For example, a person may show no emotional reaction to illnesses or accidents that occur to family members.

Movement Symptoms of Frontotemporal Disorders

• Dystonia—Abnormal postures of body parts such as the hands or feet. A limb may be bent stiffly or not used when performing activities that are normally done with two hands.
• Gait disorder—Abnormalities in walking, such as walking with a shuffle, sometimes with frequent falls.
• Tremor—Shakiness, usually of the hands.
• Clumsiness—Dropping of small objects or difficulty manipulating small items like buttons or screws.
• Apraxia—Loss of ability to make common motions, such as combing one’s hair or using a knife and fork, despite normal strength.
• Neuromuscular weakness—Severe weakness, cramps, and rippling movements in the muscles.

For more information visit the National Institute of Health’s website: “What are the Symptoms of Frontotemporal Disorders?“

 Creutzfeldt-Jakob disease (CJD) is the most common human form of a group of rare, fatal brain disorders known as prion diseases.

Prion diseases, such as Creutzfeldt-Jakob disease, occur when prion protein, which is found throughout the body but whose normal function isn’t yet known, begins folding into an abnormal three-dimensional shape. This shape change gradually triggers prion protein in the brain to fold into the same abnormal shape.

Creutzfeldt-Jakob disease causes a type of dementia that gets worse unusually fast. More common causes of dementia, such as Alzheimer’s, Lewy body dementia, and frontotemporal dementia, typically progress more slowly.

Through a process scientists don’t yet understand, misfolded prion protein destroys brain cells. Resulting damage leads to a rapid decline in thinking and reasoning as well as involuntary muscle movements, confusion, difficulty walking, and mood changes.

Creutzfeldt-Jakob disease is rare, occurring in about one in 1 million people annually worldwide.

Specific Creutzfeldt-Jakob disease symptoms experienced by an individual and the order in which they appear can differ significantly. Some common symptoms include:

• Depression.
• Agitation, apathy, and mood swings.
• Rapidly worsening confusion.
• Disorientation.
• Problems with memory, thinking, planning, and judgment.
• Difficulty walking.
• Muscle stiffness, twitches, and involuntary jerky movements.
• Vision problems, such as double vision and hallucinations

Diagnosis of Cruetzfeldt-Jakob disease

Rapid symptom progression is one of the most important clues that a person may have Creutzfeldt-Jakob disease.

There is no single test — or any combination of tests — that can conclusively diagnose sporadic Creutzfeldt-Jakob disease in a living person, but the following tests may help determine whether an individual has Creutzfeldt-Jakob disease:

• An electroencephalogram (EEG) measures the brain’s patterns of electrical activity similar to the way an electrocardiogram (ECG) measures the heart’s electrical activity.
• Brain magnetic resonance imaging (MRI) can detect certain brain changes consistent with Creutzfeldt-Jakob disease.
• Lumbar puncture (spinal tap) tests spinal fluid for the presence of certain proteins.
• Protein misfolding cyclic amplification (PMCA): PMCA is an amplification technique for the detection of misfolded protein aggregates.

Age has an influence on sporadic CJD, which tends to develop later in life, usually around age 60. The onset of familial CJD occurs slightly earlier and CJD has affected people at a much younger age, usually in their late 20s.

Treatment and outcomes

There is no treatment that can slow or stop the underlying brain cell destruction caused by Creutzfeldt-Jakob disease and other prion diseases. Various drugs have been tested but have not shown any benefit. Clinical studies of potential Creutzfeldt-Jakob disease treatments are complicated by the rarity of the disease and its rapid progression.

Current therapies focus on treating symptoms and on supporting individuals and families coping with Creutzfeldt-Jakob disease. Doctors may prescribe painkillers such as opiates to treat pain if it occurs. Muscle stiffness and twitching may be treated with muscle-relaxing medications or antiseizure drugs. In the later stages of the disease, individuals with Creutzfeldt-Jakob disease become completely dependent on others for their daily needs and comfort.

Creutzfeldt-Jakob disease progresses rapidly. Those affected lose their ability to move or speak and require full-time care to meet their daily needs. An estimated 90 percent of those diagnosed with sporadic Creutzfeldt-Jakob disease die within one year. Those affected by familial Creutzfeldt-Jakob disease tend to develop the disorder at an earlier age and survive somewhat longer than those with the sporadic form, as do those diagnosed with variant Creutzfeldt-Jakob disease. Scientists have not yet learned the reason for these differences in survival.

Resources:

• Creutzfeldt-Jakob Disease Foundation is a nonprofit organization that offers support, information, and guidance to those dealing with Creutzfeldt-Jakob disease. Call the Foundation at 800.659.1991.
• The Alzheimer’s Association can help you learn more about Alzheimer’s and other dementias, and help you find local support services. Call our 24/7 Helpline at 800.272.3900.
• Social Security Administration (SSA) has a “compassionate allowance” program in which workers diagnosed with Creutzfeldt-Jakob disease can qualify for Social Security disability benefits. Call the SSA at 800.772.1213.
• Medline Plus: Creutzfeldt-Jakob disease is a consumer health information service of the U.S. National Library of Medicine and National Institutes of Health (NIH). This gateway page links to resources from NIH agencies, major medical centers, and other sources.