Alzheimer's disease (AD) is the most common form of dementia among older people. Dementia is a brain disorder that seriously affects a person's ability to carry out daily activities.

AD begins slowly. It first involves the parts of the brain that control thought, memory and language. People with AD may have trouble remembering things that happened recently or names of people they know. A related problem, mild cognitive impairment (MCI), causes more memory problems than normal for people of the same age. Many, but not all, people with MCI will develop AD.

In AD, over time, symptoms get worse. People may not recognize family members. They may have trouble speaking, reading or writing. They may forget how to brush their teeth or comb their hair. Later on, they may become anxious or aggressive, or wander away from home. Eventually, they need total care. This can cause great stress for family members who must care for them.

AD usually begins after age 60. The risk goes up as you get older. Your risk is also higher if a family member has had the disease.

No treatment can stop the disease. However, some drugs may help keep symptoms from getting worse for a limited time.

What is Alzheimer’s Disease?

• Alzheimer’s disease is the most common type of dementia.
• It is a progressive disease beginning with mild memory loss and possibly leading to loss of the ability to carry on a conversation and respond to the environment.
• Alzheimer’s disease involves parts of the brain that control thought, memory, and language.
• It can seriously affect a person’s ability to carry out daily activities.

Who has Alzheimer’s Disease?

• In 2020, as many as 5.8 million Americans were living with Alzheimer’s disease.¹
• Younger people may get Alzheimer’s disease, but it is less common.
• The number of people living with the disease doubles every 5 years beyond age 65.
• This number is projected to nearly triple to 14 million people by 2060.¹
• Symptoms of the disease can first appear after age 60, and the risk increases with age.

What is known about Alzheimer’s Disease?

Scientists do not yet fully understand what causes Alzheimer’s disease. There likely is not a single cause but rather several factors that can affect each person differently.

• Age is the best known risk factor for Alzheimer’s disease.
• Family history—researchers believe that genetics may play a role in developing Alzheimer’s disease. However, genes do not equal destiny. A healthy lifestyle may help reduce your risk of developing Alzheimer’s disease. Two large, long term studies indicate that adequate physical activity, a nutritious diet, limited alcohol consumption, and not smoking may help people.
• Changes in the brain can begin years before the first symptoms appear.
• Researchers are studying whether education, diet, and environment play a role in developing Alzheimer’s disease.
• There is growing scientific evidence that healthy behaviors, which have been shown to prevent cancer, diabetes, and heart disease, may also reduce risk for subjective cognitive decline.

What are the warning signs of Alzheimer’s disease?

“Memory Loss is Not a Normal Part of Aging”

Alzheimer’s disease is not a normal part of aging. Memory problems are typically one of the first warning signs of Alzheimer’s disease and related dementias.

In addition to memory problems, someone with symptoms of Alzheimer’s disease may experience one or more of the following:

• Memory loss that disrupts daily life, such as getting lost in a familiar place or repeating questions.
• Trouble handling money and paying bills.
• Difficulty completing familiar tasks at home, at work or at leisure.
• Decreased or poor judgment.
• Misplacing things and being unable to retrace steps to find them.
• Changes in mood, personality, or behavior.

Even if you or someone you know has several or even most of these signs, it doesn’t mean it’s Alzheimer’s disease.

What to do if you suspect Alzheimer’s disease

Getting checked by your healthcare provider can help determine if the symptoms you are experiencing are related to Alzheimer’s disease, or a more treatable conditions such as a vitamin deficiency or a side effect from medication. Early and accurate diagnosis also provides opportunities for you and your family to consider financial planning, develop advance directives, enroll in clinical trials, and anticipate care needs.

How is Alzheimer’s disease treated?

Medical management can improve quality of life for individuals living with Alzheimer’s disease and for their caregivers. There is currently no known cure for Alzheimer’s disease. Treatment addresses several areas:

• Helping people maintain brain health.
• Managing behavioral symptoms.
• Slowing or delaying symptoms of the disease.

Support for family and friends

Currently, many people living with Alzheimer’s disease are cared for at home by family members. Caregiving can have positive aspects for the caregiver as well as the person being cared for. It may bring personal fulfillment to the caregiver, such as satisfaction from helping a family member or friend, and lead to the development of new skills and improved family relationships.

Although most people willingly provide care to their loved ones and friends, caring for a person with Alzheimer’s disease at home can be a difficult task and may become overwhelming at times. Each day brings new challenges as the caregiver copes with changing levels of ability and new patterns of behavior. As the disease gets worse, people living with Alzheimer’s disease often need more intensive care.

What is the burden of Alzheimer’s disease in the United States?

• Alzheimer’s disease is one of the top 10 leading causes of death in the United States.
• The 6th leading cause of death among US adults.
• The 5th leading cause of death among adults aged 65 years or older.

In 2020, an estimated 5.8 million Americans aged 65 years or older had Alzheimer’s disease. This number is projected to nearly triple to 14 million people by 2060.

In 2010, the costs of treating Alzheimer’s disease were projected to fall between $159 and $215 billion. By 2040, these costs are projected to jump to between $379 and more than $500 billion annually.

Death rates for Alzheimer’s disease are increasing, unlike heart disease and cancer death rates that are on the decline.⁵ Dementia, including Alzheimer’s disease, has been shown to be under-reported in death certificates and therefore the proportion of older people who die from Alzheimer’s may be considerably higher.

What is known about reducing your risk of Alzheimer’s Disease?

The science on risk reduction is quickly evolving, and major breakthroughs are within reach. For example, there is growing evidence that people who adopt healthy lifestyle habits — like regular exercise and blood pressure management — can lower their risk of dementia. There is growing scientific evidence that healthy behaviors, which have been shown to prevent cancer, diabetes, and heart disease, may also reduce risk for subjective cognitive decline. To learn more about the current state of evidence on dementia risk factors and the implications for public health, please read the following summaries on Cardiovascular Health, Exercise, Diabetes and Obesity, Traumatic Brain Injury (TBI), Tobacco and Alcohol, Diet and Nutrition, Sleep, Sensory Impairment, and Social Engagement or the Compiled Report (includes all reports in this list).

Alzheimer’s disease is a brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. People with Alzheimer’s also experience changes in behavior and personality.

More than 6 million Americans, many of them age 65 and older, are estimated to have Alzheimer’s disease. That’s more individuals living with Alzheimer’s disease than the population of a large American city. Many more people experience Alzheimer's in their lives as family members and friends of those with the disease.

The symptoms of Alzheimer’s disease — changes in thinking, remembering, reasoning, and behavior — are known as dementia. That’s why Alzheimer’s is sometimes referred to as “dementia.” Other diseases and conditions can also cause dementia, with Alzheimer’s being the most common cause of dementia in older adults.

Alzheimer’s disease is not a normal part of aging. It’s the result of complex changes in the brain that start years before symptoms appear and lead to the loss of brain cells and their connections.

What Causes Alzheimer’s?

The causes of Alzheimer’s disease are not yet fully understood, but probably include a combination of:

• Age-related changes in the brain, like shrinking, inflammation, blood vessel damage, and breakdown of energy within cells, which may harm neurons and affect other brain cells.
• Changes or differences in genes, which may be passed down by a family member. Both types of Alzheimer's — the very rare early-onset type occurring between age 30 and mid-60s, and the most common late-onset type occurring after a person’s mid-60s — can be related to a person’s genes in some way. Many people with Down syndrome, a genetic condition, will develop Alzheimer’s as they age and may begin to show symptoms in their 40s.
• Health, environmental, and lifestyle factors that may play a role, such as exposure to pollutants, heart disease, stroke, high blood pressure, diabetes, and obesity.

What Are the Signs and Symptoms of Alzheimer’s?

Memory problems are often one of the first signs of Alzheimer’s. Symptoms vary from person to person, and may include problems with:

• Word-finding, or having more trouble coming up with words than other people the same age.
• Vision and spatial issues, like awareness of the space around them.
• Impaired reasoning or judgment, which can impact decisions.

Other symptoms may be changes in the person’s behavior, including:

• Taking longer to complete normal daily tasks.
• Repeating questions.
• Trouble handling money and paying bills.
• Wandering and getting lost.
• Losing things or misplacing them in odd places.
• Mood and personality changes.
• Increased anxiety and/or aggression.

How Is Alzheimer’s Diagnosed and Treated?

Doctors may ask questions about health, conduct cognitive tests, and carry out standard medical tests to determine whether to diagnose a person with Alzheimer’s disease. If a doctor thinks a person may have Alzheimer’s, they may refer the person to a specialist, such as a neurologist, for further assessment. Specialists may conduct additional tests, such as brain scans or lab tests of spinal fluid, to help make a diagnosis. These tests measure signs of the disease, such as changes in brain size or levels of certain proteins.

There is currently no cure for Alzheimer’s, though there are several medicines approved by the U.S. Food and Drug Administration (FDA) that can help manage some symptoms of the disease along with coping strategies to manage behavioral symptoms. There are also medications emerging to treat the progression of the disease by targeting its underlying causes.

Most medicines work best for people in the early or middle stages of Alzheimer’s. Researchers are exploring other drug therapies and nondrug interventions to delay or prevent the disease as well as treat its symptoms.

What Are the Stages of Alzheimer’s?

Alzheimer’s disease slowly gets worse over time. People with this disease progress at different rates and in several stages. Symptoms may get worse and then improve, but until an effective treatment for the disease itself is found, the person’s ability will continue to decline over the course of the disease.

Early-stage Alzheimer’s is when a person begins to experience memory loss and other cognitive difficulties, though the symptoms appear gradual to the person and their family. Alzheimer’s disease is often diagnosed at this stage.

During middle-stage Alzheimer’s, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. People at this stage may have more confusion and trouble recognizing family and friends.

In late-stage Alzheimer’s, a person cannot communicate, is completely dependent on others for care, and may be in bed most or all the time as the body shuts down.

How long a person can live with Alzheimer’s disease varies. A person may live as few as three or four years if he or she is older than 80 when diagnosed, to as long as 10 or more years if the person is younger. Older adults with Alzheimer’s disease need to know their end-of-life care options and express their wishes to caregivers as early as possible after a diagnosis, before their thinking and speaking abilities fail.

What Is Mild Cognitive Impairment?

Mild cognitive impairment, or MCI, is a condition in which people have more memory problems than normal for their age but are still able to carry out their normal daily activities. A doctor can do thinking, memory, and language tests to see if a person has MCI. People with MCI are at a greater risk for developing Alzheimer’s disease, so it’s important to see a doctor or specialist regularly if you have this condition.

What Can You Do?

If you are concerned about memory problems or other symptoms, call your doctor. If you or someone you know has recently been diagnosed, explore the resources on this website and linked below to find out more about the disease, care, support, and research.

Dementia is an umbrella term used to describe a range of neurological conditions affecting the brain that get worse over time.

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Neurons are nerve cells that send messages all over your body to allow you to do everything from breathing to talking, eating, walking, and thinking. Until recently, most neuroscientists (scientists who study the brain) thought we were born with all the neurons we were ever going to have. As children, we might grow some new neurons to help build the pathways—called neural circuits—that act as information highways between different areas of the brain. However, scientists believed that once a neural circuit was in place, adding any new neurons would change the flow of information and break the brain’s communication system

In 1962, scientist Joseph Altman challenged this belief when he saw evidence of neurogenesis (the birth of neurons) in a region of the adult rat brain called the hippocampus. He later reported that newborn neurons traveled from their birthplace in the hippocampus to other parts of the brain. In 1979, another scientist, Michael Kaplan, confirmed Altman’s findings in the rat brain; and in 1983, he found special kinds of cells—called neural precursor cells—with the ability to become brain cells like neurons, in adult monkeys.

These discoveries about neurogenesis in the adult brain were surprising to other researchers who thought they were not true in humans. Fortunately, in the early 1980s, a scientist trying to understand how birds learn to sing began to see how neurogenesis in the adult brain might make sense. In a series of experiments, Fernando Nottebohm and his research team showed that the numbers of neurons in the forebrains (areas controlling complex behaviors) of male canaries dramatically increased during the mating season, when the birds learn new songs to attract females.

Why did these bird brains add neurons at such an important time in learning? Nottebohm believed it was because newborn neurons helped store new song patterns within the pathways of the forebrain; these new neurons made learning new songs possible! If birds made new neurons to help them remember and learn, Nottebohm thought the brains of mammals—like humans—might too.

Other scientists, like Elizabeth Gould, later found evidence of newborn neurons in a distinct area of the brain in monkeys, and Fred Gage and Peter Eriksson showed that the adult human brain produced new neurons in a similar area.

Neurogenesis in the adult human brain is still tricky for neuroscientists to show, let alone learn about, how it impacts the brain and its functions. Still, scientists are intrigued by current research on neurogenesis and the possible role of new neurons in the adult brain for learning and memory.

Although neurons are the longest living cells in the body, large numbers of them die during migration and differentiation.

The lives of some neurons can take abnormal turns. Some diseases of the brain are the result of the unnatural deaths of neurons.

- In Parkinson’s disease, neurons that produce the neurotransmitter dopamine die off in the basal ganglia, an area of the brain that controls body movements. This causes difficulty initiating movement.

- In Huntington’s disease, a genetic mutation causes over-production of a neurotransmitter called glutamate, which kills neurons in the basal ganglia. As a result, people twist and writhe uncontrollably.

- In Alzheimer’s disease, unusual proteins build up in and around neurons in the neocortex and hippocampus, parts of the brain that control memory. When these neurons die, people lose their capacity to remember and their ability to do everyday tasks. Physical damage to the brain and other parts of the central nervous system can also kill or disable neurons.

- Blows to the brain, or the damage caused by a stroke, can kill neurons outright or slowly starve them of the oxygen and nutrients they need to survive.

- Spinal cord injury can disrupt communication between the brain and muscles when neurons lose their connection to axons located below the site of injury. These neurons may still live, but they lose their ability to communicate.

Scientists don't yet fully understand what causes Alzheimer's disease in most people. The causes probably include a combination of age-related changes in the brain, along with genetic, environmental, and lifestyle factors. The importance of any one of these factors in increasing or decreasing the risk of Alzheimer's disease may differ from person to person.

Alzheimer's disease is a progressive brain disease. It is characterized by changes in the brain—including amyloid plaques and neurofibrillary, or tau, tangles—that result in loss of neurons and their connections. These and other changes affect a person’s ability to remember and think and, eventually, to live independently.

Aging and Alzheimer's Risk

Older age does not cause Alzheimer’s, but it is the most important known risk factor for the disease. The number of people with Alzheimer’s disease doubles about every 5 years beyond age 65. About one-third of all people age 85 and older may have Alzheimer's disease.

Scientists are learning how age-related changes in the brain may harm neurons and affect other types of brain cells to contribute to Alzheimer’s damage. These age-related changes include atrophy (shrinking) of certain parts of the brain, inflammation, vascular damage, production of unstable molecules called free radicals, and breakdown of energy production within cells.

However, age is only one risk factor for Alzheimer’s disease. Many people live into their 90s and beyond without ever developing dementia.

Genetics of Alzheimer's Disease

Many people worry about developing Alzheimer’s disease, especially if a family member has had it. Having a family history of the disease does not mean for sure that you’ll have it, too. But it may mean you are more likely to develop it.

People’s genes, which are inherited from their biological parents, can affect how likely they are to develop Alzheimer’s disease. Genetic risk factors are changes or differences in genes that can influence the chance of getting a disease. These risk factors are the reason some diseases run in families.

There are two types of Alzheimer's—early-onset and late-onset. Both types have a genetic component.

Late-Onset Alzheimer's Disease

Most people with Alzheimer's have late-onset Alzheimer's disease, in which symptoms become apparent in their mid-60s. Researchers have not found a specific gene that directly causes the late-onset form of the disease. However, one genetic risk factor—having one form, or allele, of the apolipoprotein E (APOE) gene on chromosome 19—does increase a person's risk. APOE ɛ4 is called a risk-factor gene because it increases a person's risk of developing the disease. However, inheriting an APOE ɛ4 allele does not mean that a person will definitely develop Alzheimer's. Some people with an APOE ɛ4 allele never get the disease, and others who develop Alzheimer's do not have any APOE ɛ4 alleles.

Early-Onset Alzheimer's Disease

Early-onset Alzheimer's disease occurs between a person's 30s to mid-60s and represents less than 10 percent of all people with Alzheimer's. Some cases are caused by an inherited change in one of three genes. For other cases, research shows that other genetic components are involved. Researchers are working to identify additional genetic risk variants for early-onset Alzheimer's disease.

Health, Environmental, and Lifestyle Factors that May Contribute to Alzheimer's Disease

Research suggests that a host of factors beyond genetics may play a role in the development and course of Alzheimer's disease. There is a great deal of interest, for example, in the relationship between cognitive decline and vascular conditions such as heart disease, stroke, and high blood pressure, as well as metabolic conditions such as diabetes and obesity. Ongoing research will help us understand whether and how reducing risk factors for these conditions may also reduce the risk of Alzheimer's.

A nutritious diet, physical activity, social engagement, sleep, and mentally stimulating pursuits have all been associated with helping people stay healthy as they age. These factors might also help reduce the risk of cognitive decline and Alzheimer's disease. Clinical trials are testing some of these possibilities.

Early-life factors may also play a role. For example, studies have linked higher levels of education with a decreased risk of dementia. There are also differences in dementia risk among racial groups and sexes—all of which are being studied to better understand the causes of Alzheimer’s disease and to develop effective treatments and preventions for all people.

Some cases of early-onset Alzheimer's disease are caused by gene variants (also called mutations) that can be passed from parent to child. This results in what is known as early-onset familial Alzheimer's disease (FAD). Researchers have found that this form of the disorder can result from variants in the APP, PSEN1, or PSEN2 genes. When any of these genes is altered, large amounts of a toxic protein fragment called amyloid beta peptide are produced in the brain. This peptide can build up in the brain to form clumps called amyloid plaques, which are characteristic of Alzheimer's disease. A buildup of toxic amyloid beta peptide and amyloid plaques may lead to the death of nerve cells and the progressive signs and symptoms of this disorder. Other cases of early-onset Alzheimer's disease may be associated with changes in different genes, some of which have not been identified.

Some evidence indicates that people with Down syndrome have an increased risk of developing Alzheimer's disease. Down syndrome, a condition characterized by intellectual disability and other health problems, occurs when a person is born with an extra copy of chromosome 21 in each cell. As a result, people with Down syndrome have three copies of many genes in each cell, including the APP gene, instead of the usual two copies. Although the connection between Down syndrome and Alzheimer's disease is unclear, the production of excess amyloid beta peptide in cells may account for the increased risk. People with Down syndrome account for less than 1 percent of all cases of Alzheimer's disease. This type of Alzheimer's disease is not inherited.

The causes of late-onset Alzheimer's disease are less clear. The late-onset form does not clearly run in families, although clusters of cases have been reported in some families. Alzheimer's disease is probably related to variations in one or more genes in combination with lifestyle and environmental factors. A gene called APOE has been studied extensively as a risk factor for the disease. In particular, a variant of this gene called the e4 allele seems to increase an individual's risk for developing late-onset Alzheimer's disease.

Many more genes have been associated with Alzheimer's disease, and researchers are investigating the role that additional genes may play in Alzheimer's disease risk.

Frequency

Alzheimer's disease currently affects more than 5 million Americans. Because the risk of developing Alzheimer's disease increases with age and more people are living longer, the number of people with this disease is expected to increase significantly in coming decades.

Early-onset familial Alzheimer's disease is inherited in an autosomal dominant pattern, which means one copy of an altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person inherits the altered gene from one affected parent.

The inheritance pattern of late-onset Alzheimer's disease is uncertain. People who inherit one copy of the APOE e4 allele have an increased chance of developing the disease; those who inherit two copies of the allele are at even greater risk. It is important to note that people with the APOE e4 allele inherit an increased risk of developing Alzheimer's disease, not the disease itself. Not all people with Alzheimer's disease have the e4 allele, and not all people who have the e4 allele will develop the disease.

The symptoms of Alzheimer’s can vary from one person to another. Memory problems are typically one of the first signs of the disease. Decline in non-memory aspects of cognition, such as finding the right word, trouble understanding visual images and spatial relationships, and impaired reasoning or judgment, may also signal the early stages of Alzheimer’s. As the disease progresses, symptoms become more severe and include increased confusion and behavior changes.

For most people with Alzheimer’s — those who have the late-onset variety — symptoms first appear in their mid-60s or later. When the disease develops before age 65, it’s considered early-onset Alzheimer’s, which can begin as early as a person’s 30s, although this is rare.

Alzheimer’s typically progresses clinically in several stages: preclinical, mild (sometimes called early-stage), moderate, and severe (sometimes called late-stage).

Preclinical Alzheimer’s disease

Research suggests that the complex brain changes associated with Alzheimer’s, such as the formation of amyloid plaques or tau tangles, start a decade or more before memory and thinking problems appear. This stage, in which changes in the brain appear before the onset of dementia, is called preclinical Alzheimer’s. However, it’s important to note that not everyone with these brain changes develops dementia.

Signs of Mild Alzheimer’s disease

In mild Alzheimer’s, a person may seem healthy but has more and more trouble making sense of the world around them. The realization that something is wrong often comes gradually to the person and their family. Problems can include:

• Memory loss that disrupts daily life
• Poor judgment, leading to bad decisions
• Loss of spontaneity and sense of initiative
• Losing track of dates or knowing current location
• Taking longer to complete normal daily tasks
• Repeating questions or forgetting recently learned information
• Trouble handling money and paying bills
• Challenges in planning or solving problems
• Wandering and getting lost
• Losing things or misplacing them in odd places
• Difficulty completing tasks such as bathing
• Mood and personality changes
• Increased anxiety and/or aggression

Alzheimer’s is often diagnosed at this stage.

Signs of moderate Alzheimer’s disease

In this stage, more intensive supervision and care become necessary. These changes and increasing needs can be difficult for many spouses and families. Symptoms may include:

• Increased confusion and memory loss, such as forgetting events or personal history
• Withdrawal from social activities
• Inability to learn new things
• Difficulty with language and problems with reading, writing, and working with numbers
• Difficulty organizing thoughts and thinking logically
• Shortened attention span
• Problems coping with new situations
• Changes in sleeping patterns, such as sleeping more during the day and being restless at night
• Difficulty carrying out familiar, multistep tasks, such as getting dressed
• Occasional problems recognizing family and friends
• Hallucinations, delusions, and paranoia
• Impulsive behavior, such as undressing at inappropriate times or places, or using vulgar language
• Inappropriate emotional outbursts
• Restlessness, agitation, anxiety, tearfulness, wandering — especially in the late afternoon or evening
• Repetitive statements or movement, occasional muscle twitches

Signs of severe Alzheimer's disease

People with severe Alzheimer’s cannot communicate and are completely dependent on others for their care. Near the end of life, the person may be in bed most or all of the time as their body shuts down. Symptoms often include:

• Inability to communicate
• No awareness of recent experiences or surroundings
• Weight loss with little interest in eating
• Seizures
• General physical decline, including dental, skin, and foot problems
• Difficulty swallowing
• Groaning, moaning, or grunting
• Increased sleeping
• Loss of bowel and bladder control

A common cause of death for people with Alzheimer’s is aspiration pneumonia. This type of pneumonia develops when a person cannot swallow properly and takes food or liquids into the lungs instead of air.

While there is currently no cure for Alzheimer’s, there are medicines approved by the U.S. Food and Drug Administration that may help treat the disease. There are also changes that can be made to the home environment and daily activities to help a person manage their changes in thinking.

• Symptoms of mild cognitive impairment

  Some people have a condition called mild cognitive impairment (MCI), which can be an early sign of Alzheimer’s. However, not everyone with MCI will develop Alzheimer’s. People with MCI can still take care of themselves and perform their normal activities. MCI memory problems may include:

  • Losing things often
  • Forgetting to go to events or appointments
  • Problems communicating because of difficulty finding words

Recognizing Symptoms of Dementia and Seeking Help

As we age, our brains change, but Alzheimer’s disease and related dementias are not an inevitable part of aging. In fact, up to 40% of dementia cases may be prevented or delayed. It helps to understand what’s normal and what’s not when it comes to brain health.

Normal brain aging may mean slower processing speeds and more trouble multitasking, but routine memory, skills, and knowledge are stable and may even improve with age. It’s normal to occasionally forget recent events such as where you put your keys or the name of the person you just met.

Symptoms of Dementia or Alzheimer’s Disease

In the United States, 6.2 million people age 65 and older have Alzheimer’s disease, the most common type of dementia. People with dementia have symptoms of cognitive decline that interfere with daily life—including disruptions in language, memory, attention, recognition, problem solving, and decision-making. Signs to watch for include:

• Not being able to complete tasks without help.
• Trouble naming items or close family members.
• Forgetting the function of items.
• Repeating questions.
• Taking much longer to complete normal tasks.
• Misplacing items often.
• Being unable to retrace steps and getting lost.

If you have one or more of the 10 warning signs of Alzheimer’s Disease, please see your health care provider. Early diagnosis gives you the best chance to seek treatment and time to plan for the future.

Conditions That Can Mimic Dementia

Symptoms of some vitamin deficiencies and medical conditions such as vitamin B12 deficiency, infections, hypothyroidism (underactive thyroid), or normal pressure hydrocephalus (a neurological condition caused by the build-up of fluid in the brain) can mimic dementia. Some prescription and over-the-counter medicines can cause dementia-like symptoms. If you have these symptoms, it is important to talk to your health care provider to find out if there are any underlying causes for these symptoms

How is Dementia Diagnosed?

A healthcare provider can perform tests on attention, memory, problem solving and other cognitive abilities to see if there is cause for concern. A physical exam, blood tests, and brain scans like a CT or MRI can help determine an underlying cause.

What To Do If a Loved One is Showing Symptoms

Talk with your loved one about seeing a health care provider if they are experiencing symptoms of Alzheimer’s dementia to get a brain health check up.

Be Empowered to Discuss Memory Problems

More than half of people with memory loss have not talked to their healthcare provider, but that doesn’t have to be you. Get comfortable with starting a dialogue with your health care provider if you observe any changes in memory, or an increase in confusion, or just if you have any questions. You can also discuss health care planning, management of chronic conditions, and caregiving needs.

Memory often changes as people grow older. Some people notice changes in themselves before anyone else does. For other people, friends and family are the first to see changes in memory, behavior, or abilities. Memory loss that disrupts daily life is not a typical part of aging. People with one or more of these 10 warning signs should see a doctor to find the cause. Early diagnosis gives them a chance to seek treatment and plan for the future.

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.

Chances are you’ve walked into a room and forgotten why you went there. And misplaced your keys or eyeglasses at least a few times. Many people worry about these memory lapses. They fear they’re heading toward a serious condition like Alzheimer’s disease, an irreversible brain illness.

Occasional forgetfulness is a normal part of life that becomes more common as we grow older. In most cases, it’s no cause for alarm—unless it begins to hamper daily activities. Forgetting where you left the car keys is one thing; forgetting what they do is quite another.

Over the past few years, scientists have learned a lot about memory and why some memory problems are serious but others are not. As we age, changes occur throughout the body, including the brain. As a result, you may begin to notice that it takes longer to learn new things. Perhaps you can’t remember information as well as before, or you may misplace things. These memory lapses may be signs of normal aging. But if increasing forgetfulness begins to worry you, it’s a good idea to check with your doctor. If a medical problem exists, it’s best to start treatment as early as possible.

No matter what your age, several underlying causes can bring about memory problems. Forgetfulness can arise from stress, depression , lack of sleep or thyroid problems. Other causes include side effects from certain medicines, an unhealthy diet or not having enough fluids in your body (dehydration). Taking care of these underlying causes may help resolve your memory problems.

For some older people, though, episodes of memory loss may be a sign of a more serious problem called dementia . Two of the most common forms of dementia in older people are Alzheimer’s disease and multi-infarct dementia (or vascular dementia).

In Alzheimer’s disease, memory loss begins slowly and gets worse over time. People with Alzheimer’s disease have trouble thinking clearly. They find it hard to do everyday things like shopping, driving, cooking or having a conversation. Medications can help during the early or middle stages. As the illness progresses, though, patients may need someone to take care of all their needs (like feeding and bathing) at home or in a nursing home.

Vascular dementia also causes serious memory problems. But unlike Alzheimer’s disease, the signs of vascular dementia may appear suddenly. This is because the memory loss and confusion are caused by small strokes or changes in the blood supply to the brain. Further strokes can make the situation worse. Taking care of your high blood pressure can lower your chances of getting this illness.

See your doctor if you’re concerned that you or someone you know has a memory problem. Your doctor may be able to diagnose the problem or refer you to an expert who specializes in memory problems.

Forgetfulness: When To Seek Help

People who have a sudden loss of memory or become very confused should get medical help right away. Make an appointment to see a doctor if you notice these symptoms:

• Asking the same question or repeating the same story over and over
• Becoming lost in familiar places
• Not being able to follow directions
• Getting confused about time, people and places
• Not taking care of yourself—eating poorly, not bathing or being unsafe
• Having memory or concentration problems that concern you

As we age, our brains change, but Alzheimer’s disease and related dementias are not an inevitable part of aging. In fact, up to 40% of dementia cases may be prevented or delayed. It helps to understand what’s normal and what’s not when it comes to brain health.

Normal brain aging may mean slower processing speeds and more trouble multitasking, but routine memory, skills, and knowledge are stable and may even improve with age. It’s normal to occasionally forget recent events such as where you put your keys or the name of the person you just met.

Symptoms of Dementia or Alzheimer’s Disease

In the United States, 6.2 million people age 65 and older have Alzheimer’s disease, the most common type of dementia. People with dementia have symptoms of cognitive decline that interfere with daily life—including disruptions in language, memory, attention, recognition, problem solving, and decision-making. Signs to watch for include:

• Not being able to complete tasks without help.
• Trouble naming items or close family members.
• Forgetting the function of items.
• Repeating questions.
• Taking much longer to complete normal tasks.
• Misplacing items often.
• Being unable to retrace steps and getting lost.

Conditions That Can Mimic Dementia

Symptoms of some vitamin deficiencies and medical conditions such as vitamin B12 deficiency, infections, hypothyroidism (underactive thyroid), or normal pressure hydrocephalus (a neurological condition caused by the build-up of fluid in the brain) can mimic dementia. Some prescription and over-the-counter medicines can cause dementia-like symptoms. If you have these symptoms, it is important to talk to your health care provider to find out if there are any underlying causes for these symptoms

How is Dementia Diagnosed?

A healthcare provider can perform tests on attention, memory, problem solving and other cognitive abilities to see if there is cause for concern. A physical exam, blood tests, and brain scans like a CT or MRI can help determine an underlying cause.

What To Do If a Loved One is Showing Symptoms

Talk with your loved one about seeing a health care provider if they are experiencing symptoms of Alzheimer’s dementia to get a brain health check up.

Be Empowered to Discuss Memory Problems

More than half of people with memory loss have not talked to their healthcare provider, but that doesn’t have to be you. Get comfortable with starting a dialogue with your health care provider if you observe any changes in memory, or an increase in confusion, or just if you have any questions. You can also discuss health care planning, management of chronic conditions, and caregiving needs.

Many people wonder if Alzheimer’s disease runs in their family. Is it in your genes? This question isn’t easy to answer. Researchers have identified several genetic variants that are associated with Alzheimer’s and may increase or decrease a person’s risk of developing the disease. What does that mean? Let’s first learn about the role of genes.

What Are Genes?

Human cells contain the instructions needed for a cell to do its job. These instructions are made up of DNA, which is packed tightly into structures called chromosomes. Each chromosome has thousands of segments called genes.

Genes are passed down from a person’s biological parents. They carry information that defines traits such as eye color and height. Genes also play a role in keeping the body’s cells healthy.

Variations in genes — even small changes to a gene — can affect the likelihood of a person developing a disease such as Alzheimer’s.

Do Genes Cause Diseases?

Permanent changes in one or more specific genes are called genetic variants. Some of these variants are quite common in the human population. While most genetic variants don’t cause diseases, some do. In some cases, a person inherits a genetic variant that will almost certainly lead to that individual developing a disease. Sickle cell anemia, cystic fibrosis, and some cases of early-onset Alzheimer’s are examples of inherited genetic disorders. However, other variants may simply increase, or even decrease, a person’s risk of developing that disease. Identifying genetic variants and their effects can help researchers uncover the most effective ways to treat or prevent diseases in an individual.

Additionally, factors such as exercise, diet, chemicals, or smoking can have positive or negative effects by changing the way certain genes work. In the field of epigenetics, researchers are studying how such factors can alter a cell’s DNA in ways that affect gene activity.

Genetic research is a component of precision medicine, an emerging approach that considers individual variability in genes, environment, and lifestyle. Precision medicine will enable researchers and doctors to predict more accurately which treatment and prevention strategies will work in particular groups of people.

Genes and Alzheimer's Disease

In most cases, Alzheimer’s does not have a single genetic cause. Instead, it can be influenced by multiple genes in combination with lifestyle and environmental factors. Consequently, a person may carry more than one gene or group of genes that can either increase or reduce the risk of Alzheimer’s.

Importantly, people who develop Alzheimer’s do not always have a history of the disease in their families. Still, those who have a parent or sibling diagnosed with the disease have a higher risk of developing Alzheimer’s than those without that association.

Genetic variants that affect Alzheimer's disease risk

Ten years ago, researchers knew of only 10 genes linked with Alzheimer’s. Today, scientists have identified more than 70 genetic regions associated with Alzheimer’s. Understanding which genes play a role — and what role they play — may help identify new methods to prevent, delay, or treat dementia.

One well-known gene that influences Alzheimer’s risk is the apolipoprotein E (APOE) gene. The APOE gene is involved in making a protein that helps carry cholesterol and other types of fat in the bloodstream. Problems in this process are thought to contribute to the development of Alzheimer’s. APOE comes in several forms, called alleles (e.g., ε2, ε3).

• APOE ε2 may provide some protection against the disease. If Alzheimer’s occurs in a person with this allele, it usually develops later in life than it would in someone with the APOE ε4 gene. Roughly 5% to 10% of people have this allele.
• APOE ε3, the most common allele, is believed to have a neutral effect on the disease — neither decreasing nor increasing risk of Alzheimer’s.
• APOE ε4 increases risk for Alzheimer’s and is associated with an earlier age of disease onset in certain populations. About 15% to 25% of people have this allele, and 2% to 5% carry two copies.

Each person inherits two APOE alleles, one from each biological parent, meaning people can have one of six possible combinations: 2/2, 2/3, 2/4, 3/3, 3/4, and 4/4. Having two copies of APOE ε4 is associated with a higher risk of Alzheimer’s than having one copy. While inheriting APOE ε4 increases a person’s risk of Alzheimer’s, some people with an APOE ε4 allele never develop the disease.

Researchers are also finding other rare genetic variants, in addition to APOE ε2, that appear to provide some protection against developing Alzheimer’s.

However, prevalence and risk associated with APOE and other genetic variants may not be the same across all population groups. Research suggests that the degree of risk may be affected by genetic ancestry — the global geographic region from which a person is biologically descended — and differ among people of African, Asian, American Indian, and European descent. More research is needed to better understand how certain genetic variants might affect a person’s or group’s risk for Alzheimer’s and to identify treatment and prevention strategies that will work best for that particular group.

Genetic variants that cause Alzheimer's disease

Of the genetic variants so far associated with Alzheimer’s, three rare single-gene variants are known to cause the disease:

• Amyloid precursor protein (APP) on chromosome 21
• Presenilin 1 (PSEN1) on chromosome 14
• Presenilin 2 (PSEN2) on chromosome 1

A child whose biological parent carries a genetic variant for one of these three genes has a 50/50 chance of inheriting that altered version of the gene. If the variant is inherited, the child has a very strong probability of developing Alzheimer’s before age 65 and sometimes much earlier. When someone develops Alzheimer’s before age 65, it’s known as “early-onset Alzheimer’s” or sometimes “younger-onset Alzheimer’s” or “earlier-onset Alzheimer’s.” Less than 10% of all people with Alzheimer’s develop symptoms this early. Of those who do, 10% to 15% can be attributed to changes in APP, PSEN1, and PSEN2.

Changes in these three genes result in the production of abnormal proteins that are associated with the disease. Each of these mutations contributes to the breakdown of APP, a protein that’s function isn’t completely understood. The breakdown of APP is part of a process that makes harmful forms of sticky amyloid fragments. These fragments cluster to form plaques in the brain, which is a hallmark of Alzheimer’s.

In addition to the three genetic variants that are known to cause Alzheimer’s, people with Down syndrome have an extra copy of chromosome 21, which carries the APP gene, and a higher risk of developing early-onset Alzheimer’s. Estimates suggest that 50% or more of people living with Down syndrome will develop Alzheimer’s with symptoms appearing in their 50s and 60s.

Genetic testing for Alzheimer's disease

Genetic tests are not routinely used in clinical settings to diagnose or predict the risk of developing Alzheimer’s or a related dementia.

In some cases, if a person has symptoms at an early age with a strong family history of Alzheimer’s, a neurologist or other medical specialist may order a genetic test for APP, PSEN1, and PSEN2.

Although APOE testing is also available, the results cannot fully predict who will or won’t develop Alzheimer’s. Rather, this type of testing is used primarily in research settings to identify study participants who may have an increased risk of developing Alzheimer’s. This approach helps scientists look for early brain changes and compare the effectiveness of possible treatments for people with different APOE profiles.

Some people learn their APOE status through consumer genetic testing. These products are available for a fee and provide some information around the results and what they mean. While at-home genetic tests are convenient, people considering them may also benefit from talking with a doctor or genetic counselor to better understand this type of test and their test results.

Normal Function

The APP gene provides instructions for making a protein called amyloid precursor protein. This protein is found in many tissues and organs, including the brain and spinal cord (central nervous system). Little is known about the function of amyloid precursor protein. Researchers speculate that it may bind to other proteins on the surface of cells or help cells attach to one another. Studies suggest that in the brain, it helps direct the movement (migration) of nerve cells (neurons) during early development.

Amyloid precursor protein is cut by enzymes to create smaller fragments (peptides), some of which are released outside the cell. Two of these fragments are called soluble amyloid precursor protein (sAPP) and amyloid beta (β) peptide. Recent evidence suggests that sAPP has growth-promoting properties and may play a role in the formation of neurons in the brain both before and after birth. The sAPP peptide may also control the function of certain other proteins by turning off (inhibiting) their activity. Amyloid β peptide is likely involved in the ability of neurons to change and adapt over time (plasticity). Other functions of sAPP and amyloid β peptide are under investigation.

Health Conditions Related to Genetic Changes

Alzheimer's disease

Many variants (also called mutations) in the APP gene can cause early-onset Alzheimer's disease, which begins before age 65. These variants are responsible for less than 10 percent of all early-onset cases of Alzheimer's disease.

The most common APP gene variant changes one of the protein building blocks (amino acids) in the amyloid precursor protein. This variant replaces the amino acid valine with the amino acid isoleucine at protein position 717 (written as Val717Ile or V717I). Variants in the APP gene can lead to an increased amount of the amyloid β peptide or to the production of a slightly longer and stickier form of the peptide. When these protein fragments are released from the cell, they can accumulate in the brain and form clumps called amyloid plaques. These plaques are characteristic of Alzheimer's disease. A buildup of toxic amyloid β peptide and amyloid plaques may lead to the death of neurons and the progressive signs and symptoms of Alzheimer's disease.

Hereditary cerebral amyloid angiopathy

Variants in the APP gene have been found to cause hereditary cerebral amyloid angiopathy, a condition characterized by stroke and a decline in intellectual function (dementia), which begins in mid-adulthood. These variants change single amino acids in the amyloid precursor protein. Each of these variants causes a different type of the condition. The Dutch type, the most common of all the types, is caused by the replacement of the amino acid glutamic acid with the amino acid glutamine at position 22 in the protein sequence (written as Glu22Gln or E22Q). The Italian type and Arctic type are also caused by changes to glutamic acid at position 22. In the Italian type, glutamic acid is replaced with the amino acid lysine (written as Glu22Lys or E22K) and in the Arctic type, glutamic acid is replaced with the amino acid glycine (written as Glu22Gly or E22G). The Flemish type is caused by replacement of the amino acid alanine with glycine at position 21 (written as Ala21Gly or A21G). In the Iowa type, the amino acid aspartic acid is switched with the amino acid asparagine at position 23 (written as Asp23Asn or D23N). The Piedmont type of hereditary cerebral amyloid angiopathy is caused by the replacement of the amino acid leucine at position 34 with the amino acid valine (written as Leu34Val or L34V).

The result of all of these variants is the production of an amyloid β peptide that is more prone to cluster together (aggregate) than the normal peptide. The aggregated protein forms amyloid deposits that accumulate in the blood vessels of the brain. The amyloid deposits replace the muscle fibers and elastic fibers that give blood vessels flexibility, causing the blood vessels to become weak and prone to breakage. In the brain, such a break causes bleeding (hemorrhagic stroke), which can lead to brain damage and dementia or be life-threatening. Amyloid deposits in specific parts of the brain can interfere with normal brain function, leading to dementia, seizures, movement problems, and other neurological features in some people with hereditary cerebral amyloid angiopathy.

Other Names for This Gene

• A4_HUMAN
• AAA
• ABETA
• ABPP
• AD1
• amyloid beta (A4) precursor protein
• amyloid beta-peptide
• amyloid beta-protein precursor
• amyloid precursor protein
• APPI
• cerebral vascular amyloid peptide
• CVAP
• PN-II
• PN2
• protease nexin 2
• protease nexin-II

Genomic Location

Normal Function

The PSEN1 gene provides instructions for making a protein called presenilin 1. This protein is one part (subunit) of a complex called gamma- (γ-) secretase. Presenilin 1 carries out the major function of the complex, which is to cut apart (cleave) other proteins into smaller pieces called peptides. This process is called proteolysis, and presenilin 1 is described as the proteolytic subunit of γ-secretase.

The γ-secretase complex is located in the membrane that surrounds cells, where it cleaves many different proteins that span the cell membrane (transmembrane proteins). This cleavage is an important step in several chemical signaling pathways that transmit signals from outside the cell into the nucleus. One of these pathways, known as Notch signaling, is essential for the normal growth and maturation (differentiation) of hair follicle cells and other types of skin cells. Notch signaling is also involved in normal immune system function.

The γ-secretase complex may be best known for its role in processing amyloid precursor protein (APP), which is made in the brain and other tissues. γ-secretase cuts APP into smaller peptides, including soluble amyloid precursor protein (sAPP) and several versions of amyloid-beta (β) peptide. Evidence suggests that sAPP has growth-promoting properties and may play a role in the formation of nerve cells (neurons) in the brain both before and after birth. Other functions of sAPP and amyloid-β peptide are under investigation.

Health Conditions Related to Genetic Changes

Alzheimer's disease

Dozens of PSEN1 gene variants (also known as mutations) have been identified in patients with early-onset Alzheimer's disease, a degenerative brain condition that begins before age 65. Variants in the PSEN1 gene are the most common cause of early-onset Alzheimer's disease, accounting for up to 70 percent of cases.

Almost all PSEN1 gene variants change single building blocks of DNA (nucleotides) in a particular segment of the PSEN1 gene. These variants result in the production of an abnormal presenilin 1 protein. Defective presenilin 1 interferes with the function of the γ-secretase complex, which alters the processing of APP and leads to the overproduction of a longer, toxic version of amyloid-β peptide. Copies of this protein fragment stick together and build up in the brain, forming clumps called amyloid plaques that are a characteristic feature of Alzheimer's disease. A buildup of toxic amyloid-β peptide and the formation of amyloid plaques likely lead to the death of neurons and the progressive signs and symptoms of Alzheimer's disease.

Hidradenitis suppurativa

At least one variant (also known as a mutation) in the PSEN1 gene has been found to cause hidradenitis suppurativa, a chronic skin disease characterized by recurrent boil-like lumps (nodules) under the skin that develop in hair follicles. The nodules tend to become inflamed and painful, and they produce significant scarring as they heal.

The identified variant deletes a single DNA building block (nucleotide) from the PSEN1 gene, written as 725delC. This genetic change reduces the amount of functional presenilin 1 produced in cells, so less of this protein is available to act as part of the γ-secretase complex. The resulting shortage of normal γ-secretase impairs cell signaling pathways, including Notch signaling. Although little is known about the mechanism, studies suggest that abnormal Notch signaling may promote the development of recurrent nodules in hair follicles and trigger inflammation in the skin.

Studies suggest that the PSEN1 gene variant that causes hidradenitis suppurativa has a different effect on γ-secretase function than the variants that cause early-onset Alzheimer's disease. These differences may explain why no single PSEN1 gene variant has been reported to cause the signs and symptoms of both diseases.

Familial dilated cardiomyopathy

MedlinePlus Genetics provides information about Familial dilated cardiomyopathy

Other Names for This Gene

• AD3
• FAD
• presenilin 1 (Alzheimer disease 3)
• presenilin 1 protein
• PS1
• PSN1_HUMAN
• PSNL1 gene product
• S182 protein

Genomic Location

Normal Function

The PSEN2 gene provides instructions for making a protein called presenilin 2. Presenilin 2 helps process proteins that transmit chemical signals from the cell membrane into the nucleus. Once in the nucleus, these signals turn on (activate) genes that are important for cell growth and maturation.

Presenilin 2 is best known for its role in processing amyloid precursor protein, which is found in the brain and other tissues. Research suggests that presenilin 2 works together with other enzymes to cut amyloid precursor protein into smaller segments (peptides). One of these peptides is called soluble amyloid precursor protein (sAPP), and another is called amyloid beta peptide. Recent evidence suggests that sAPP has growth-promoting properties and may play a role in the formation of neurons in the brain both before and after birth. Other functions of sAPP and amyloid beta peptide are under investigation.

Health Conditions Related to Genetic Changes

Alzheimer's disease

At least 11 mutations in the PSEN2 gene have been shown to cause early-onset Alzheimer's disease. Mutations in this gene account for less than 5 percent of all early-onset cases of the disorder.

Two of the most common PSEN2 mutations that cause early-onset Alzheimer's disease change single protein building blocks (amino acids) used to make presenilin 2. One mutation replaces the amino acid asparagine with the amino acid isoleucine at position 141 (written as Asn141Ile or N141I). The other mutation changes the amino acid methionine to the amino acid valine at position 239 (written as Met239Val or M239V). These mutations appear to disrupt the processing of amyloid precursor protein, leading to the overproduction of amyloid beta peptide. This protein fragment can build up in the brain and form clumps called amyloid plaques that are characteristic of Alzheimer's disease. A buildup of toxic amyloid beta peptide and amyloid plaques may lead to the death of neurons and the progressive signs and symptoms of this disorder.

Familial dilated cardiomyopathy

MedlinePlus Genetics provides information about Familial dilated cardiomyopathy

Other Names for This Gene

• AD3-like protein
• AD3L
• AD3LP
• AD4
• AD5
• Alzheimer's disease 3-like
• E5-1
• presenilin 2 (Alzheimer disease 4)
• PS2 protein (alzheimer-associated)
• PSN2_HUMAN
• PSNL2
• STM2

Genomic Location