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HomeExclusiveWill There Ever Be A Cure For Dementia

Will There Ever Be A Cure For Dementia

Finding A Cure For Alzheimers Using Yeast

Ayurvedic Treatment for Dementia | The Natural Therapy for Absolute Healing of Dementia Patients

Founded in 2014, Cambridge, Massachusetts-based Yumanity Therapeutics is also developing their therapies from technology spun-out of MIT. The startup has raised $82.1 million, including $31.1 million from a Series A in June. Yumanity Therapeutics relies on a technology involving bioengineered bakers yeast that overexpresses misfolded proteins to screen for drug candidates that target these proteins. The low cost and easy use of these petri dishes full of yeast allow the company to search for compounds that correct the misfolding more quickly than previous methods. This biotechnology might just be the best thing since sliced bread.

So What Could Future Treatments Offer

Heres a few of the drugs and therapies that are currently being researched and developed in the fight against dementia.

1. Disease Modification Therapies

The current drugs available to treat Alzheimers and dementia tackle the symptoms of the disease, but a new type of medication called Disease Modification Therapies works by tackling the disease itself and could potentially be of far more benefit. These drugs are being hailed as a transformative event in the search for a cure. Watch out for one called Solanezumab which is currently undergoing clinical trials.

2. The diabetes connection

A drug called Liraglutide, currently used to treat type 2 Diabetes could become the first treatment to reverse the progression of Alzheimers disease. A £5m study is currently under way in the UK after the drug was shown to reduce the damage caused by dementia when tested on mice. It is thought that the drug could be particularly beneficial to people in the later stages of dementia.

3. Ultrasound

Canadian researchers have found a way to remove toxic amyloid plaques in brain cells by using a non- invasive form of ultrasound. Although it hasnt been tested on humans yet human trials are at least two years away scientists say this could be a breakthrough which fundamentally changes our understanding of how to treat Alzheimers.

4. A vaccine

5. A drug to ease agitation

Treatment For Moderate To Severe Alzheimers

A medication known as memantine, an N-methyl D-aspartate antagonist, is prescribed to treat moderate to severe Alzheimers disease. This drugs main effect is to decrease symptoms, which could enable some people to maintain certain daily functions a little longer than they would without the medication. For example, memantine may help a person in the later stages of the disease maintain his or her ability to use the bathroom independently for several more months, a benefit for both the person with Alzheimer’s and caregivers.

Memantine is believed to work by regulating glutamate, an important brain chemical. When produced in excessive amounts, glutamate may lead to brain cell death. Because NMDA antagonists work differently from cholinesterase inhibitors, the two types of drugs can be prescribed in combination.

The FDA has also approved donepezil, the rivastigmine patch, and a combination medication of memantine and donepezil for the treatment of moderate to severe Alzheimers.

Drug NameFor More Information
  • Intravenous: Dose is determined by a persons weight given over one hour every four weeks most people will start with a lower dose and over a period of time increase the amount of medicine to reach the full prescription dose
  • Tablet: Once a day dosage may be increased over time if well tolerated
  • Orally disintegrating tablet: Same dosing regimen as above

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What The Data Show

The late-stage development program for Aduhelm consisted of two phase 3 clinical trials. One study met the primary endpoint, showing reduction in clinical decline. The second trial did not meet the primary endpoint. In all studies in which it was evaluated, however, Aduhelm consistently and very convincingly reduced the level of amyloid plaques in the brain in a dose- and time-dependent fashion. It is expected that the reduction in amyloid plaque will result in a reduction in clinical decline.

We know that the Peripheral and Central Nervous System Drugs Advisory Committee, which convened in November 2020 to review the clinical trial data and discuss the evidence supporting the Aduhelm application, did not agree that it was reasonable to consider the clinical benefit of the one successful trial as the primary evidence supporting approval. The option of Accelerated Approval was not discussed by the Advisory Committee. As mentioned above, treatment with Aduhelm was clearly shown in all trials to substantially reduce amyloid beta plaques. This reduction in plaques is reasonably likely to result in clinical benefit. After the Advisory Committee provided its feedback, our review and deliberations continued, and we decided that the evidence presented in the Aduhelm application met the standard for Accelerated Approval. We thank the Advisory Committee for its independent review of the data and valuable advice.

Will A Treatment For Alzheimers Ever Be Found

Neuroscientists Receive The Brain Prize for Crucial ...

In the 90s, Alzheimers researchers were full of optimism. New genetic studies all pointed to one culprithard 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. In animals, the drugs appeared to improve memory. But the results of human clinical trials that followed were disheartening: One after one, these drugsall designed to target amyloidhave failed to slow the disease.

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

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

Theres 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 Alzheimers treatments and prevention.

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Curing Alzheimers With Light Therapy

Founded in 2016, early stage startup Cognito Therapeutics was also spun out from MIT. The technology relies on treating patients with a device that exposes them to hour-long ultrafast oscillating light pulses to break down amyloid beta plaques in the brain. Think LED party strobe lights set to max. After a Series A round of funding from Chinese-based Morningside Venture Capital for an undisclosed amount and support through medical device incubator TheraNova, the strobing LED technology behind Cognito Therapeutics just began Phase I/II clinical trials in April 2018 with 60 patients using a wristband Flicker device over a six-month period. Sorry, looks like were not about to see Alzheimers-curing rave parties any time soon.

Are We Any Closer To A Cure For Dementia

The most common causes of dementia include Alzheimers and vascular dementia. There are a number of treatments to manage these, both established and emerging. There are also ways in which you can modify your lifestyle and risk factors to help maintain health, function and independence. Weve published a separate piece on the treatment of dementia, this article will focus on innovative new forms of research and potential therapies that could offer hope for people with dementia.

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Alzheimers Vaccine And Immunotherapy

Researchers have been attempting to develop a vaccine for Alzheimers disease for almost a decade. The strategy behind the immunotherapy approach is to use the bodys own immune system to destroy beta-amyloid plaques.

The first Alzheimers vaccine was tested in clinical trials in 2001. However, the trial was prematurely halted because six percent of participants developed serious brain inflammation. However, the vaccination did appear to benefit thinking and memory in some unaffected participants who were monitored after the end of the trial. Researchers have now developed a safer vaccine by using antibodies against a smaller fragment of the beta-amyloid protein, which they hope will avoid the complications of the previous trial.

Another approach to developing a vaccine involves using immunoglobulin, a filtered human blood product containing antibodies. Immunoglobulin was shown to be successful in a very small trial of 8 people with mild Alzheimers disease, with most showing improvement on tests of cognitive function after treatment. Although this trial is very small, it suggests the potential for larger trials of immunoglobulin therapy, which may have safety advantages over other vaccination techniques. Although this initial research is promising, much more research needs to be done before we know whether this approach will work.

The Apoe Gene Can Modify Your Risk Of Alzheimers

Could a treatment for Alzheimer’s disease be in the near future?

Many people have read or heard about variations in the APOE gene as a risk factor for Alzheimers. Interestingly, in their inquiry into why this woman with a mutation for early-onset Alzheimers had not yet developed dementia, the researchers found that she had an additional mutation in her APOE gene.

APOE has been linked to ordinary, late-onset Alzheimers disease and comes in three common forms. Most people, about 70% to 75%, have APOE3. About 15% to 20% of people have an APOE4 gene, and about 5% to 10% of people have an APOE2 gene.

  • If you have one APOE4 gene, your risk of developing Alzheimers disease is three to four times more likely than if you only have APOE3 genes.
  • If you have one APOE2 gene, your risk of developing Alzheimers disease is somewhat less than if you only have APOE3 genes.

This womans mutation of her APOE gene is an unusual variant called APOE3Christchurch , named after the New Zealand city where it was first discovered. Even more unusual is the fact that she had two versions of this mutation, meaning that both her father and her mother gave it to her. The researchers wondered if this APOE3ch mutation could be the cause of her resistance to Alzheimers disease.

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The Devastation Of Alzheimers Disease

With all this said, we are extremely aware of the gradual and cumulative devastation that Alzheimers disease causes, as patients lose their memory and cognitive functioning over time. In late-stage disease, people can no longer hold a conversation or respond to their environment. On average, a person with Alzheimers disease lives four to eight years after diagnosis, but some patients can live up to 20 years with the disease.

The need for treatments is urgent: right now, more than 6 million Americans are living with Alzheimers disease and this number is expected to grow as the population ages. Alzheimer’s is the sixth leading cause of death in the United States.

Although the Aduhelm data are complicated with respect to its clinical benefits, FDA has determined that there is substantial evidence that Aduhelm reduces amyloid beta plaques in the brain and that the reduction in these plaques is reasonably likely to predict important benefits to patients. As a result of FDAs approval of Aduhelm, patients with Alzheimers disease have an important and critical new treatment to help combat this disease.

Fdas Accelerated Approval Program

Aducanumab was approved through the FDAs Accelerated Approval Program, which provides a path for earlier approval of drugs that treat certain serious conditions. This helps people living with the disease gain earlier access to the treatment. The approval of aducanumab was based on the ability of the drug to reduce amyloid in the brain. When using the accelerated approval pathway, drug companies are required to conduct additional studies to determine whether there is in fact clinical benefit after the drug is approved. If the follow-up trial fails to verify clinical benefit, the FDA may withdraw approval of the drug. Results of the phase 4 clinical trial for aducanumab are expected to be available by early 2030.

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Debate Over Targeting Beta Amyloid Formations

Known among scientists as aducanumab, it works by offering an array of identical antibodies that are cloned from white blood cells. These antibodies are chosen for their targeting abilities, since they can identify specific proteins, called beta amyloids, that have constructed particular formations in the body.

There is extensive evidence suggesting that these beta amyloid formations, also known as “pathological aggregates” or”plaques,” are a major driver of Alzheimer’s disease, though the exact causal mechanisms are still not fully understood, according to Christian Pike of USC’s Leonard Davis School of Gerontology. Nonetheless, he says the antibodies can help prevent these plaques from forming, before directing other particles to break them apart, a process that’s clearly identifiable in before-and-after neural imaging.

For an analogy, it may be helpful to think of the beta amyloid proteins as young people walking around a city over the course of the day, where the city is the human body, and the day is a human lifespan. In certain cities, as afternoon turns into evening, individual young people start to congregate, and some of those congregations can turn toxic, and begin to cause problems. The antibodies delivered by Aduhelm act like law enforcement officers, arriving on the scene, identifying troublesome gatherings, surrounding them, separating them, then ordering bystanders to make the young people disperse.

The Difficulty Of Diagnosis

Dementia drug news:

Because Alzheimers disease has a wide array of causes, symptoms can vary tremendously from person to person.

For Diane, one unexpected symptom was hallucinations. She began seeing visions of her husband and seeing images of her two daughters as young children.

Alzheimers presents itself differently in every single person, said Chris Riley. Theres some very general things that can happen, but when people have Alzheimers, each persons experience is unique to themselves.

This makes a clinical diagnosis, or a diagnosis off the basis of symptoms, tricky.

The clinical diagnosis of Alzheimers disease by a physician due to his experience in the area is usually right but not always, said Dr. Victor Henderson, professor of health research and policy and of neurology and neurological sciences at Stanford University, and director of the Stanford Alzheimers Disease Research Center, in an interview with Healthline. Maybe 90 percent of the time the clinical diagnosis is accurate, a little bit less where there are atypical features.

In 2011, the National Institute on Aging developed a report with new guidelines for diagnosis. It incorporated a wealth of new research, including a number of tests that look at biomarkers in the body to diagnose Alzheimers disease.

For a rare few, a genetic test can reveal whether the person is likely to develop early-onset Alzheimers, a particularly swift-moving version of the disease.

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Medically Reviewed By: Lisa Cooper










Treatment For Mild To Moderate Alzheimers

Treating the symptoms of Alzheimers can provide people with comfort, dignity, and independence for a longer period of time and can encourage and assist their caregivers as well. Galantamine, rivastigmine, and donepezil are cholinesterase inhibitors that are prescribed for mild to moderate Alzheimers symptoms. These drugs may help reduce or control some cognitive and behavioral symptoms.

Scientists do not yet fully understand how cholinesterase inhibitors work to treat Alzheimers disease, but research indicates that they prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking. As Alzheimers progresses, the brain produces less and less acetylcholine, so these medicines may eventually lose their effect. Because cholinesterase inhibitors work in a similar way, switching from one to another may not produce significantly different results, but a person living with Alzheimers may respond better to one drug versus another.

Before prescribing aducanumab, doctors may require PET scans or an analysis of cerebrospinal fluid to evaluate whether amyloid deposits are present in the brain. This can help doctors make an accurate diagnosis of Alzheimers before prescribing the medication. Once a person is on aducanumab, their doctor or specialist may require routine MRIs to monitor for side effects such as brain swelling or bleeding in the brain.

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How Close Are We To A Cure For Alzheimer’s


    Answer by Sai Janani Ganesan, Postdoctoral Scholar at UCSF, on Quora:

    If you regularly read the newseither the politics or the science and technology section, you have read at least a couple of articles in the last year on Alzheimers disease or more broadly, dementia.

    AD is a neurodegenerative disease and is the leading cause of dementiaa syndrome or a condition that manifests as a group of symptoms that affect cognitive and behavioral skills due to death of neurons, arising from a multitude of largely unknown causes . There arent any medications available today that either slow or stop neuronal damage, the drugs available in the market are involved in only marginally improving symptoms and are highly patient dependent. With a total number of affected individuals predicted to increase to 13 million in the US and over 100 million worldwide by 2050, and skyrocketing costs for dementia care and expected to grow to $1 trillion by 2050), it is safe to call dementia one of the biggest public health problems of our times.

    Although first identified in 1906, it wasnt until the 70s that we began to accept AD as a leading cause of death. To quote Robert Kutzman from a 1973 Journal of the American Medical Association editorial :

    Q. Why have we not been successful or close to preventing or slowing down the disease?

    Q. Is Obamas 2025 target realistic?

    Q. How many years will it be before we see a cure for Alzheimers?


    Study Limitations And Conclusions

    Medications that can be dangerous for dementia

    The study has several limitations. Firstly, because of the limited database for the APOE4 genotype, the sample size the researchers used was restricted to only one dataset containing 213 samples.

    Secondly, the efficacy of bumetanide was validated only among the top predicted drugs in animal models and human EHR databases.

    Lastly, the two EHR databases the scientists used in this study did not contain APOE genotype information, which means that further studies are now necessary.

    Nevertheless, the study results spell exciting possibilities for the potential future treatment of Alzheimers disease.

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