Controlling The Risk Factors For Dementia
It is advised that if you have any of the risk factors like a positive family history of dementia, uncontrolled chronic conditions , an excessive drinking habit, high BMI , or a sedentary lifestyle, then your chances of having dementia are increased.
These factors have been recognized also to escalate the progression of dementia.
Some of the factors mentioned above are non-modifiable ones that you cant do much to change , but others can be quite manageable.
Furthermore, lifestyle modification strategies like having a healthy diet, doing regular exercise, stimulation of cognitive abilities, maintaining good sleep hygiene all have been quite effective in slowing the progression of the disease.
Although you cant reverse the progression of dementia, modifying lifestyle habits can have a positive effect on slowing further progression.
Education Health Literacy Is Key
The challenge is translating this to middle and low-income countries with larger, more diverse populations where the burden of dementia is fast increasing. Education and health literacy is a key element of protection against dementia, a measure that requires investment.
But the elephant in the room is the serious lack of investment to support people already living with dementia. Removing the stigma related to dementia, and improving environments, access to care, connectedness to communities, and health services should be supported by investment, research effort and actions equal to, if not greater than, the resources directed towards the finding of a magic cure.
Originally published under Creative Commons by 360info
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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What Medications Can Help
The FDA has approved the drug aducanumab-avwa as the first therapy that targets the fundamental pathophysiology of the disease by reducing amyloid beta plaques in the brain. It is not without controversy because of concerns it may cause swelling of bleeding in the brain.
Some drugs curb the breakdown of a chemical in the brain, called acetylcholine, thatâs important for memory and learning. They may slow down how fast symptoms get worse for about half of people who take them. The effect lasts for a limited time, on average 6 to 12 months. Common side effects are usually mild for these medications and include diarrhea, vomiting, nausea, fatigue, insomnia, loss of appetite, and weight loss. There are three drugs of this type: donepezil , galantamine , and rivastigmine .
Doctors can also prescribe medicines for other health problems that happen along with the disease, including depression, sleeplessness, and behavior problems like agitation and aggression.
Medicines To Treat Challenging Behaviour
In the later stages of dementia, a significant number of people will develop what’s known as behavioural and psychological symptoms of dementia .
The symptoms of BPSD can include:
- increased agitation
- aggression
- delusions and hallucinations
These changes in behaviour can be very distressing for both the person with Alzheimer’s disease and their carer.
If coping strategies do not work, a consultant psychiatrist can prescribe risperidone or haloperidol, antipsychotic medicines, for those showing persistent aggression or extreme distress.
These are the only medicines licensed for people with moderate to severe Alzheimer’s disease where there’s a risk of harm to themselves or others.
Risperidone should be used at the lowest dose and for the shortest time possible as it has serious side effects. Haloperidol should only be used if other treatments have not helped.
Antidepressants may sometimes be given if depression is suspected as an underlying cause of anxiety.
Sometimes other medications may be recommended to treat specific symptoms in BPSD, but these will be prescribed “off-label” .
It’s acceptable for a doctor to do this, but they must provide a reason for using these medications in these circumstances.
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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 Name | For More Information |
|---|---|
| Aducanumab |
|
|
Icipants Were Nearly 70% Less Likely To Develop Alzheimers Disease
After a 6-year follow-up, Cleveland Clinic researchers found that people who took sildenafil were 69 percent less likely to develop Alzheimers disease than those who didnt take the medication.
To further examine the drugs potential to treat Alzheimers disease, Cheng and team created a lab model that showed sildenafil targeted tau protein and increased brain cell growth, revealing how the drug might work against the degenerative condition.
Its important to note the study did not find sildenafil actually reduced the risk of Alzheimers disease. It was only associated with it. Cheng admitted there were limiting factors that indicate a need for more research.
Although we adjusted many confounding factors in our patient data analysis based on our sizeable efforts, possible confounding factors may exist by our limited clinical knowledge of this complex disease, he said.
Cheng emphasized that the findings must be confirmed in clinical trials before sildenafil can be used as a treatment for Alzheimers disease.
We are working hard to pursue a RCT in the next step, said Cheng.
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How Does Aducanumab Work
Amyloid is a protein that can build up in the brain and may cause Alzheimers disease. Aducanumab travels to the brain, sticks to amyloid, and removes it.
You may be eligible to participate in clinical research studying aducanumab or other drugs that could fight Alzheimers disease and other types of dementia.
Study Had Significant Limitations
This study looks at data from a very large number of people, but there are several important limitations to consider, Professor Tara Spires-Jones, DPhil, deputy director of the Centre for Discovery Brain Sciences at the University of Edinburgh, said in a statement.
According to Spires-Jones, study data came from insurance claims, arent very detailed, and did not include information on other important risk factors for Alzheimers, like sex, risk genes, and socioeconomic status.
Spires-Jones pointed out there are other possible explanations for these findings.
For example, we know that brain changes start decades before dementia symptoms and it is possible that these early Alzheimers changes reduce sex drive, thus people wouldnt ask for a prescription for erectile dysfunction, she explained.
is a recently FDA approved drug to treat Alzheimers disease. So far, its the only drug approved for this purpose.
It was granted accelerated FDA approval . This program allows for earlier approval of drugs to treat serious conditions and fill an unmet medical need based on a marker, such as laboratory measurement, physical sign, or other measure that might predict clinical benefit.
Aducanumab is not a cure for Alzheimer disease, Dr. Winston Chiong, member of the American Academy of Neurology Ethics, Law, and Humanities Committee, told the Psychiatric Times.
The condition involves brain bleeding, brain swelling, or both.
The behaviors were:
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Challenges To Finding A Cure
The path towards a cure is not going to be easy, and even if these theories do lead to the development of drugs, these drugs may fail for a host of other reasons.
Alzheimers is a very long, chronic disease, probably present 20 to 30 years before the first symptoms become obvious. Giving the drug when a person becomes symptomatic may be too late for it to make any difference. But we do not have the ability to diagnose it 30 years before the first symptoms, and even if we could, we would need to consider the ethics of giving a potentially toxic drug long-term to someone who may or may not get a disease in three decades.
Also, unlike developing antibiotics in which the researchers know within days if the drug works, the chronic nature of Alzheimers requires long, expensive trials years in duration before an answer can be attained. Such time and expense is a further impediment to drug development.
One final problem is that Alzheimers may not simply be one disease. It may in fact be a collection of similar diseases. A 52-year-old with early onset Alzheimers certainly has a clinical course distinct and different from an 82-year-old with late onset Alzheimers. Will a drug that works in an 82-year-old also work in a 52-year-old persons disease? Maybe, or maybe not.
Can Alzheimer’s Be Cured
P. Murali Doraiswamy discusses recent breakthroughs in diagnosing Alzheimer’s disease and what everyone can do to postpone the onset of memory loss.
Are you a scientist? Have you recently read a peer-reviewed paper that you want to write about? Then contact Mind Matters editor Jonah Lehrer, the science writer behind the blog The Frontal Cortex and the book Proust Was a Neuroscientist. His latest book isHow We Decide.
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No Cure For Alzheimer’s Disease In My Lifetime
by Norman A. Paradis, The Conversation
Biogen recently announced that it was abandoning its late stage drug for Alzheimer’s, aducanumab, causing investors to lose billions of dollars.
They should not have been surprised.
Not only have there been more than 200 failed trials for Alzheimer’s, it’s been clear for some time that researchers are likely decades away from being able to treat this dreaded disease. Which leads me to a prediction: There will be no effective therapy for Alzheimer’s disease in my lifetime.
Clinically, I am an emergency physician. But my research interests include diagnostic biomarkers, which are molecular indicators of disease, and a diagnostic test for Alzheimer’s is something of a holy grail.
Alzheimer’s sits right at the confluence of a number unfortunate circumstances. Stick with me on this it’s mostly bad news for anyone middle-aged or older, but there’s a reward of sorts at the end. If you understand why there won’t be much headway on Alzheimer’s, you’ll also understand a bit more why modern medicine has been having fewer breakthroughs on major diseases.
We don’t know what causes this disease
It was always possible that the classic plaques and tangles first seen by Alois Alzheimer, and now known to be made of abnormal proteins, were epiphenomena of aging and not the cause of the disease. Epiphenomena are characteristics that are associated with the disease but are not its cause.
Not one disease with one cause
We’ve ignored the biology of aging
How Can We Reduce The Burden
A logical question that follows is, what can be done about reducing the burden of dementia?
The answer is in fact, quite a lot.
There are several things people and governments can do to drive down symptoms of dementia and flatten the curve of dementia in whole populations.
For the general public, this means promotion of healthy diets and physical activity. For people with risk factors such as high blood pressure, diabetes, heart rhythm abnormalities, and high cholesterol, good management of cardiovascular health is required.
In high-income populations, theres evidence of a reducing incidence of new cases, most likely due to the benefits of improvements in lifestyle and cardiovascular health over the past three decades.
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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.
The Road To 202: Will A Treatment For Alzheimers Be Available
World leaders have committed to the prevention and treatment of Alzheimer’s Disease by 2025, but contemporary drug development is often slow. In this post, Dr. Jeffrey Cummings draws from his recent review in Alzheimers Research & Therapy to discuss how likely success will be, and suggests ways to make it more likely that this ambitious target will be met.
Our review sought to put the laudable goal of having a cure or meaningful treatment for Alzheimers disease approved by 2025 into the perspective of contemporary drug development. There are two main points from this paper:
In addition to abbreviating recruitment times, other approaches such as creating a central, efficient Research Review Board for multi-site trials would decrease redundancy and shorten time currently devoted to Institutional Review Board review and approval.
Advocacy groups and Congressional and Presidential candidates are lobbying for increased NIH funding including substantial new funds for Alzheimers disease. This is terrific and we should be fully behind the groups and candidates that share our passion as scientists to find new truths and new treatments. At the same time, we need to educate the public that basic science advances take more than a decade to result in new treatments and cannot produce a drug by 2025 only 9 years away!
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‘cure’ Could Take Many Forms
As varied as the research pipeline is, most experts agree on one thing: When it comes to finding a way to stop, slow or prevent dementia, it wont boil down to one drug treatment or even one drug target. Rather, it will be a combination approach, perhaps involving drugs that clear the amyloid plaques, knock out the tau tangles, target problem proteins and improve the synaptic health of the nerve cells in the brain.
Patients may also receive nonpharmacological prescriptions from their doctors. Some of the most recent research has shown that cardiovascular health and cerebral vascular health play a critical role in overall brain health throughout ones lifetime. Exercise, diet and sleep have all been shown to reduce risk of cognitive decline in adults. Whats more, a landmark study in 2018 showed that intensive blood pressure control significantly lowered the chances that participants developed mild cognitive impairment.
The mishmash of therapies likely wont cure dementia, but as Rafii explains, we have very few cures in medicine. He and others in the field, including the DDFs Grant, are optimistic, however, that the ongoing advancements will lead to treatments that can delay the disease and improve the lives of millions.
What Im seeing is great progress in the building blocks, the foundation of new future therapeutic approaches, Grant says.
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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.
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