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More People Are Cured of HIV… But Is It a Practical Way Forward?

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With all of this scientific work on using stem cell transplants to treat HIV , along with the media coverage of people being cured of their HIV, there is understandably a lot of interest in this area of research now. However, there are several challenges involved with using stem cell transplants for HIV/AIDS patients. While you may think that everyone with HIV can be cured with a stem cell transplant, most people aren’t able to get this treatment. Scientists are on the road to curing HIV, but they haven’t yet found a treatment that can work for everyone. Read on for more about this new area of medicine and research.

Road To the Cure of HIV

In the last few decades since the emergence of HIV/AIDS, scientists have tried using stem cell transplantation as a treatment . The idea was to replace the immune cells that are deficient in HIV/AIDS patients. It wasn’t until recently that they could do stem cell transplants with cells that are actually resistant to the HIV virus . And since that success, there was a launch of a new research initiative, the European Project to Guide and Investigate the Potential for HIV Cure by Stem Cell Transplantation (or EpiStem).

HIV and Its Treatment

Human immunodeficiency virus (HIV ) is a virus that invades a type of immune cell in your body called a CD4+ T-cell. When HIV infects many of your CD4+ T cells, your immune system becomes severely weak, and your body can’t fight off infections. If HIV is left untreated for a long time, you can develop acquired immune deficiency syndrome (or AIDS).

The standard treatment for HIV is antiretroviral therapy or ART. This is a medication therapy where you use multiple drugs in combination to prevent HIV from doing further damage to your immune cells. 

Who Is Cured of HIV?

A few people have been cured of HIV , but stem cell transplant treatment won’t work for everyone. The first person to be cured of HIV was a man referred to as the Berlin patient. He was diagnosed with cancer in 2006, and his doctor treated him with a stem cell transplant. 

Stem cells are young cells that can still grow into many different cell types. A stem cell transplant is a procedure where a doctor places stem cells in your body, and doctors sometimes give patients stem cell transplants to treat cancer.

But the stem cells transplanted into the Berlin patient were unique. They had a mutation called CCR5-delta32 that prevents HIV from infecting immune cells. After the transplant, not only did his cancer symptoms go away, but his HIV symptoms went away too. Doctors checked to see if HIV was still in any part of his body and couldn’t find the virus anywhere. He lived without HIV for 13 years before passing away when his cancer symptoms returned in 2020.

Some doctors tried treating other people with HIV with stem cell transplants but weren’t as successful. In general, it’s difficult to cure HIV because it’s a virus that can escape treatment by becoming latent . This means it is no longer replicating and just sits quietly in your cells. It took many years after the Berlin patient for doctors to cure other HIV-positive patients with stem cell transplants. Similar to the Berlin patient, there are four HIV-positive patients who had cancer cured of HIV by getting stem cell transplants with the CCR5-delta32 mutation.

Why Can’t We Cure Everyone?

While stem cell transplants seem to be an effective HIV cure for some patients, there are some challenges to using this treatment, such as:

Finding the right donor

The donor must be compatible with the recipient by human leukocyte antigen (or HLA) type. This indicates the type of protein found on the surface of your cells. The donor must also have the CCR5-delta32 mutation in their DNA, which is the mutation needed for providing HIV resistance to the transplanted cells. This mutation is rare in the population of stem cell donors. When combined with the HLA compatibility requirement, each patient has even fewer potential donors.

Rejecting the transplant

Stem cell transplants also can cause a complication called graft versus host disease (or GVHD). This occurs when you receive a transplant, and the cells in that transplant attack your body. Just like your body has an immune system that protects you from things that can cause you harm (like bacteria), transplanted stem cells may view your body as foreign and attack you once inside your body. In fact, some of the patients cured of HIV developed GVHD. It is a serious but treatable complication of transplantation.


Most people who have HIV/AIDS live in low and middle-income countries . They generally don’t have access to the specialized doctors who perform stem cell transplants. Stem cell transplants are expensive. One study estimated that it could cost hundreds of thousands of dollars. This treatment must be administered at specialized hospital facilities with doctors and nurses who are trained in this type of treatment. The facilities must also have the resources to care for these complicated patients and manage any serious side effects. As a result, these treatments tend to be available in resource-rich settings. This is not necessarily aligned with the areas of greatest disease burden. 

Overall, there are several challenges with treating HIV/AIDS patients with stem cell transplants. However, there are still ongoing research efforts to make this treatment safer, more effective, and more widely available in the future.

What’s Next?

While stem cell transplants are often used to treat cancer patients, it’s not yet confirmed to be a safe and effective treatment for HIV/AIDS patients. However, scientists hope that further research on the CCR5-delta32 mutation may produce a more accessible cure for HIV. If you have HIV/AIDS, you should speak with your doctor about what treatment options are right for you. And you can continue to look out for new treatments as they become available in the coming years. 


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Dementia Causes and Symptoms

Do you know a friend or family member who is experiencing a decline in their mental abilities? If this decline is interfering with their daily life, they could be experiencing dementia. Read on to learn more about dementia causes and symptoms.

What Is Dementia?

What many may not realize is that dementia isn’t a disease. Instead, it describes a group of symptoms that affect social abilities, an individual’s ability to think and their memory. When combined with each other, these symptoms can interfere with an individual’s day-to-day functions. Memory loss doesn’t necessarily mean someone is suffering from dementia, because the loss of memory has many causes. If someone is suffering from memory loss without any of the other symptoms, they aren’t necessarily going to receive a dementia diagnosis.

Dementia Symptoms

The symptoms of dementia will vary according to the cause. However, there are some common symptoms and signs to watch for, including cognitive and psychological changes. Some of the cognitive changes include memory loss, difficulty finding or communicating words, difficulty with problem-solving or reasoning, difficulty with complex tasks, the inability to organize or plan tasks easily, challenges with motor functions or coordination, and experiencing disorientation and confusion. Some psychological changes include agitation, anxiety, depression, hallucinations, inappropriate behavior, paranoia and personality changes. Patients should consult with their primary care physician as soon as peers notice they are experiencing memory loss in conjunction with other symptoms.

Dementia’s Causes

It isn’t uncommon for the symptoms of dementia to manifest slowly. They often appear progressively over time, and become more noticeable during later stages of dementia. When this occurs, the impact on the individual’s core mental functions can become quite detrimental. Several factors contribute to this damage, including a stroke, excessive alcohol use, thyroid issues, vitamin deficiencies, genetic factors, medication side-effects and the brain not receiving enough blood or oxygen.

Signs of Dementia

Those who receive a diagnosis of dementia typically have two core mental functions that are significantly impaired. Signs could include vision issues, difficulty concentrating and paying attention, sleep disturbances, peers noticing them wandering, weight loss or no longer having physical control over their bodies.

Dementia Prevention

While there’s no way to guarantee dementia won’t happen, there are some steps to take to help with prevention. Individuals can keep their minds active, keep themselves physically fit, remain socially active, avoid or quit smoking, make sure they’re receiving enough vitamin D, maintain a healthy diet and reduce their blood sugar. If you make sure you monitor your medications, ensure you have good sleep habits and maintaining a healthy weight, these are all good ways of preventing dementia. The latest dementia treatments include talk-therapy, medications, person-centered care and alternative treatments.


research on dementia cure

Is there a cure for dementia?

There is currently no "cure" for dementia. In fact, because dementia is caused by different diseases it is unlikely that there will be a single cure for dementia.

Research is aimed at finding cures for dementia-causing diseases, such as Alzheimer's disease , frontotemporal dementia and dementia with Lewy bodies .

Read more about the causes of dementia

Huge strides have been made in understanding how different diseases cause damage in the brain and so produce dementia. And with increased funding over the past few years, there are now many more research studies and clinical trials taking place.

Although a cure may be some years away, there are some very promising advances.

Here are some of the areas researchers are working on and their findings so far.

Stem cells and dementia

Stem cells are "building block" cells. They can develop into many different cell types, including brain or nerve cells.

Scientists have taken skin cells from people with certain types of dementia, such as Alzheimer's disease, and "reprogrammed" them into stem cells in the lab. They've then triggered these stem cells to become brain cells.

By studying these cells, scientists have gained important insights into how the damage to the brain begins and how it might be halted.

These brain cells can also be used to test potential treatments at a very early stage.

Read more about Alzheimer's Research UK stem cell research centre


Immunotherapy involves boosting the body's own defences to fight disease. It's one of the approaches that has been very effective in other diseases such as cancer.

In dementia, some studies have used vaccination against abnormal proteins that build up in the brain in Alzheimer's disease. Other studies have used monoclonal antibodies (manmade versions of immune system proteins) to target these proteins to slow the disease.

For example, monoclonal antibodies have been designed to target the amyloid protein, which builds up in the brains of people with Alzheimer's disease.

Several studies involving vaccination or monoclonal antibodies targeting amyloid have so far been unsuccessful. However, lessons have been learnt from these failed studies and a number of new clinical trials are taking place.

One such trial is the CLARITY study, which is measuring how effective the monoclonal antibody BAN2401 (lecanemab) is at preventing or delaying the very early stages of Alzheimer's disease.

More recent trials have shown promise and one treatment using an antibody called aducanumab is currently under consideration by the US Food and Drug Administration (FDA).

In addition, immunotherapies are also being used to target the tau protein in Alzheimer's disease and in some other diseases.

Read more about the specific trials at Join Dementia Research

Another area being explored by researchers involves specialised immune cells in the brain called microglia. These cells are involved in clearing out debris from the brain.

In Alzheimer's disease, these immune cells appear to become overactive, which may be causing further damage to the brain. Current studies are trying to identify how to prevent this.

Gene-based therapies

There is great interest in using gene-based therapies to target genes that can cause dementia, such as Alzheimer's disease or frontotemporal dementia.

These gene-based therapies are also being used to reduce the production of proteins involved in a dementia-causing disease, such as tau in Alzheimer's disease.

Repurposing medicines

Developing new medicines to treat dementia takes many years and millions of pounds.

Repurposing existing drugs used for other conditions is another, often quicker, way of finding medicines to treat dementia.

Current medicines being explored as possible treatments for Alzheimer's and vascular dementia include those used for:

  • type 2 diabetes
  • high blood pressure
  • rheumatoid arthritis

Find out more about Alzheimer's Society Drug Discovery programme

Identifying who's at risk of dementia

Experts know that damage to the brain caused by Alzheimer's disease can start many years before symptoms appear. If people at risk of Alzheimer's could be identified at an early stage, it is hoped that treatments could be offered that would slow down or even stop the disease.

A major study, called PREVENT , concentrates on people in their 40s and 50s to identify those who are at greater risk of developing Alzheimer's (based on family history and genetics). It aims to understand what is happening in their brains before symptoms appear.

Specialised brain scans, known as PET scans , have been developed to study two proteins (amyloid and tau) in the brains of those with Alzheimer's disease. The aim is to increase the understanding of the disease process, and also to identify those people who will benefit most from new drug treatments.

Although PET scans are sometimes used to help with a dementia diagnosis, these highly specialised scans are usually only available as part of clinical trials.

A number of different trials are now under way in people who are currently well but are at increased risk of Alzheimer's disease.

Prevention is important

Even if we find an effective cure for dementia, it would be better to try to prevent it happening in the first place.

Research has shown that the risk factors for heart disease and stroke – such as raised blood pressure, diabetes, obesity and smoking – are also risk factors for dementia. By modifying or changing these risk factors in mid-life, the risk of dementia could be reduced by up to 30%.

Find out more about risk factors for dementia

Join dementia research

There are dozens of dementia research projects going on around the world, many of which are based in the UK.

If you have a dementia diagnosis or are worried about memory problems, you can help scientists understand more about the disease, and develop future treatments, by taking part in research.

If you are a carer, you can also take part as there are studies into the best ways to care for someone with a dementia diagnosis.

You can sign up to take part in trials on the NHS Join Dementia Research  website.

Sign up for the Dementia Information Service emails

Page last reviewed: 8 April 2021 Next review due: 8 April 2024

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Alzheimer's treatments: what's on the horizon.

Despite many promising leads, new treatments for Alzheimer's are slow to emerge.

Current Alzheimer's treatments temporarily improve symptoms of memory loss and problems with thinking and reasoning.

These Alzheimer's treatments boost the performance of chemicals in the brain that carry information from one brain cell to another. They include cholinesterase inhibitors and the medicine memantine (Namenda). However, these treatments don't stop the underlying decline and death of brain cells. As more cells die, Alzheimer's disease continues to progress.

Experts are cautious but hopeful about developing treatments that can stop or delay the progression of Alzheimer's. Experts continue to better understand how the disease changes the brain. This has led to the research of potential Alzheimer's treatments that may affect the disease process.

Future Alzheimer's treatments may include a combination of medicines. This is similar to treatments for many cancers or HIV / AIDS that include more than one medicine.

These are some of the strategies currently being studied.

Taking aim at plaques

Some of the new Alzheimer's treatments target clumps of the protein beta-amyloid, known as plaques, in the brain. Plaques are a characteristic sign of Alzheimer's disease.

Strategies aimed at beta-amyloid include:

Recruiting the immune system. Medicines known as monoclonal antibodies may prevent beta-amyloid from clumping into plaques. They also may remove beta-amyloid plaques that have formed. They do this by helping the body clear them from the brain. These medicines mimic the antibodies your body naturally produces as part of your immune system's response to foreign invaders or vaccines.

In 2023, the U.S. Food and Drug Administration (FDA) approved lecanemab (Leqembi) for people with mild Alzheimer's disease and mild cognitive impairment due to Alzheimer's disease.

A phase 3 clinical trial found that the medicine slowed cognitive decline in people with early Alzheimer's disease. The medicine prevents amyloid plaques in the brain from clumping. The phase 3 trial was the largest so far to study whether clearing clumps of amyloid plaques from the brain can slow the disease.

Lecanemab is given as an IV infusion every two weeks. Your care team likely will watch for side effects and ask you or your caregiver how your body reacts to the drug. Side effects of lecanemab include infusion-related reactions such as fever, flu-like symptoms, nausea, vomiting, dizziness, changes in heart rate and shortness of breath.

Also, people taking lecanemab may have swelling in the brain or may get small bleeds in the brain. Rarely, brain swelling can be serious enough to cause seizures and other symptoms. Also in rare instances, bleeding in the brain can cause death. The FDA recommends getting a brain MRI before starting treatment. It also recommends being monitored with brain MRI s during treatment for symptoms of brain swelling or bleeding.

People who carry a certain form of a gene known as APOE e4 appear to have a higher risk of these serious complications. The FDA recommends being tested for this gene before starting treatment with lecanemab.

If you take a blood thinner or have other risk factors for brain bleeding, talk to your health care professional before taking lecanemab. Blood-thinning medicines may increase the risk of bleeds in the brain.

More research is being done on the potential risks of taking lecanemab. Other research is looking at how effective lecanemab may be for people at risk of Alzheimer's disease, including people who have a first-degree relative, such as a parent or sibling, with the disease.

Another medicine being studied is donanemab. It targets and reduces amyloid plaques and tau proteins. It was found to slow declines in thinking and functioning in people with early Alzheimer's disease.

Aducanumab (Aduhelm) has been approved for the treatment of Alzheimer's disease in some people, but it's not widely used. Results were mixed in studies about how effective aducanumab is at slowing cognitive decline. Insurance coverage of the medicine is limited.

The monoclonal antibody solanezumab did not show benefits for individuals with preclinical, mild or moderate Alzheimer's disease. Solanezumab did not lower beta-amyloid in the brain, which may be why it wasn't effective.

Preventing destruction. A medicine initially developed as a possible cancer treatment — saracatinib — is now being tested in Alzheimer's disease.

In mice, saracatinib turned off a protein that allowed synapses to start working again. Synapses are the tiny spaces between brain cells through which the cells communicate. The animals in the study experienced a reversal of some memory loss. Human trials for saracatinib as a possible Alzheimer's treatment are now underway.

Production blockers. These therapies may reduce the amount of beta-amyloid formed in the brain. Research has shown that beta-amyloid is produced from a "parent protein" in two steps performed by different enzymes.

Several experimental medicines aim to block the activity of these enzymes. They're known as beta- and gamma-secretase inhibitors. Recent studies showed that the beta-secretase inhibitors did not slow cognitive decline. They also were associated with significant side effects in those with mild or moderate Alzheimer's. This has decreased enthusiasm for the medicines.

Keeping tau from tangling

A vital brain cell transport system collapses when a protein called tau twists into tiny fibers. These fibers are called tangles. They are another common change in the brains of people with Alzheimer's. Researchers are looking at a way to prevent tau from forming tangles.

Tau aggregation inhibitors and tau vaccines are currently being studied in clinical trials.

Reducing inflammation

Alzheimer's causes chronic, low-level brain cell inflammation. Researchers are studying ways to treat the processes that lead to inflammation in Alzheimer's disease. The medicine sargramostim (Leukine) is currently in research. The medicine may stimulate the immune system to protect the brain from harmful proteins.

Researching insulin resistance

Studies are looking into how insulin may affect the brain and brain cell function. Researchers are studying how insulin changes in the brain may be related to Alzheimer's. However, a trial testing of an insulin nasal spray determined that the medicine wasn't effective in slowing the progression of Alzheimer's.

Studying the heart-head connection

Growing evidence suggests that brain health is closely linked to heart and blood vessel health. The risk of developing dementia appears to increase as a result of many conditions that damage the heart or arteries. These include high blood pressure, heart disease, stroke, diabetes and high cholesterol.

A number of studies are exploring how best to build on this connection. Strategies being researched include:

  • Current medicines for heart disease risk factors. Researchers are looking into whether blood pressure medicines may benefit people with Alzheimer's. They're also studying whether the medicines may reduce the risk of dementia.
  • Medicines aimed at new targets. Other studies are looking more closely at how the connection between heart disease and Alzheimer's works at the molecular level. The goal is to find new potential medicines for Alzheimer's.
  • Lifestyle choices. Research suggests that lifestyle choices with known heart benefits may help prevent Alzheimer's disease or delay its onset. Those lifestyle choices include exercising on most days and eating a heart-healthy diet.

Studies during the 1990s suggested that taking hormone replacement therapy during perimenopause and menopause lowered the risk of Alzheimer's disease. But further research has been mixed. Some studies found no cognitive benefit of taking hormone replacement therapy. More research and a better understanding of the relationship between estrogen and cognitive function are needed.

Speeding treatment development

Developing new medicines is a slow process. The pace can be frustrating for people with Alzheimer's and their families who are waiting for new treatment options.

To help speed discovery, the Critical Path for Alzheimer's Disease (CPAD) consortium created a first-of-its-kind partnership to share data from Alzheimer's clinical trials. CPAD 's partners include pharmaceutical companies, nonprofit foundations and government advisers. CPAD was formerly called the Coalition Against Major Diseases.

CPAD also has collaborated with the Clinical Data Interchange Standards Consortium to create data standards. Researchers think that data standards and sharing data from thousands of study participants will speed development of more-effective therapies.

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FDA-approved drugs for Alzheimer's

  • Alternative treatments and supplements  

Research into future treatments

Participate in clinical trials.

The U.S. Food and Drug Administration (FDA) has approved medications that fall into two categories: drugs that change disease progression in people living with Alzheimer’s, and drugs that may temporarily mitigate some symptoms of the disease. Treatments may be available in different forms (pill, patch or other). When considering any treatment, it is important to have a conversation with a health care professional to determine whether it is appropriate. A physician who is experienced in using these types of medications should monitor people who are taking them and ensure that the recommended guidelines are strictly observed.

Drugs that change disease progression

Drugs in this category slow disease progression by going after the underlying biology of the disease process. They aim to slow the decline of memory and thinking, as well as function, in people living with Alzheimer's disease.

Amyloid-targeting approaches

Anti-amyloid treatments work by attaching to and removing beta-amyloid, a protein that accumulates into plaques, from the brain. Each works differently and targets beta-amyloid at a different stage of plaque formation. These treatments change the course of the disease in a meaningful way for people in the early stages, giving them more time to participate in daily life and live independently. Clinical trial participants who received anti-amyloid treatments experienced reduction in cognitive decline observed through measures of cognition and function. Examples of cognition measures include:

  • Orientation. 

Examples of functional measures include:

  • Conducting personal finances.
  • Performing household chores such as cleaning.

Anti-amyloid treatments do have side effects. These treatments can cause serious allergic reactions. Side effects can also include amyloid-related imaging abnormalities (ARIA), infusion-related reactions, headaches and falls. ARIA is a common side effect that does not usually cause symptoms but can be serious. It is typically a temporary swelling in areas of the brain that usually resolves over time. Some people may also have small spots of bleeding in or on the surface of the brain with the swelling, although most people with swelling in areas of the brain do not have symptoms. Some may have symptoms of ARIA such as headache, dizziness, nausea, confusion and vision changes. Some people have a genetic risk factor (ApoE ε4 gene carriers) that may cause an increased risk for ARIA. The FDA encourages that testing for ApoE ε4 status should be performed prior to initiation of treatment to inform the risk of developing ARIA. Prior to testing, doctors should discuss with patients the risk of ARIA and the implications of genetic testing results. These are not all the possible side effects, and individuals should talk with their doctors to develop a treatment plan that is right for them, including weighing the benefits and risks of all approved therapies. Aducanumab (Aduhelm®) Aducanumab (Aduhelm ) is an anti-amyloid antibody intravenous (IV) infusion therapy that is delivered every month. It has received accelerated approval from the FDA to treat early Alzheimer's disease, including people living with mild cognitive impairment (MCI) or mild dementia due to Alzheimer's disease who have confirmation of elevated beta-amyloid in the brain. Aducanumab was the first therapy to demonstrate that removing beta-amyloid from the brain reduces cognitive and functional decline in people living with early Alzheimer's. Lecanemab (Leqembi®) Lecanemab (Leqembi) is an anti-amyloid antibody intravenous (IV) infusion therapy that is delivered every two weeks. It has received traditional approval from the FDA to treat early Alzheimer's disease, including people living with mild cognitive impairment (MCI) or mild dementia due to Alzheimer's disease who have confirmation of elevated beta-amyloid in the brain. There is no safety or effectiveness data on initiating treatment at earlier or later stages of the disease than were studied. Lecanemab was the second therapy to demonstrate that removing beta-amyloid from the brain reduces cognitive and functional decline in people living with early Alzheimer's. Learn more: Medications for Memory

Drugs that treat symptoms

Cognitive (memory and thinking) symptoms These medications are prescribed to treat symptoms related to memory and thinking. While these drugs cannot stop the damage Alzheimer’s causes to brain cells, they may help lessen or stabilize symptoms for a limited time by affecting certain chemicals involved in carrying messages between the brain's nerve cells. The drugs currently approved to treat cognitive symptoms are cholinesterase inhibitors and glutamate regulators. Learn more: Medications for Memory

Tips from people living with Alzheimer's: Medication safety

  • Keep a calendar and check off each dose as it's taken.
  • Set up a pill box each night for use the next day.
  • Set the alarm on your cell phone or schedule dosing around meal times.
  • See More Tips

Alternative treatments and supplements

Research suggests that lifestyle habits, such as eating a healthy diet, may reduce a person’s risk for cognitive decline and dementia. However, there isn’t a single food, ingredient or supplement that has been shown to prevent, treat or cure Alzheimer’s or other dementias. There are remedies, supplements and “medical foods” that are often referred to as alternative treatments. Alternative treatments are not regulated and do not need to adhere to the same standards as FDA-approved treatments. Claims about their safety and effectiveness are based largely on testimonials, tradition or a small body of scientific research. If you are considering taking an alternative treatment or dietary supplement, it’s important to talk to your physician. He or she can provide you with the best possible advice for your situation and make you aware of any risks. Even if advertised as “natural,” alternative treatments can involve potentially powerful substances that have not met FDA standards for effectiveness or safety, and some alternative medicines can cause unintended reactions when taken with prescription medications. Learn more: Alternative Therapies Here is a list of questions to ask when considering an alternative treatment or supplement: Has the FDA approved this product for the treatment of Alzheimer’s or dementia symptoms? The FDA may have reviewed the data on a product, but found it to be ineffective for the intended purpose. In this instance, the company may still release the product as a medical food, either with or without changes. In the United States, a product can only be considered a medical food if it is designed to treat a condition that has a “distinctive nutritional requirement.” According to the FDA, Alzheimer’s, as currently understood, does not have distinctive nutritional requirements, and therefore, in the United States, no product can legitimately be described as a medical food for Alzheimer’s. Is there independent research to support the safety and effectiveness of this product for treating Alzheimer's or other dementia? If the testing entity has a vested interest in the outcome (e.g., testing done by the company developing the product), the results may not be reliable. To best serve individuals living with Alzheimer’s and their families, the Alzheimer’s Association strongly encourages makers of products that claim to be beneficial for those with Alzheimer’s or other dementia to conduct definitive clinical trials. Does the developer of the product or the person recommending it to you have a potential financial gain from the use of the medication? If so, use extreme caution. Check with your care team to see if they have any questions or concerns with your plan to use it. Does the FDA oversee how dietary supplements are manufactured? No. It is up to each manufacturer and distributer of dietary supplements to meet all safety and labeling requirements of the Dietary Supplement Health and Education Act of 1994 (DSHEA) and the FDA. Most in the industry act responsibly, but some adulterated or misbranded products have made it to market. Therefore, people with Alzheimer’s and their families have no absolute guarantee that supplements contain the ingredients listed on the label in the specified amounts. Is the product compatible with the other medications you are taking or with your diagnoses? Be sure to check with your doctor or pharmacist to find out whether the product could cause negative outcomes given your diagnoses and any FDA-approved medications you are taking. The lack of rigorous research for these products means little (or nothing) is known about the effects, both when taken alone or in combination with approved drugs. We often don’t know whether the products will interact with, and possibly decrease, the effectiveness of approved drugs taken for Alzheimer’s and other dementia.

Researchers are conducting studies to find new interventions and treatments for Alzheimer’s. Because the disease is complex and not fully understood — with a multitude of factors that may contribute to risk — today’s research focuses on several areas of study. Many drugs and medical devices in development aim to interrupt the disease process by impacting one or more of the brain changes associated with Alzheimer’s. These changes offer potential "targets" for new drugs or devices to slow or stop the progress of the disease. These promising targets include the buildup of beta-amyloid and tau protein (hallmarks of Alzheimer's), neuroinflammation, immune response, metabolic changes and more. Researchers believe that future treatments will involve a combination of medications or devices aimed at several targets, along with risk reduction strategies similar to current treatments for many cancers and AIDS. As the leading nonprofit funder of Alzheimer’s research, the Alzheimer’s Association has played a vital role in every significant development in dementia science. Learn more: Research and Progress , Part the Cloud

Recruiting and retaining clinical trial participants is now the greatest obstacle, other than funding, to developing the next generation of Alzheimer's treatments. Individuals with dementia, caregivers and healthy volunteers are all needed to participate in clinical studies focused on Alzheimer's and all other dementia. If you are interested in participating in a current clinical study, Alzheimer's Association TrialMatch® is a free, easy-to-use clinical studies matching service that generates customized lists of studies based on user-provided information. The TrialMatch database includes:

  • Trials for new drugs or non-drug-based dementia treatments.
  • Studies on new tests or procedures for diagnosis.
  • Trials that investigate ways to prevent the onset of diseases.
  • Studies exploring ways to improve quality of life for individuals living with a chronic illness, their caregivers and family members.
  • Online studies.

Learn more: Clinicial Trials and Alzheimer's Association TrialMatch®

Help Advance Research

At the heart of all medical advances are clinical trials. You can participate in clinical research, helping to find new treatments, and, ultimately, a cure.

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Recent breakthroughs in Alzheimer’s research provide hope for patients

While there is no cure, researchers say a newly approved drug, advanced testing, and increasing knowledge about the disease may improve patients’ lives..

Lori Weiss, 65, a retired teacher, has early onset Alzheimer’s disease. She is enrolled in a drug clinical trial and is hopeful about recent progress in disease research.

A few years ago, Lori Weiss, a high school math and engineering teacher, noticed it was taking her longer to do her lesson plans and grading. She also repeatedly needed to ask for help using spreadsheets she’d once mastered and she struggled to answer her students’ questions.

The symptoms were all too familiar to Weiss. Not only had she cared for her grandfather with Alzheimer’s disease when she was a teenager, she’d also watched her mother slowly lose her memory to the disease for nearly two decades. She had aunts, uncles, and a cousin as well who were diagnosed with the neurological disorder, which gradually steals a person’s memory and cognitive abilities.

“It’s rampant in my family,” Weiss says.

Weiss decided to speak with her primary care physician, who referred her to a neurologist for testing. In 2020, at the age of 62, Weiss was diagnosed with mild cognitive impairment. Two years after that, a PET scan revealed amyloid plaques, a buildup of toxic proteins in the brain that disrupt neural function and are a hallmark of Alzheimer’s disease.

Soon, Weiss began to lose her sense of direction, which prompted fears that she might be forced into a full-time care facility at a young age.

“Losing my freedom was just more than I could handle,” she says. Around that time, a friend saw a TV advertisement for a clinical trial for a drug that would attempt to slow progression of the disease using manmade monoclonal antibodies to attack and remove the amyloid plaques in the brain.

“I don’t even think that I thought twice about” enrolling in the trial, says Weiss, who has been receiving monthly infusions of the drug, called donanemab , near her home in Portland, Oregon, for about a year. “I just said, ‘Yeah, sign me up!’”

Although donanemab is not approved by the Food and Drug Administration (FDA), it uses a similar approach to the drug lecanemab, which received accelerated FDA approval on Jan. 6, and which showed biological and clinical benefits for patients in trials. In November, drugmaker Eli Lilly and Company announced promising results for donanemab, but last week, the FDA denied the company’s request for accelerated approval, saying it needed more data for participants receiving the drug for at least 12 months.

Nonetheless, this recent progress has given people like Weiss hope that previous generations have not had.

“Alzheimer’s research is getting to a place where cancer research was maybe 30, 40 years ago.” Anton Porsteinsson, MD, University of Rochester Medical Center in New York

Participating in the clinical trial “has had a huge impact,” Weiss says. “It’s given me the drive to do things while I can; it’s given me the desire to talk to more people about getting treatment, getting diagnosed early, and getting in drug trials.”

Weiss says that since she’s begun taking donanemab, she’s regained her sense of direction and has not noticed significant cognitive decline. For her, even the hope that the trial has given her has made all the difference.

“For my husband and I, it’s totally changed our lives. Instead of living in fear … we treat each day like it’s Valentine’s Day,” Weiss says. Getting diagnosed early has “given me so much more life. [I thought] getting the disease was a death sentence for me, but I’m taking a water painting class, I’m in a walking group and a music group. I thrive on my relationships with my Alzheimer’s friends and other friends, and I’m connected with my family. I feel like I’m living my life. It’s so much better than I imagined.”

Lori Weiss, 65, with her husband, Kevin Weiss, 60, at Rockaway Beach in Oregon.

And while Alzheimer’s researchers are careful to emphasize that they are still a long way from a cure, many say the hope is not a false one. The field has had several breakthroughs in recent years, from identifying easier and cheaper ways to diagnose the disease early to better understanding how individuals with the disease might require a variety of interventions.

“Alzheimer’s research is getting to a place where cancer research was maybe 30, 40 years ago,” says Anton Porsteinsson, MD, director of the Alzheimer’s Disease Care, Research and Education Program at the University of Rochester Medical Center in New York. “I think we’re at a point where we’re going to see a logarithmic increase in discovery.”

Fighting a complex disease

Alzheimer’s disease, which was discovered in 1906 and is now the seventh leading cause of death in the United States, has long boggled the scientific community. Though research over the decades has identified characteristics of the disease — such as the presence of amyloid plaques between neurons and the buildup, known as tangles, of another toxic protein, tau, inside neurons — questions remain about what causes the disease and how best to treat it in a clinically meaningful way.

“It’s a complex disease. It’s not just a single molecule that’s gone awry. It’s not an infection that has a viral particle,” says Ronald C. Petersen, MD, PhD, director of the Mayo Clinic Alzheimer’s Disease Research Center in Rochester, Minnesota. “We’ve defined it by the presence of amyloid , neuritic plaques , and neurofibrillary tangles , but that’s just the tip of the iceberg.”

Many researchers now believe that the precursors to developing Alzheimer’s begin to accumulate in the brain 10 or more years before symptoms begin to show.

Alzheimer’s disease progression affects the brain much like a forest fire, with many factors affecting how it spreads, says Rudolph E. Tanzi, PhD, director of the Genetics and Aging Research Unit at Massachusetts General Hospital in Boston.

Amyloid plaques and tau tangles can build up over years, at some point triggering an inflammatory response that can quickly destroy brain cells. These conditions can be influenced by a range of factors, from genetic predisposition to environmental exposures to lifestyle, he explains.

That’s why the solution to treating — or ideally, preventing — Alzheimer’s disease will likely require a combination of interventions, Petersen says.

One important part of the puzzle — and a part that has been the focus of much pharmaceutical development — is targeting the amyloid plaques.

This approach has been controversial. In 2021, the FDA granted accelerated approval to the anti-amyloid drug aducanumab, sold as Aduhelm, despite objections from an advisory committee and outcry from the scientific community that the lack of clinical benefit made the drug’s high cost, initially set at $56,000 a year and later reduced to $28,000 a year, unjustifiable. A Congressional investigation found numerous flaws and irregularities in the process the FDA used when approving the drug.

Lecanemab, on the other hand, has been met with more optimism in the Alzheimer’s research community because its clinical trials demonstrated an actual clinical benefit to patients early in the disease progression.

“The field is feeling that, finally, we have a drug that didn’t have the controversy aducanumab had,” Petersen says. “It looks like it does what it’s supposed to do biologically [and] this looks like it could be meaningful for patients.”

In clinical trials , lecanemab showed a modest but tangible decrease in cognitive decline (of 27%) over 18 months in Alzheimer’s patients who were early in the disease’s progression, compared with patients who were given a placebo. Though it’s far from a cure, experts say it could give patients months of retaining memory and cognition that they might otherwise lose, a prospect that could be meaningful for patients and their families who have no other options.

But this drug, too, has stirred some controversy because of its high price tag and potentially deadly side effects, including swelling and bleeding in the brain. The pharmaceutical company Eisai has priced lecanemab, sold as Leqembi, at $26,000 a year, and the Centers for Medicare and Medicaid Services has yet to decide if it will cover the drug.

“It’s very expensive,” Tanzi says, explaining that patients who take the drug will also need several MRIs to check for brain bleeds on top of the cost of the infusions. “There is a health care disparity this could create; those who want to remove amyloid can pay out of pocket [but] the average person can’t afford that. The wealthy can protect themselves.”

Equity starting in research

The high costs of treatment could also exacerbate existing racial disparities when it comes to Alzheimer’s outcomes. Although Black Americans are about twice as likely as White Americans to have Alzheimer’s, and Hispanics are about 1.5 times as likely to have it, White people make up a disproportionate majority of clinical trial participants and non-White people report greater barriers to diagnosis and access to care, according to the Alzheimer’s Association .

“Most of the research operations are either based at large academic institutions or private professional research sites,” Porsteinsson explains about pharmaceutical company trials. “The temptation [for researchers] is to go where the treatment is ‘easiest’; where you’ve recruited before.”

In its clinical trial recruitment for lecanemab, the University of Rochester succeeded in increasing the representation of Hispanic participants, but struggled to include a representative number of Black patients.

“We can’t just wait until the brain deteriorates.” Rudolph E. Tanzi, PhD, Massachusetts General Hospital in Boston

“If we want to go after historically underrepresented groups in research, first we need to recognize they’re underrepresented for a reason,” Porsteinsson says. “There might have been a poor experience with researchers coming [into their community], doing a study [the researchers] needed, and then basically leaving. There isn’t an ongoing commitment.”

He says that if Alzheimer’s treatments are going to be meaningful to all people affected by the disease, it will take a concerted effort to include more diversity in clinical trial participants, not only in race and ethnicity, but in health status and inclusion of people with comorbidities. Often, trials tend to select for the healthiest patients possible, he explains.

“[We must] secure making our research more representative of the American population,” Porsteinsson says. “It’s going to take an investment in infrastructure and it’s going to take an investment of time.”

A stage set for discovery

Alzheimer’s disease already affects more than six million people living in the United States, and that number is projected to grow to 13 million by 2050. It’s also an incredibly financially costly disease, with an economic impact of $321 billion in health care costs in 2022, expected to rise to $1 trillion by 2050, according to the Alzheimer’s Association. That prospect prompted the U.S. Congress to approve an additional $226 million to the National Institutes of Health for Alzheimer’s research in December, bringing the annual federal funding outlay to more than $3.7 billion .

Experts say it is not in vain. Research efforts, particularly those at teaching hospitals, have helped unlock mysteries about the genetic underpinnings of the disease, ways to identify biomarkers in the blood that can more easily diagnose the disease in its earliest states, and complex treatment approaches that use lifestyle interventions and a combination of drug therapies.

Tanzi believes that the future of Alzheimer’s treatment and prevention will be similar to current management of heart disease and diabetes. It could mean more regular screenings and early interventions, such as taking anti-amyloid drugs and incorporating lifestyle and diet changes before the disease gets out of control. And for those already diagnosed, it means using a combination of therapies that target different aspects of the disease, such as neuroinflammation and plaque buildup.

“We can’t just wait until the brain deteriorates,” he says.

With the current momentum, Porsteinsson hopes that young and aspiring physician-scientists will be inspired to join the field and continue the research for generations to come.

“What many medical students and young doctors have historically been hesitant about is that dementia is very nebulous, there is a lot of gray there. … They felt things were pretty bleak, too uncertain, and there was too little you could offer,” he says. “Now, I think we are at the dawn of a very different era.”

  • Health Care
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As populations age, Alzheimer’s and dementia are becoming more prevalent. A new drug could offer hope

Alzheimer’s dementia population age brain injury

As populations age, the number of cases of dementia rises. Image:  Unsplash/centelm

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Illustration of cells in an Alzheimer’s affected brain.

Expert discusses recent lecanemab trial, why it appears to offer hope for those with deadly disease

By Alvin Powell Harvard Staff Writer

Date June 5, 2023 June 5, 2023

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Researchers say we appear to be at the start of a new era for Alzheimer’s treatment. Trial results published in January showed that for the first time a drug has been able to slow the cognitive decline characteristic of the disease. The drug, lecanemab, is a monoclonal antibody that works by binding to a key protein linked to the malady, called amyloid-beta, and removing it from the body. Experts say the results offer hope that the slow, inexorable loss of memory and eventual death brought by Alzheimer’s may one day be a thing of the past.

The Gazette spoke with Scott McGinnis , an assistant professor of neurology at Harvard Medical School and Alzheimer’s disease expert at Brigham and Women’s Hospital , about the results and a new clinical trial testing whether the same drug given even earlier can prevent its progression.

Scott McGinnis

GAZETTE: The results of the Clarity AD trial have some saying we’ve entered a new era in Alzheimer’s treatment. Do you agree?

McGINNIS: It’s appropriate to consider it a new era in Alzheimer’s treatment. Until we obtained the results of this study, trials suggested that the only mode of treatment was what we would call a “symptomatic therapeutic.” That might give a modest boost to cognitive performance — to memory and thinking and performance in usual daily activities. But a symptomatic drug does not act on the fundamental pathophysiology, the mechanisms, of the disease. The Clarity AD study was the first that unambiguously suggested a disease-modifying effect with clear clinical benefit. A couple of weeks ago, we also learned a study with a second drug, donanemab, yielded similar results.

GAZETTE: Hasn’t amyloid beta, which forms Alzheimer’s characteristic plaques in the brain and which was the target in this study, been a target in previous trials that have not been effective?

McGINNIS: That’s true. Amyloid beta removal has been the most widely studied mechanism in the field. Over the last 15 to 20 years, we’ve been trying to lower beta amyloid, and we’ve been uncertain about the benefits until this point. Unfavorable results in study after study contributed to a debate in the field about how important beta amyloid is in the disease process. To be fair, this debate is not completely settled, and the results of Clarity AD do not suggest that lecanemab is a cure for the disease. The results do, however, provide enough evidence to support the hypothesis that there is a disease-modifying effect via amyloid removal.

GAZETTE: Do we know how much of the decline in Alzheimer’s is due to beta amyloid?

McGINNIS: There are two proteins that define Alzheimer’s disease. The gold standard for diagnosing Alzheimer’s disease is identifying amyloid beta plaques and tau neurofibrillary tangles. We know that amyloid beta plaques form in the brain early, prior to accumulation of tau and prior to changes in memory and thinking. In fact, the levels and locations of tau accumulation correlate much better with symptoms than the levels and locations of amyloid. But amyloid might directly “fuel the fire” to accelerated changes in tau and other downstream mechanisms, a hypothesis supported by basic science research and the findings in Clarity AD that treatment with lecanemab lowered levels of not just amyloid beta but also levels of tau and neurodegeneration in the blood and cerebrospinal fluid.

GAZETTE: In the Clarity AD trial, what’s the magnitude of the effect they saw?

McGINNIS: The relevant standards in the trial — set by the FDA and others — were to see two clinical benefits for the drug to be considered effective. One was a benefit on tests of memory and thinking, a cognitive benefit. The other was a benefit in terms of the performance in usual daily activities, a functional benefit. Lecanemab met both of these standards by slowing the rate of decline by approximately 25 to 35 percent compared to placebo on measures of cognitive and functional decline over the 18-month studies.

Scott McGinnis.

“In a perfect world, we’d have treatments that completely stop decline and even restore function. We’re not there yet, but this represents an important step toward that goal.”

GAZETTE: What are the key questions that remain?

McGINNIS: An important question relates to the stages at which the interventions were done. The study was done in subjects with mild cognitive impairment and mild Alzheimer dementia. People who have mild cognitive impairment have retained their independence in instrumental activities of daily living — for example, driving, taking medications, managing finances, errands, chores — but have cognitive and memory changes beyond what we would attribute to normal aging. When people transition to mild dementia, they’re a bit further along. The study was for people within that spectrum but there’s some reason to believe that intervening even earlier might be more effective, as is the case with many other medical conditions.

We’re doing a study here called the AHEAD study that is investigating the effects of lecanemab when administered earlier, in cognitively normal individuals who have elevated brain amyloid, to see whether we see a preventative benefit. The hope is that we would at least see a delay to onset of cognitive impairment and a favorable effect not only on amyloid biomarkers, but other biomarkers that might capture progression of the disease.

GAZETTE: Is anybody in that study treatment yet or are you still enrolling?

McGINNIS: There’s a rolling enrollment, so there are people who are in the double-blind phase of treatment, receiving either the drug or the placebo. But the enrollment target hasn’t been reached yet so we’re still accepting new participants.

GAZETTE: Is it likely that we may see drug cocktails that go after tau and amyloid? Is that a future approach?

McGINNIS: It has not yet been tried, but those of us in the field are very excited at the prospect of these studies. There’s been a lot of work in recent years on developing therapeutics that target tau, and I think we’re on the cusp of some important breakthroughs. This is key, considering evidence that spreading of tau from cell to cell might contribute to progression of the disease. Additionally, for some time, we’ve had a suspicion that we will likely have to target multiple different aspects of the disease process, as is the case with most types of cancer treatment. Many in our field believe that we will obtain the most success when we identify the most pertinent mechanisms for subgroups of people with Alzheimer’s disease and then specifically target those mechanisms. Examples might include metabolic dysfunction, inflammation, and problems with elements of cellular processing, including mitochondrial functioning and processing old or damaged proteins. Multi-drug trials represent a natural next step.

GAZETTE: What about side effects from this drug?

McGINNIS: We’ve known for a long time that drugs in this class, antibodies that harness the power of the immune system to remove amyloid, carry a risk of causing swelling in the brain. In most cases, it’s asymptomatic and just detected by MRI scan. In Clarity AD, while 12 to 13 percent of participants receiving lecanemab had some level of swelling detected by MRI, it was symptomatic in only about 3 percent of participants and mild in most of those cases.

Another potential side effect is bleeding in the brain or on the surface of the brain. When we see bleeding, it’s usually very small, pinpoint areas of bleeding in the brain that are also asymptomatic. A subset of people with Alzheimer’s disease who don’t receive any treatment are going to have these because they have amyloid in their blood vessels, and it’s important that we screen for this with an MRI scan before a person receives treatment. In Clarity AD, we saw a rate of 9 percent in the placebo group and about 17 percent in the treatment group, many of those cases in conjunction with swelling and mostly asymptomatic.

The scenario that everybody worries about is a hemorrhagic stroke, a larger area of bleeding. That was much less common in this study, less than 1 percent of people. Unlike similar studies, this study allowed subjects to be on anticoagulation medications, which thin the blood to prevent or treat clots. The rate of macro hemorrhage — larger bleeds — was between 2 and 3 percent in the anticoagulated participants. There were some highly publicized cases including a patient who had a stroke, presented for treatment, received a medication to dissolve clots, then had a pretty bad hemorrhage. If the drug gets full FDA approval, is covered by insurance, and becomes clinically available, most physicians are probably not going to give it to people who are on anticoagulation. These are questions that we’ll have to work out as we learn more about the drug from ongoing research.

GAZETTE: Has this study, and these recent developments in the field, had an effect on patients?

McGINNIS: It has had a considerable impact. There’s a lot of interest in the possibility of receiving this drug or a similar drug, but our patients and their family members understand that this is not a cure. They understand that we’re talking about slowing down a rate of decline. In a perfect world, we’d have treatments that completely stop decline and even restore function. We’re not there yet, but this represents an important step toward that goal. So there’s hope. There’s optimism. Our patients, particularly patients who are at earlier stages of the disease, have their lives to live and are really interested in living life fully. Anything that can help them do that for a longer period of time is welcome.

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Research on Alzheimer’s Disease and Related Dementias

Breadth of NIH-supported research on Alzheimer’s and related dementias

Alzheimer’s disease and related dementias are a series of complex brain disorders that affect millions of Americans and many more worldwide. They have an enormous impact on individuals and their families, long-term care facilities, health care providers, health care systems and infrastructure, and the communities in which we all live. As the economic, social, and personal costs of these diseases climb, the research community is working to discover solutions that will improve the lives of those with dementia, their caregivers, and their communities.

The federal government’s Alzheimer’s and related dementias research strategy focuses on engaging a cross-disciplinary team of geneticists, epidemiologists, gerontologists, behavioral scientists, disease and structural biologists, pharmacologists, clinical researchers, and others to bring the greatest and most diverse expertise to the field. This includes training new generations of researchers and clinician-scientists and engaging in innovative partnerships with private industry, nonprofit groups, and more to foster collaboration and broaden access to research resources and data.

Critically, the government’s research strategy includes the search to find treatment and prevention strategies, as well as interventions, services, and supports to improve quality of life for those already living with these diseases and their families.

Who Funds Alzheimer’s and Related Dementias Research?

The National Institutes of Health (NIH) is made up of Institutes, Centers, and Offices that conduct and fund research into all aspects of human health. The National Institute on Aging (NIA) leads NIH’s efforts in clinical, behavioral, and social research in Alzheimer’s and related dementias through efforts aimed at finding ways to treat and ultimately prevent the disorder. NIA collaborates closely with the National Institute of Neurological Disorders and Stroke (NINDS), which manages a research portfolio targeting Alzheimer’s disease-related dementias. While some of this research takes place in NIH laboratories, the vast majority of NIH support is provided through a competitive grants process to institutions and small businesses across the country. Other federal agencies support a range of activities focused on public health and community programs.

Advances in Alzheimer's and Related Dementias Research

As the nation’s biomedical research agency, the National Institutes of Health (NIH) supports research spanning from basic biology to drug development to clinical studies to evaluating public health outcomes. Within the past several decades, researchers have made great strides toward better understanding what causes Alzheimer’s and related dementias and discovering approaches that may prevent, diagnose, and treat them. Some highlights of these efforts include:

  • Early detection and diagnosis. Researchers have made significant progress in developing, testing, and validating biomarkers that detect signs of the disease process. For example, NIH-supported scientists have made advances in blood-based tests that can be used to screen volunteers for research studies. It is likely that in the future, physicians will be able to use such tests to screen their patients for Alzheimer’s and related dementias before symptoms appear. Researchers are also studying behavioral and social indicators, including problems with paying bills and a combined decline in memory and walking speed, that may be early signs of these diseases. Other early markers are also under study. Early and clear diagnoses of Alzheimer’s and related dementias will enable researchers to develop appropriate treatment and prevention strategies based on an individual’s disease profile.
  • Population studies and precision medicine. By studying large, diverse groups of people, researchers are identifying which genes, behaviors, and lifestyle choices are linked with dementia. Population studies have shown that sedentary behavior, low socioeconomic status, low level of education, and living in a poor neighborhood may increase the risk of developing dementia. These observational discoveries, along with knowledge of genetic and other factors, can be used to advance the development of methods for diagnosis, prevention, and treatment at an individualized level.
  • Lifestyle interventions. Researchers are investigating interventions around exercise, healthy eating, cognitive training, preventive health care, and management of chronic conditions that — if made early in life — may be able to prevent or delay disease symptoms. NIA currently supports more than 100 trials testing behavioral and lifestyle interventions.
  • Disease pathways. NIH’s research investments to identify the biological mechanisms that lead to Alzheimer’s and related dementias are fundamental for the discovery of potential drugs that target them. There are many biological pathways that scientists can target with investigational drugs. For example, several recent studies have further revealed how components of the immune system, brain inflammation, and possibly viruses and bacteria — including the many tiny organisms that live in the digestive system, known as the gut microbiome — contribute to the development of these diseases. Scientists are also exploring genetic variations that may contribute to or prevent disease.
  • Drug discovery. Thanks to the substantial investment in Alzheimer’s and related dementias research over the past several years, NIH has increased drug discovery significantly. Of the many compounds in NIH-supported drug development programs for Alzheimer’s and related dementias, 10 drug candidates have now matured through the pipeline, from discovery in the lab all the way through preclinical development, to reach the stage of human testing. NIA currently supports more than 40 clinical trials testing drug candidates that target many different aspects of the disease.
  • Infrastructure development. NIH is continually investing in research infrastructure to advance Alzheimer’s and related dementias research. Efforts in this area include launching a consortium for Alzheimer’s clinical trials, research efforts to validate cognitive tests in a primary care setting, and genetics and genomics sharing and collaboration initiatives.

Challenges for the Alzheimer’s Research Community

Even with the progress that we’ve made, there's still a lot of work to do before we can find treatment and prevention strategies for the millions of people affected by Alzheimer’s and related dementias. These devastating diseases are highly complex conditions caused by an interplay of genetic, lifestyle, and environmental factors. They usually develop gradually — changes in the brain take place over years and even decades, long before the first symptoms appear. This complexity presents challenges to the discovery and development of new drugs and other prevention and treatment approaches. Alzheimer’s disease does not affect all communities at the same rate, and research has found that a person’s likelihood of getting Alzheimer’s can be affected by their sex, ethnicity, race, socioeconomic status, and other factors. These differences are called health disparities.

Researchers believe Alzheimer’s disease and related dementias will likely require multiple treatments customized to individuals. We also know that as the older adult population continues to grow — aging remains the most important risk factor for dementia — we will see increased numbers of people living with these diseases. That’s why thousands of researchers around the country are working on this issue.

Setting the Federal Research Agenda

NIH takes a collaborative, methodical approach to reviewing progress, identifying gaps, and setting the future agenda for research into Alzheimer’s disease and related dementias. NIH funding in this area is guided by gaps and opportunities identified in research summits , which alternate yearly to focus on Alzheimer’s disease, Alzheimer’s disease-related dementias, or dementia care and services. Smaller, focused workshops are held more frequently on specific aspects of this research.

NIH outlines its Alzheimer’s research efforts in the  NIH AD/ADRD Research Implementation Milestones , a research framework detailing specific steps and success criteria toward achieving the goals of the  National Plan to Address Alzheimer's Disease . The milestones also showcase funding initiatives, accomplishments, and highlights of progress toward accomplishing the National Plan goals.

NIH’s research progress is highlighted in the annual  Alzheimer’s and related dementias professional judgment budget , which is submitted to Congress each year.

What Is a Professional Judgment Budget?

Each year NIH submits a professional judgment budget that estimates the additional funding needed to advance NIH-supported research into the treatment and prevention of Alzheimer’s disease and related dementias. The report also summarizes progress and promising research opportunities. Only two other areas of biomedical research — cancer and HIV/AIDS — follow a similar process designed to accelerate research discovery. This approach is often referred to as a “bypass budget” because of its direct transmission to the President and then to Congress without modification through the traditional federal budget process.

Clinical Research Into Alzheimer’s and Related Dementias

No major advance in Alzheimer’s and related dementias treatment, prevention, or care will be possible without robust clinical research. Clinical research includes studies that involve people so scientists can learn more about disease progression, how behavior and lifestyle factors may affect health, and the safety and effectiveness of an intervention. Advances made through clinical research rely on the volunteers who participate in these types of studies. NIA is working on multiple initiatives to enhance recruitment and retention of diverse populations in clinical research. View some of those resources below.

NIA-funded clinical research includes both observational studies through which researchers gather important information, and clinical trials in which researchers test interventions to treat or prevent disease, improve care and caregiver support, and enhance quality of life for people living with dementia. NIA is currently funding more than 200 active clinical trials .

NIA also funds more than 30 Alzheimer’s Disease Research Centers across the country. Scientists at these centers conduct clinical research to improve diagnosis and care for people with dementia and their families, and to find a treatment or prevention.

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You could help discover new ways to treat and prevent Alzheimer’s and related dementias.

Find More Resources on Alzheimer’s Research

Explore the resources on this website and linked below to find more information from federal government agencies.

View professional judgment budgets for Alzheimer’s and related dementias from NIH, including yearly updates on research progress.

Browse this database to learn more about research implementation plans and progress toward the goal of treating or preventing Alzheimer’s and related dementias.

Search this repository of resources to support the recruitment and retention of participants into clinical trials and studies on Alzheimer’s disease and related dementias.

Learn about the data sharing policies, considerations, resources, and guidance available to support researchers in safely and efficiently sharing data from their studies.

Visit IADRP to search a database of categorized research across public and private sources.

Learn about NIA's efforts toward the National Plan and NIH annual summits that shape research priorities.

View a list of all active NIA-funded clinical trials, including drug trials, intervention studies, and care and caregiver interventions.

Search for NIA-supported clinical research tools, datasets, samples, visualization tools, and more for Alzheimer’s and related dementias research.

Read the National Strategy for Recruitment and Participation in Alzheimer’s and Related Dementias Research and get resources to support study recruitment.

Read about the National Institute of Neurological Disorders and Stroke’s research into Alzheimer’s disease-related dementias.

Search NIH-funded research in Alzheimer’s and related dementias.

Other Articles in This Section

  • Federal Response
  • National Research Centers

Questions? Contact the ADEAR Center

The Alzheimer’s & related Dementias Education & Referral (ADEAR) Center is a service of the National Institute on Aging at the National Institutes of Health. Call 800-438-4380 or email [email protected] to talk with an information specialist.

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


An official website of the U.S. government, managed by the National Institutes on Aging at the National Institutes of Health

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Preparing for the next big thing in dementia treatment

A collaborative network of 17 Australian research organisations is working to prepare for the rollout of anticipated research and clinical initiatives as the global dementia community is poised for a step change to tackle one of the leading causes of death in Australia.

Key points:

  • Through targeted initiatives supported by the Yulgilbar Foundation, the  Australian Dementia Network is supporting research, recruiting people to participate in clinical trials, and ensuring dementia patients will be able to access new medical technologies as they emerge.
  • Nearly 500,000 Australians are living with dementia, and nearly three times that many are involved in their care
  • Dementia is the second leading cause of death, with Alzheimer’s Disease being the most prevalent form of the illness
  • Dementia affects memory, cognitive and physical functioning, and personality
  • Currently drugs to manage and sometimes defer onset of symptoms exist but there is no cure
  • With recent new outcomes, the global dementia research community is poised for a significant improvement in diagnosis and treatment.

The outcome

The Australian Dementia Network (ADNeT) is a unique dementia community that draws the expertise of researchers in 17 Australian universities and research institutions, as well as people with lived experience of dementia.

ADNeT brings together Australia’s leading dementia stakeholders to create a powerful translational research infrastructure for dementia prevention, treatment, and care. ADNeT has three key initiatives – Clinical Quality Registry, Memory Clinics, and Screening and Trials.

  • The  Clinical Quality Registry was established in Australia to measure the quality of diagnosis and care for people newly diagnosed with dementia or mild cognitive impairment. It is expected the initiative will drive improvements in the clinical quality of care of people living with dementia.
  • Development of best practice guidelines for the diagnosis and treatment of dementia in  Memory Clinics helps ensure all people living with dementia have access to quality diagnostic and care, wherever they live.
  • Detailed screening of patients suitable for participation in clinical trials  (Screening and Trials) facilitates the development of effective therapies.
  • Globally, important outcomes have recently been achieved in dementia research. Further research is crucial to demonstrate clinical usefulness. With the dementia research community on the cusp of breakthroughs in diagnosis and treatment, the coordinated ADNeT clinical and research community means Australia is ready to be at the forefront of trialling and embedding these new dementia treatments into practice

The research

ADNeT helps Australian researchers find participants to trial their therapeutic discoveries and for longitudinal observational research to learn more about the development of Alzheimer’s disease and other dementias.

Slow build-up of two toxic proteins called amyloid and tau are believed to be the cause of Alzheimer’s disease.  Previous studies have shown amyloid in all participants with Alzheimer’s disease but have also observed that amyloid begins to deposit in the brain 15 to 20 years before other symptoms develop. Amyloid may speed up the formation of the other toxic protein, called tau.

The earlier that drugs designed to slow the build-up of amyloid or to clear it from the brain are given, the greater the chance of preventing this major cause of dementia.

ADNeT developed and implemented a national network using common operating and analysis procedures to enhance research and provide new technology such as novel brain scans and blood tests that identify people suitable for early treatment trials aimed to slow the disease and prevent dementia.

ADNeT is pioneering a management impact study on implementing blood-based biomarkers into memory clinics, following recent global breakthroughs in blood tests that detect tau protein implicated in Alzheimer’s disease (pTau181), and a protein known as neurofilament light chain which is associated with brain damage in several neurodegenerative diseases, including Alzheimer’s disease.

The test will improve diagnostic accuracy allowing treatments to be started sooner. Importantly, such blood tests would be less invasive, more accessible, and more affordable with the ability to be implemented widely in clinical practice.

The partnership

The Australian Dementia Network is fully funded by a grant from the National Health and Medical Research Council (NHMRC) and two generous grants from the Wicking Trust and the Yulgilbar Foundation.

The University of Melbourne is one of 17 partners that make up the Australian Dementia Network.


See a comprehensive list of ADNeT research publications

Professor Christopher Rowe , ADNeT Director, Florey Department of Neuroscience and Mental Health, University of Melbourne

Professor Colin Masters , Professor in Dementia Research, Florey Department of Neuroscience and Mental Health, University of Melbourne

Professor Nicola Lautenschlager , Professor of Psychiatry of Old Age and Director of the Academic Unit for Psychiatry of Old Age, Department of Psychiatry at the University of Melbourne.

This article was originally published on  Research at Melbourne . Read the original article here .

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