Treating Alzheimer’s Disease
Alzheimer’s disease is a progressive, irreversible brain disorder. Alzheimer’s disease (AD) is the most common form of dementia among older people. Alzheimer’ destroys a person’s memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Genetic factors are suspected, and dominant mutations in three different genes have been identified that account for a much smaller number of cases of familial, early-onset AD. People with dementia often have trouble thinking and speaking clearly, remembering recent events, and learning new things. Over time, it becomes hard for them to handle everyday activities and take care of themselves. Age is the most important risk factor for AD; the number of people with the disease doubles every 5 years beyond age 65. Three genes have been discovered that cause early onset (familial) AD. Other genetic mutations that cause excessive accumulation of amyloid protein are associated with age-related (sporadic) AD. AD is part of an immune response that is attempting to contain the disease. The former may be more likely, since research indicates that anti-inflammatory drugs can prevent or retard AD development.
Alzheimer’s disease advances at widely different rates. Family history is another risk factor of Alzheimer’s. Several risk factor genes may interact with each other and with non-genetic factors to cause the disease. Cardiovascular Risk Factors The same factors that increase the risk for heart disease and stroke, such as high blood pressure, may also increase the risk for late-onset AD. Most people with mild forgetfulness do not have AD. In the early stage of AD, people may have trouble remembering recent events, activities, or the names of familiar people or things. Oxidative damage refers to cell damage caused by excess free radicals, which are highly reactive chemicals. Free radicals are often formed as a by-product of metabolism, or chemical processes within the cell. Excess free radicals may cause substantial neuronal damage, contributing to AD development. Type 2 Diabetes. A link between AD and type 2 diabetes, the form of diabetes in which insulin levels are high. One theory is that too much insulin in the blood promotes inflammation and oxidative damage in the brain, both of which contribute to AD development.
Symptoms of AD include memory loss, language deterioration, impaired ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. Alzheimer’s disease may also include behavioral changes, such as outbursts of violence or excessive passivity in people who have no previous history of such behavior. In the later stages, deterioration of musculature and mobility, leading to bedfastness, inability to feed oneself, and incontinence, will be seen if death from some external cause (e.g. heart attack or pneumonia) does not intervene. Moderate -As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities. Severe — As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They may even lose the ability to walk or eat without assistance. They might forget to eat and starve.
Treatment Alzheimer’s Disease Tips
1. Acetylcholinesterase (AChE)-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons).
2. Ginkgo for the treatment of “cognitive impairment and dementia,” a Cochrane Review concludes that “there is promising evidence of improvement in cognition and function associated with Ginkgo According to this review the two randomized controlled studies that focused on Alzheimer’s patients both showed significant improvement in these areas.
3. Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques.
4. R-flurbiprofen (MPC-7869) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide.
5. Leuprolide has also been studied for Alzheimer’s. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages.
6. Antihistamine drug Dimebon has also recently been found to show beneficial effects against Alzheimer’s disease in preliminary trials
7. Vaccines or immunotherapy for Alzheimer’s, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention.
8. Proposed alternative treatments for Alzheimer’s include a range of herbal compounds and dietary supplements.
9. Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacologic treatment, especially in the early to moderately advanced stages of disease.
10. DNA-based therapy is also Treating Alzheimer’s Disease.
About the Author
Juliet Cohen writes articles for health care clinic and home remedies.
The Progression of Alzheimer’s Disease
Alzheimer’s disease is marked by slow development, and its characteristic decline in cognitive and behavioral function typically takes place gradually over a period of several years. It is because of this slow onset that many cases go undiagnosed until more severe symptoms become apparent. Over time, the disease affects a person’s memory, language skills, decision making abilities and reasoning. Though the disease may be classified in individuals as mild, moderate or severe based on the extent of the symptoms, it is important to remember that each case is unique and progression will vary from one person to the next.
Although the stages of Alzheimer’s are not concrete time periods, knowing generally what to expect over time can be helpful in future care planning for anyone who has a loved one with Alzheimer’s disease. Here we examine some of the characteristic behaviors observed in the mild, moderate and severe stages of Alzheimer’s disease:
Mild/Early: In the early stages of Alzheimer’s disease, symptoms such as forgetfulness, a limited attention span and forgetting where things belong are often disregarded as typical signs of aging. Though some of the symptoms of early Alzheimer’s disease are similar to those experienced by a healthy person with age, a person with Alzheimer’s disease will exhibit such behaviors with more frequency and severity over time. A person in the mild stage of the disease may become less motivated, resist change and confuse one word with another when speaking. Often, the patient does not realize that he or she is experiencing these changes, and a close family member is the first to notice symptoms. People in the early stages of Alzheimer’s disease can usually remain at home, particularly when there is a spouse or other loved one there to help out.
Moderate/Middle: As the disease progresses into the moderate stage, symptoms become more severe, more recurrent and more apparent to other people as well as the patient. The middle stage of Alzheimer’s disease is marked by a decline in memory function, particularly short term memory, though a patient may retain his or her long term memory. Personality changes and an inability to make judgments are also extremely common in this stage. It is in the moderate stage that a person with Alzheimer’s may begin to have difficulty recognizing people they know, or confusing the identity of one person with another. People in this stage of Alzheimer’s do best having a caregiver available full time to help with daily needs and ensure their safety.
Severe/Advanced: Severe Alzheimer’s disease calls for fulltime care from a loved one or a professional caregiver. Patients at this stage have difficulty communicating and frequently do not recognize loved ones. Advanced Alzheimer’s disease causes patients to feel disoriented with their surroundings and exhibit severe mood swings.
Alzheimer’s disease affects every person differently, and all people with Alzheimer’s disease will not experience every described symptom. Though the disease is divided into stages to make understanding its progression easier, there is no set timeline for any one patient’s progression. Today, the progression of the Alzheimer’s symptoms can sometimes be delayed with medications and lifestyle changes.
About the Author
About the Author: John Trevey is the C.E.O. of Uncommon Care, a leading provider of Austin Alzheimer’s care. He is the manager of both The Barton House and the Breckinridge. For more information, please visit http://www.uncommoncare.com.
Health Matters – Ol’ Timers (Rhymes with Alzheimer’s) Disease
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My Dad is a funny guy. I owe the title of this article to him. Fortunately, he still has his mental faculties intact. However, he has what he refers to as ’senior moments’. When that happens he often says jokingly (as he abruptly feigns as if he is looking for something) “where did I place my aluminum pills?”
It’s one of those sort of funny, sort of not-so-funny things that he says, in gest.
Some people think aluminum is the cause of Alzheimer’s. Now, where would we get enough aluminum to cause aluminum poisoning? Perhaps all the soda pop cans we’ve been drinking out of for xx number of years? But is that it? Is that the only cause? And most of us don’t need much proof that having aluminum in our brains is probably not a good idea.
What else might be the cause of Alzheimer’s?
The University of Calgary has done some research and, in fact, they’ve produced an interesting video. The video shows the visual evidence of neural degeneration caused by the presence of mercury on a developing neural fiber. It is compelling information.
Granted, they did not use human brain neurons in their experiment, thankfully, but I think the point is still valid.
It appears likely, from the research and video, that mercury is a likely cause of Alzheimer’s. In other research, autopsies performed on people that were known to have Alzheimer’s showed that their brains have the same kinds of twisted neural fibers seen and described in the video (post mercury exposure).
Until more compelling evidence is available that contradicts this conclusion, for my money, I’m betting that mercury is the primary cause of Alzheimer’s Disease. How convinced am I? Enough to chelate mercury out of my system, including my brain. But then, I was already going through chelation before I saw this video. I had also already done a lot of mercury related research. Thus I didn’t need a firestorm of new information to be convinced of the connection between the two.
If that is the case, what can you do to lower your risks? Plenty. But you need to see an outstanding Doctor that understands the proper protocols for determining if you have mercury in your body and how to get it out if you do.
I can tell you that depending on your condition, chelation can be relatively easy or it can be quite a difficult process to endure. In any case, it beats the possibility of enduring the loss of your mind to “Alzheimer’s” or mercury poisoning of the brain.
Copyright 2007 Thomas Mayhew
About the Author
Thomas Mayhew is the Webmaster for Crimson Books. Since going through a death-defying health experience (in 2005), he has taken a keen interest in sharing his health knowledge with others. You can subscribe to his blog at Health Matters Blog.
Using Vitamins to Prevent Alzheimer’s
Understanding what happens when an individual develops Alzheimer’s is still something that is being investigated. What scientists do know about Alzheimer’s is that it is a slow-developing disease of the brain that is characterized by dying brain cells. While the direct cause is unknown, it is theorized that the death of the cells is attributed to a lack of chemicals necessary to keep brain cells healthy.
After the age of 20, human brain cells (neurons) start to die at a rate of about 9000 per day. This results in a natural decline of mental acuity. There are reports that some vitamins can help to restore brain cells, but these reports are highly controversial. Once brain cells die, there really is no way to restore them. What scientists focus on is how to prevent Alzheimer’s. In the last few years, scientists have been testing the effects of vitamins on the brain. Those that seem to provide the most benefit are vitamins C and E.
In the world of vitamin supplementation, vitamin C and E are building blocks of good health. These vitamins are antioxidants that has proven beneficial in numerous health conditions, including heart disease, high blood pressure, high cholesterol, and stress. The body normally produces enough vitamin C and E in the body to protect the brain from damage from free radicals. However, the amount of vitamin C may be depleted by factors, such as diet and genetics. Scientists believe that taking 500 milligrams of vitamin C and 500 milligrams of vitamin E daily protects brain cells from premature destruction, a key to Alzheimer’s prevention.
These recommended amounts of vitamin C and E supplementation to prevent Alzheimer’s is way beyond what is recommended for general health. Before you consider taking these vitamins, you should discuss your plans with a medical doctor. Excessive amounts of vitamin C are flushed out in the urine and don’t usually cause serious problems, but excessive amounts of vitamin E can result in some unpleasant side effects. As with any vitamins or medication, you should store them in a location that is out of reach from children. Vitamins C and E can cause serious problems in children.
Why not check out our nutrition guide at http://www.nutritional-supplement-guides.com/nut-ebook.html
and also what supplement we personally use for our nutrition needs at http://www.nutritional-supplement-guides.com/what-we-use.html
About the Author
John Gibb is the owner of Nutrition guides, a website offering free nutrition advice and a quality nutrition book for newsletter subscribers.
News Alzheimer’s Immune Treatment
While there are medications that can slow-slightly–the progression of Alzheimer’s, the end inevitably comes in all those affected.
While there are medications that can slow, slightly, the progression of Alzheimer’s, the end inevitably comes to all those affected. New data suggests that Immunoglobulin, used to treat multiple sclerosis patients, could work in Alzheimer’s patients as well.
Immunoglobulin contains antibodies against a protein thought to be a main suspect in Alzheimer’s disease. That protein, called beta-amyloid, causes the formation of protein deposits which can damage and destroy sensitive nerve cells, leading to the early senility of Alzheimer’s.
In the study of five patients, this drug, IVIG, given intravenously every four weeks over six months, lowered the levels of the beta-amyloid protein in the fluid around the brain by more than 30 percent.
Dr. Mark Mehler, Chairman of the Department of Neurology at Montefiore Medical Center, New York, says, “There’s evidence from other diseases that the pathology is on going. And there is some hope that if you could reverse part of the pathological process before the cells actually die, you may be able to intervene even late in a disease. But there is also a lot of evidence because theses diseases are biologically complex, that if you intervene late the chance of you effecting either a cure or a significant retardation of the progression is little. That’s the problem.”
The researchers also found four of the five patients actually improved slightly on mental status tests…none deteriorated over the six month period. Still, Dr. Mehler thinks this would only be a disease halting approach, not one that can reverse the problem.
“The only way you’re really going to cure the disease is to re-establish the neuro-networks that have been damaged in the disease. And probably the only way that you can do that and effectively in the future is through stem-cells. So I think that research in these fields really needs to happen because it’s really become an epidemic.”
There is a lot of controversy in the field as to whether or not these beta-amyloid plaques are just the by-product of the disease or if the plaques are central to the problem. That still to be worked out, but this research gives a small boost to support the thinking it does indeed contribute to the disease.
About the Author
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