Q: Is There Anything People Can Do Now To Prevent The Disease Or At Least Delay It For Several Years
In my practice, I encounter many people who have family members with Alzheimer’s and theyre worried about their genes. But in most cases, just because your mother has it doesnt mean youre going to get it.
In a complex disease, each gene and each environmental factor is like putting a pebble on a scale. None of them by themselves can prevent or cause Alzheimers. So if your parent has Alzheimers, that puts one pebble on the scale. But if you went to college, if you exercise, those are pebbles on the other side of the scale.
Many of the things that we thought historically cause Alzheimer’s have been debunkedfor example, the idea that it was caused by various heavy metals. But we do know that maintaining cardiac health is good: Exercise is good smoking is bad developing diabetes or obesity increases the risk. These recommendations, as most people know, are true for any disease.
People often ask me this question, hoping I know something that no one else does. I dont have any other answers at the moment, but everyone in the field is doing their best to find new ways to forestall this disease.
Preventing And Targeting Plaques And Tangles
As with all diseases, knowing exactly what causes Alzheimers is key to identifying ways to prevent and treat the condition.
Past research has indicated that Alzheimers occurs when two abnormal brain structures plaques and tangles damage and kill nerve cells, causing the memory, thinking and behavioral problems associated with the disease.
Plaques are fragments of a protein called beta-amyloid, which build up in areas between nerve cells. Tangles are twisted fibers of a protein called tau, which accumulate inside brain cells.
Although the jury is still out on the exact roles plaques and tangles play in the development of Alzheimers, studies have suggested that build up of these proteins begins long before symptoms develop.
Evidence suggests that the process of Alzheimers disease begins more than a decade before clinical symptoms appear, suggesting we may need to intervene earlier to have a major impact on the course of the disease, particularly when using therapies designed to prevent the development of abnormal protein structures plaques and tangles that are abundant in the brains of people with Alzheimers, says Snyder.
Other research has suggested that targeting these abnormal structures could treat Alzheimers. Earlier this year, Medical News Today reported on a study by researchers from the University of California-Irvine, suggesting that increasing brain cell connections could reduce plaque accumulation.
Will A Cure For Alzheimer’s Ever Be Found
Unless an effective treatment is found, the costs to treat people with Alzheimer’s disease will rise to more than $1 trillion by 2050, an increase from current costs estimated at $214 billion, according to data from the nonprofit Alzheimer’s Association.
Affecting some 5 million people, Alzheimer’s is the most common neurological condition, robbing the afflicted of their memories and so debilitating that many have to live in specialized care facilities. The disease is the only one in the top five causes of death that has no effective treatment or cure. While scientists have made progress in treating Alzheimer’s symptoms, they’re now focusing their efforts more on prevention and early detection, according to Dr. James Hendrix, director of the Global Science Initiative at the Alzheimer’s Association.
“We have seen great progress around early detection,” he said.
A cure — which could be worth tens of billions dollars — has proven to be elusive, however. Several drugs that scientists and drugmakers thought held promise failed during trials in recent years. Federal funding for Alzheimer’s research is about $600 million, which the Alzheimer’s Association considers inadequate. Last year, a blue-ribbon panel of scientists recommended to the U.S. Department of Health and Human Services that the figure be raised to at least $2 billion per year.
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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 . 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 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.
Will We Ever Cure Alzheimers
Few drugs have been approved for treatment of this dementia, and none works very well. It has become one of the most intractable problems in medicine.
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By Pam Belluck
Its a rare person in America who doesnt know of someone with Alzheimers disease. The most common type of dementia, it afflicts about 44 million people worldwide, including 5.5 million in the United States.
Experts predict those numbers could triple by 2050 as the older population increases. So why is there still no effective treatment for it, and no proven way to prevent or delay its effects?
Why is there still no comprehensive understanding of what causes the disease or who is destined to develop it?
The answer, you could say, is: Its complicated. And that is certainly part of it.
For nearly two decades, researchers, funding agencies and clinical trials have largely focused on one strategy: trying to clear the brain of the clumps of beta amyloid protein that form the plaques integrally linked to the disease.
But while some drugs have reduced the accumulation of amyloid, none have yet succeeded in stopping or reversing dementia. And amyloid doesnt explain everything about Alzheimers not everyone with amyloid plaques has the disease.
But, of course, that is not the same as turning back the tide of the disease.
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How Close Are We To A Cure For Alzheimer’s
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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?
Footnotes
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.
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Can We Cure Dementia
IT ALL STARTED WITH A MYSTERIOUS ILLNESS.
In the 1990s, thousands of U.S. veterans returning from combat in the Persian Gulf began suffering from what became known as Gulf War Syndrome, an undiagnosed host of chronic neurological symptoms. During the first Gulf War, deployed soldiers had been prescribed a daily dose of the drug pyridostigmine as a prophylactic against nerve gas because it was feared that Iraqi forces would resort to chemical attacks against invading troops. Although no such attack occurred, soldiers reported symptoms including headaches, dizziness, and memory problems.
Israeli neuroscientist Alon Friedman and then-grad student Daniela Kaufer, now a professor at Berkeley, wanted to know the cause. They proposed what Kaufer calls a wild hypothesis: that the anti-nerve gas drug had somehow penetrated the protective blood-brain barrier and was wreaking havoc on the soldiers brains.
Late one night in 1994, the researchers stood hunched over a tub of water in the psychobiology lab at the Hebrew University of Jerusalem, watching a mouse struggle to stay afloat. The water was intentionally coldnot quite active combat, but enough to induce a stress response in the mouse. The experiment itself was fairly simple: Mouse is forced to swim for four minutes. Researchers inject blue dye into mouses vein. If mouses brain shows blue coloration, then dye from the bloodstream has crossed the blood-brain barrier.
So what exactly is aging?
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Will We Ever Find A Cure For Dementia
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The Apoe Gene Can Modify Your Risk Of Alzheimers
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.
The Difficulty Of Diagnosis
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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We Just Got A Lot Closer To Finding A Cure For Alzheimers
In 2020, 5.8 million Americans were suffering from Alzheimers. According to the CDC, that number is expected to balloon to 14 million by 2060. A cure for those people has long remained elusive, but that might change sooner than we think thanks to a new study illustrating how Alzheimers-associated proteins accumulate in the brain. The findings, Science Advances, arm researchers with novel insights into how the disease progresses and could lead to new ideas for more effective treatments.
Alzheimers is a disease defined by misbehaving proteins, according to Tuomas Knowles, a researcher at the University of Cambridge and a co-senior author of the new study. One of these proteins is called tau. In Alzheimers disease, tau starts to misbehave, forming clumps inside brain cells, interfering with their ability to communicate with one another.
Reducing the accumulation of these tau clumps might be one way to fight Alzheimers disease, but first, scientists have to figure out how the accumulation is happening.
Knowles told The Daily Beast there are two main processes at work in taus takeover of the brain. One process involves tau clumps spreading from one part of the brain to another. The other process involves tau replicationthe clumps growing and multiplying in place.
Will We Ever Cure Dementia
As with cancer, there is currently no cure for dementia
If there is one dreaded word uttered by doctors to rival cancer, it’s dementia. Patients the world over fear its impacts: the lack of independence the higher likelihood of ending up in a nursing home. As with cancer, there is currently no cure for dementia.
But the prognosis is not entirely bleak. It’s now becoming more apparent we may be able to prevent or delay the onset of dementia symptoms by living more healthily in our earlier years.
An often forgotten and more pressing need is how do we care for people living with dementia? Doing so will require investment both now and into the future.
Meanwhile, a large section of the scientific community is squarely focused on the search for effective treatments. Millions of dollars have been invested over the last three decades in search of a holy grail.
This despite the reality that dementia is a complex condition, an enigma to researchers.
For two important reasons, dementia cannot be fixed quickly and with great effectiveness – like a heart attack or angina is with a stent, or like some cancers can be with surgery.
First, it’s a cumulative condition with multiple causes that impact on the brain at various times during a person’s life span. Second, dementia creeps up on a person with changes in the brain beginning decades before a person actually starts to show symptoms.
A logical question that follows is, what can be done about reducing the burden of dementia?
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Scientists Discover Possible Cure For Alzheimer’s Seeks Funds For Trials
A team of Bengaluru-based scientists led by T Govindaraju a Professor of Jawaharlal Nehru Centre for Advanced Scientific Research has discovered a possible cure for Alzheimer’s disease, the leading cause of dementia worldwide.
The breakthrough is a small molecule, named TGR 63 that has shown the ability to disrupt the mechanism through which neurons become dysfunctional in Alzheimer’s disease.
Govindaraju and scientists from JNCASR and an Indian-origin scientist at the KTH Royal Institute of Technology in Sweden, the molecule, called TGR63, has been shown in animal studies to to not only halt the progress of the disease but even reverse it.
The research has been ongoing for the past 10 years, the result of which was published recently in the journal ‘Advanced Therapeutics’.
“After identifying the molecule we started with a test tube experiment, then tested the molecules in cellular models. We treated an Alzheimer’s affected animal model and a healthy mouse with the same drug. We detected that the molecule is significantly reducing amyloid aggregates which resulted in a reversal of the cognitive decline in the animal,” said Govindaraju.
“Under some adverse physiological conditions, amyloid-beta a peptide clumps into toxic aggregates in the brain which results in volume and mass of the brain decreasing significantly disrupting the neural connections causing cognitive decline,” he explained.
He also thanked the government for the financial support it has lent.