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What is the name/nicknames of Alzheimer's

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What is the name/nicknames of Alzheimer's

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The actual name for Alzheimer's is Alzheimer's Disease.

Some common nicknames for Alzheimer's Disease are AD or Dementia

Dr. Alois Alzheimer found changes in the brain of a deceased female and discovered the neurological disease. That's why it is named Alzheimer's.
https://www.nia.nih.gov/health/alzheimers-disease

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Alzheimer's Association offers virtual/in person support groups and message boards for individuals with Alzheimer's. They offer support for family members and advice to those who seek it.
Support Groups | Alzheimer's Association

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What is the long-term outlook for an individual with Alzheimer's? 

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What is the long-term outlook for an individual with Alzheimer's? 

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The progression of the disease varies widely.  On average someone diagnosed with Alzheimer's will live 3-11 after diagnosis. An individual with high blood pressure and does not treat themselves can also cause the Alzheimer's to have a faster progression.
Alzheimer's stages: How the disease progresses - Mayo Clinic

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Even though there are no cures for Alzheimer's there are in fact treatments to help slow down the disease. Some treatments consist of medicine prescriptions such as Donepezil that help nerve cells communicate with each other better. Therapy such as Cognitive Stimulation Therapy can also help stimulate the patient's mind through talking and other activities to help them maintain memory better.

https://www.nhs.uk/conditions/alzheimers-disease

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The symptoms and effects on an individual with Alzheimer's 

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The symptoms and effects on an individual with Alzheimer's 

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Memory loss is the key symptom of Alzheimer's. Early signs of this disease are failure to remember recent conversations or events. As time goes on, memory gets worse and other diseases develop as well. Alzheimer's disease causes difficulty concentrating and thinking, especially about abstract concepts such as numbers.  Here is a list of effects people with Alzheimer's do.

-Repeat statements and questions over and over.
-Forget conversations, appointments or events.
-Misplace items, often putting them in places that don't make sense.
-Get lost in places they used to know well.
-Eventually forget the names of family members and everyday objects.
-Have trouble finding the right words for objects, expressing thoughts or taking part in conversations.
Alzheimer's disease - Symptoms and causes - Mayo Clinic

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The basic understanding of what causes Alzheimer's is when the brain's protein fails to function as usual on chromosome 21. This disrupts the work of brain cells, also called neurons, and triggers. The neurons become damaged and lose connections to each other.  Which leads to their death.
Alzheimer's disease - Symptoms and causes - Mayo Clinic

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What is the current status of research on Alzheimer's?

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What is the current status of research on Alzheimer's?

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According to Scott Small, it might take a while to figure out a cure for Alzheimer's, but they are getting closer and closer every year.

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Columbia University Irving Medical Center

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In the 90s, Alzheimer's researchers were full of optimism. New genetic studies all pointed to one culprit-hard clumps of protein, called amyloid, that litter the brains of people with the disease.

Scott Small, MD. Photo: Alzheimer's Disease Research Center at Columbia University.

With the emergence of the first tangible target, pharmaceutical companies jumped in to develop drugs to clear amyloid from the brain. In animals, the drugs appeared to improve memory. But the results of human clinical trials that followed were disheartening: One after one, these drugs-all designed to target amyloid-have failed to slow the disease.

The onslaught of news about these failures has left the public wondering whether amyloid has anything to do with Alzheimer's-and whether a new approach is needed.

The field has already begun to redirect its focus, says Scott Small, MD, director of Columbia's Alzheimer's Disease Research Center and the Boris and Rose Katz Professor of Neurology at Columbia University Vagelos College of Physicians and Surgeons.

"There's now reason to be cautiously optimismistic," he says, "because we have uncovered new pathways that lead to the disease, and we know that they truly make a difference."

The CUIMC Newsroom spoke with Small about the current state of research into Alzheimer's treatments and prevention.

Q: First, the bad news. Why have all drugs tested in the past several years failed?

In retrospect, the idea that reducing amyloid in the brain-which all the failed drugs do-is based on an incomplete picture of the disease.

To treat a disease, we need to treat what's broken. But it's very difficult to find what's broken in these slowly progressive brain disorders.

One way to find what's broken is through genetics, but the first wave of genetic studies in the 80s and 90s only had the technical capabilities to investigate Alzheimer's cases that run in families, those caused by a single gene.

The results of these studies all seemed to converge on one biological process: amyloid.

But these single-gene forms of Alzheimer's are rare-and account for maybe 2% to 3% of cases. Most cases of Alzheimer's are caused by a complex interplay of many genes and the environment.

The field made the assumption that amyloid is the primary culprit in all forms of Alzheimer's. It made perfect sense, because we see amyloid in all patients with Alzheimer's, whether their disease is caused by a single gene or not. The amyloid finding was extremely exciting, and there was a sense that we were on the cusp of curing this devastating, horrible disease.

Q: Does that mean the amyloid hypothesis is completely wrong?

The amyloid hypothesis is that amyloid is the trigger of everything in Alzheimer's. That seems now to be wrong.

New studies from the past decade tell us that amyloid is part of the story of Alzheimer's disease, but it's the smoke, not the fire. We've learned that the single-gene and more common, complex forms of Alzheimer's are not identical, though they do overlap.

There's been a lot of backlash against the amyloid hypothesis lately, but in the 90s, it was the right idea. The pharmaceutical industry was right to jump on the amyloid bandwagon. And they're now right to give it up, I think.

Q: If drugs against amyloid aren't the answer, what is?

Back in the 80s and 90s, genetic tools weren't quite developed enough to address the real question we had: What genes are involved in most cases of Alzheimer's disease?

Techniques have advanced and we can now answer this question. New studies-many led by Richard Mayeux, MD [chair of neurology at Columbia]-have been pointing to other processes in the brain. We also have better biological tools that can reveal the basic problem inside neurons.

Based on this research, the new consensus in the field is that there are two other pathways that cause the disease.

One involves "protein trafficking," which is how proteins are shipped to different sites within a single cell. The health of neurons, more so than other cells, depends on protein trafficking in and out of one particular site: the endosome.

In Alzheimer's, the flow of proteins out of the endosome is blocked, and we think that causes the other problems we see in the disease: the amyloid, the tau tangles also common in the Alzheimer's brain, and the neurodegeneration. Essentially it's a plumbing problem.

Our research here at Columbia provided some early evidence for an endosomal trafficking problem in Alzheimer's. And genetic studies-including those led by Dr. Mayeux-have now found that some endosomal genes are linked to Alzheimer's, which provides more support.

The second pathway involves microglia, which are cells in the brain that help maintain the health of neurons and help keep the spaces between neurons clear of pathogens, protein aggregates, and other cellular debris.

Recently discovered genes-by Phil De Jager, MD, PhD, in our center and others-point us to these cells. But what exactly is wrong with the microglia is still hotly debated. We don't know if they're working too well or not well enough, but we do know they're not working properly.

Q: What makes you so optimistic that we will find a treatment that slows or stops the disease?

We now, I believe, have evidence to help us understand why the first hypothesis was wrong. Scientifically, we have very good justification to argue why our new hypotheses are correct.

We're now seeing that companies are getting back into drug development because these new pathways are so compelling.

In the coming years, our biggest focus at the Alzheimer's Disease Research Center at Columbia will be accelerating drug discovery. One of the most important goals is to develop new biomarkers-for the new Alzheimer's pathways. These biomarkers are crucial for developing the new generation of therapeutic agents. These biomarkers will be useful for enrolling patients into new anticipated clinical trials, following the logic of precision medicine. Also, just as biomarkers of amyloid were important for testing assumptions about the primacy of amyloid in the disease, these biomarkers are important for testing-or potentially refuting-the new pathways.

We're also testing gene therapies and other ways to restore endosomal trafficking to see if that prevents neurodegeneration in animal models.

Frank Provenzano and Adam Brickman are developing new techniques, with imaging and cognitive testing, to detect patients with endosomal defects as early as possible. We think the sooner we can treat people, the better. Sabrina Simoes, one of our newest members, is developing new ways to use spinal fluid and blood to remotely monitor endosomal trafficking. That's a critical step in measuring a drug's effectiveness when the drug moves to clinical testing.

In science, though, you never can be sure. The only way we'll know we're right is by developing drugs and testing the hypothesis in clinical trials in patients, like we did with the amyloid hypothesis.

Q: Is there anything people can do now to prevent the disease, or at least delay it for several years?

In my practice, I encounter many people who have family members with Alzheimer's and they're worried about their genes. But in most cases, just because your mother has it doesn't mean you're going to get it.

In a complex disease, each gene and each environmental factor is like putting a pebble on a scale. None of them by themselves can prevent or cause Alzheimer's. So if your parent has Alzheimer's, that puts one pebble on the scale. But if you went to college, if you exercise, those are pebbles on the other side of the scale.

Many of the things that we thought historically cause Alzheimer's have been debunked-for example, the idea that it was caused by various heavy metals. But we do know that maintaining cardiac health is good: Exercise is good; smoking is bad; developing diabetes or obesity increases the risk. These recommendations, as most people know, are true for any disease.

People often ask me this question, hoping I know something that no one else does. I don't have any other answers at the moment, but everyone in the field is doing their best to find new ways to forestall this disease.

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Will a Treatment for Alzheimer's Ever Be Found?

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In the 90s, Alzheimer's researchers were full of optimism. New genetic studies all pointed to one culprit-hard clumps of protein, called amyloid, that litter the brains of people with the disease. With the emergence of the first tangible target, pharmaceutical companies jumped in to develop drugs to clear amyloid from the brain.

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Are there prenatal tests for Alzheimers?

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Are there prenatal tests for Alzheimers?

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According to Alzheimers.org, there are no approved prenatal tests to see if one will have Alzheimer's.

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Genes play a role in the development of many types of dementia, although the extent of this role varies between dementia types. A person with a parent or sibling with a dementia such as Alzheimer's disease has on average a higher risk of developing the same condition themselves, although other factors such as lifestyle can also play a part.

At present, the relationship between genetics and dementia is not fully understood. We do know that a mutation (change) in one of a small number of genes can cause someone to develop frontotemporal dementia or rarer, inherited forms of Alzheimer's disease. These conditions both often start in people under the age of 65.

Predictive genetic testing is where the genes of someone who is related by birth to a person with diagnosed dementia are tested. The genetic test aims to see whether the relative has inherited the same mutation and so will go on to develop the dementia. At present such predictive genetic testing is only possible for inherited Alzheimer's disease, in which very rare mutations in three genes are implicated, and frontotemporal dementia, which has known mutations in at least six genes. The most common form of Alzheimer's disease affects about 520,000 people in the UK and most often starts in people over the age of 65. There are no approved predictive genetic tests for this form of the condition.

In the vast majority of people, any genetic risk of Alzheimer's disease - increased or decreased - is linked not to rare mutations but to variations in a large number of susceptibility genes that they have inherited. The most common risk gene is called APOE. This gene has a number of variants, and a variant called e4 has been shown to increase risk of developing Alzheimer's disease. However, risk genes such as APOE have a more subtle influence on someone's chances of developing Alzheimer's disease than the genes that are used in tests for the inherited forms of dementia.

Predictive testing for APOE variants outside of approved research studies is currently available in the UK only on a commercial basis: for a fee, companies not based in the UK will analyse a saliva sample sent off in the post. However, the results of APOE testing have low predictive value. Someone who has two copies of the higher risk APOE variant e4 is not certain to develop Alzheimer's disease, while someone who has other variants still might. This poor predictive value is why APOE testing is not recommended (outside research studies) or available within the NHS.

Genetic testing can be difficult emotionally, not provide conclusive results and cause practical difficulties. Before considering genetic tests, it is vital that proper genetic counselling is provided to ensure it is the correct decision for the individual. It is also vital that, if someone does have testing, they receive full genetic counselling about what the results mean. No counselling is currently provided with the commercially available APOE test.

For more information on genetic testing, please see our factsheet, Genetics of dementia.

Alzheimer's Society strongly believes that there should be legal protection against discrimination on the grounds of genetic information. There is currently a moratorium on the use of genetic information by UK insurance companies until November 2019. Alzheimer's Society campaigns for the continued prevention of insurers and employers using genetic information to discriminate against people at risk of dementia.

What Alzheimer's Society calls for

Proper and timely genetic counselling for all individuals who choose to consider predictive genetic tests. There are no approved predictive genetic tests for the most common form of Alzheimer's disease. However, regional genetics clinics offer testing for people whose family history of dementia suggests they might carry one of the causative mutations for inherited Alzheimer's or frontotemporal dementia. It is important to note that testing can be difficult emotionally, not provide conclusive results and cause practical difficulties. Before this test, it is vital that proper genetic counselling is provided to ensure it is the correct decision for the individual. For more information, please see our page: Genetics of dementia.

Continued prevention of insurers using genetic information to discriminate against people at risk of dementia in the future. People receiving a positive result in a genetic test can face discrimination that affects their ability to buy property, get insurance or plan financially for old age. There is, however, a moratorium on the use of genetic information by UK insurance companies until November 2019. Alzheimer's Society campaigns for the continued prevention of insurers and employers using genetic information to discriminate against people at risk of dementia.

Research into the genetic risk factors for dementia. Progress in genetics has meant that more than 20 susceptibility genes have been identified that affect a person's risk of developing Alzheimer's disease. The genetic basis of frontotemporal dementia is also a very active research field. These conditions are now the subject of intense scientific investigation. Ultimately, this research may identify causes of the disease. Alzheimer's Society supports, and funds, genetic research.

This information was last updated in April 2015 by Laurence Thraves

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Alzheimer's Society's view on genetic testing

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Genes play a role in the development of many types of dementia, although the extent of this role varies between dementia types. A person with a parent or sibling with a dementia such as Alzheimer's disease has on average a higher risk of developing the same condition themselves, although other factors such as lifestyle can also play a part.

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When being diagnosed with Alzheimer's doctors may ask the following questions.
-how is your ability to carry out daily activities
-Any changes in behavior or personality
-Any past medical diseases
-how is your diet
The questions are very simple but another way doctors diagnose someone with Alzheimer's are done by specific tests.  -Conduct tests of memory, problem solving, attention, counting, and language.
-Perform brain scans, such as computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET), to support an Alzheimer’s diagnosis or rule out other possible causes
How Is Alzheimer's Disease Diagnosed? | National Institute on Aging (nih.gov)

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Alzheimer's does not affect one group more than others. According to Alzheimers.org, the most susceptible group are people over the age of 65.
www.alzheimers.org.uk

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How does a person get Alzheimer's? (Mutation or inherited?)

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How does a person get Alzheimer's? (Mutation or inherited?)

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Alzheimer's is a genetic mutation, but could also have a higher chance of being inherited if one's mom or dad or grandma or grandpa have it.

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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

Share this infographic and help spread the word about Alzheimer's genetics.

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 , 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:

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. Learn more about Alzheimer's disease in people with Down syndrome.

For resources related to early-onset Alzheimer's, see NIA's Early-Onset Alzheimer's Disease: A Resource List.

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.

General information about genetic testing can be found at:

Understanding Alzheimer's genetics in diverse populations

Research shows the rates of dementia vary among different racial and ethnic groups. While the concepts of race and ethnicity are socially defined, these social definitions offer researchers another way of looking at risk factors that may affect certain groups. These risk factors can include external influences, such as the environment, education, and income levels, as well as biological factors like genetics.

One way researchers are using genetics to advance health disparities research is to look at genetic ancestry. Genetic ancestry refers to the region from which a person is biologically descended. People of the same race and ethnicity may share genetic ancestry, but this is not always the case. Large genetic research studies can help scientists identify unique factors that are linked to genetic ancestry. Understanding these factors in diverse populations is important to identifying ways to prevent, diagnose, and treat Alzheimer's in all people.

Alzheimer's genetics research

Discovering as much as possible about the role of Alzheimer's genetic risk and protective factors across populations is an important area of research. NIA funds several major genetics research programs. Understanding more about the genetic basis of the disease will help researchers:

Answer a number of basic questions, such as: What makes the disease process begin? Why do some people with memory and other thinking problems develop Alzheimer's while others don't?

Determine how genetic risk and protective factors may interact with other genes and lifestyle or environmental influences to affect Alzheimer's risk in any one person.

Identify people who are at high risk for developing Alzheimer's so they can benefit from new interventions and treatments as much and as soon as possible.

Explain differences in Alzheimer's risks and protections among racial groups and genders.

Use individual gene discoveries to develop potential therapies to prevent or treat the disease.

Research needs volunteers of all different races, ethnicities, ancestries, ages, and genders to participate in clinical trials and studies. Talk with a doctor if you're interested in participating in Alzheimer's research or search the Alzheimers.gov Clinical Trials Finder to find a study near you or online.

For more information about Alzheimer's disease genetics

NIA Alzheimer's and related Dementias Education and Referral (ADEAR) Center
800-438-4380
adear@nia.nih.gov
www.nia.nih.gov/alzheimers
The NIA ADEAR Center offers information and free print publications about Alzheimer's and related dementias for families, caregivers, and health professionals. ADEAR Center staff answer telephone, email, and written requests and make referrals to local and national resources.

Alzheimers.gov
www.alzheimers.gov
Explore the Alzheimers.gov website for information and resources on Alzheimer's and related dementias from across the federal government.

This content is provided by the NIH National Institute on Aging (NIA). NIA scientists and other experts review this content to ensure it is accurate and up to date.

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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?