With these startling statistics, can anything be done to save our brains from this horrific deterioration? Will more seniors be able to avoid falling victim to Alzheimer’s as the elderly population increases? Are we finally getting close to a cure?
One of the biggest problems for an Alzheimer’s cure has been finding a way to stop deadly plaques from forming in the brains of patients. If the disease has progressed past an early diagnosis, drugs need to be safely delivered to the affected areas to destroy plaque build-up.
Here are three dramatic new discoveries which are now giving millions more hope for a future cure.
1. Gene Transfer Therapy: Dr. Zoe Arvanitakis of the Rush University Medical Center is currently working with gene transfer. By inserting tiny needles into the brain’s area affected by Alzheimer’s, he believes the drug CERE 110 can be delivered directly where is its needed.
CERE110’s purpose is to stimulate nerve growth, but not to spread the drug throughout the brain which could cause side effects.
Current trials are showing a great deal of promise. The very first patient in the trial, Ron Shellady, claims he is no longer losing his memory. It is still too early to gage long lasting results but CERE 110 shows promise.
2. Nutritional Combat: As more studies about Alzheimer’s and diet are coming in, more evidence seems to be pointing to diet as a deterrent to the disease.
The interesting discovery made by the Aberdeen University researchers is that people who eat diets rich in omega-3 oils do better on mental tests. This is strong indication the omega-3 oils may actually help slow down the early stages of Alzheimer’s.
Omega-3 oils are found in walnut oil, flaxseed oil, canola oil and fish such as Salmon. How do Omega-3 oils work? According to Greg Cole, professor of medicine and neurology at the David Geffen School of Medicine at UCLA, these oils expand the productions of LR11, an important protein that runs low in Alzheimer’s patients.
LR11’s function is to destroy harmful proteins which form dangerous plaques which destroy nerve cells in the brain. Plaque build-up is one of the major problems caused by the disease.
3. Molecular Attacks: German scientists are researching ways to prevent harmful brain plaques from forming in the first place. The fact that an enzyme called beta-secretase causes plaque damage is nothing new, but how to deliver well targeted drugs to the damaged areas has been puzzling researchers for some time.
The Germans have discovered that by blocking beta-secretase via the blood, this harmful enzyme can be better targeted, without harming other brain cells. What is needed now is to find a way around the blood-brain barrier which guards the brain from most molecules entering it. If scientists can get past this natural wall they will be closer to delivering the beta secretase inhibitor to target only those areas where the therapy is needed.
Alzheimer’s is one of the most deadly diseases of old age because it robs the brain of its ability to function. This keeps many elderly people in nursing homes and away from their own homes and families. It is also very painful for their loved ones to watch their decline.
Although Alzheimer’s was first discovered over 100 years ago, most of what we now know about the disease has been learned within the last fifteen years. As world wide efforts continue in the fight against brain destruction due to Alzheimer’s, a cure may be possible as breakthroughs surge.
Although the world has only focused its attention on this disease for jus over thirty years, it was actually discovered back in 1906 by the German physician, Alois Alzheimer; even though it has been scientifically studied for many years, knowledge surrounding this disease is minimal.
Studies have shown that the greatest known risk for developing Alzheimer’s is increasing age. Unfortunately, the person experiencing the early symptoms of Alzheimer’s will know something is wrong but won’t admit it to others or even to themselves; to make matters worse, this situation creates a delay in the person and family learning what is wrong.
As far as treatment is concerned, Alzheimer’s disease is treated in the same manner as other types of dementia. Some drugs can now slow down and sometimes improve the symptoms but so far no treatment has been discovered that can cure the disorder. Most Alzheimer’s disease sufferers will be prescribed one of the following drugs Donepezil, Tacrine, and Rivastigmine; these have helped many patients with improvements in their mental faculties although this is only in the short term.
Another drug, Memantine, a relative of the older anti-influenza drug Amantadine, is proving successful at slowing down the mental decline of sufferers; it is now normally given to those on Donepezil who are suffering moderate to severe Alzheimer’s. Memantine is the first medicine to show such positive results with sufferers with few problems associated with its use; most of the drug is passed out again when the patient urinates (about 80 percent), virtually without any change taking place.
Alzheimer’s disease is thought to be one of the largest public health problems, primarily due to an increase in the life expectancy of people in the world; it is already the fourth largest killer in the United States. It is not just the human cost of Alzheimer’s that has to be taken into consideration but also the monetary costs surrounding long term care; the annual cost of treatment and care for sufferers is in excess of 40 billion dollars and is expected to rise well beyond this in the future. Last year alone, the National Institute on Aging spent nearly one-half of its funding on research related to this insidious disease; currently there are over 300 different compounds at various stages of development for its treatment.
One way to help lower the risk of dementia and one that you can have responsibility for is to change how you live by eating healthily and taking regular exercise. Studies have also indicated that a number of Alzheimer’s patients have reduced their rate of decline by staying healthy and happy. At the time of writing this condition primarily affects men and women over sixty years of age; nevertheless, there have been occasional incidences of people contracting it before the age of 60.
Judith
To understand Alzheimers better, we should consider and understand dementia. Dementia is a mental disorder characterized by the deprivation of cognitive abilities. It’s an exceedingly debilitating disease that afflicts some individuals in their senior years. Alzheimers information shows that Alzheimer’s is the most common form of this disorder that greatly impairs normal mental abilities.
There’s no certain prevention or remedy for Alzheimer’s right now but continuous studies and tests are being made towards this effort because according to Alzheimers information, this disease is irreversible. The disease also continues to advance into different levels and symptoms that worsen over time.
One of the earliest symptoms of Alzheimer’s is short term memory loss. It then advances into a gradual decay of other cognitive abilities. After the disease has advanced further, one may see a noticeable change in the sufferer’s conduct and at the very last stages of the disease, the individual with Alzheimer’s will have to depend upon others for simple actions such as eating and mobility.
Alzheimer’s information tells us that the course of the disease changes from one to another with a range of five to twenty years. Alzheimer’s in time ends in death due to complications and infections.
Although increasingl Alzheimer’s information has been collated and explored through the years, the advancement has been steady but slow. For example, the Alzheimer’s information on what causes the disease is still uncertain. There are some major hypotheses that appear to center on two ingredients: genetic or hereditary and a complex environmental interaction.
Alzheimer’s information tells us that it’s mainly a disease that affects the brain. It’s in the abnormalities in the brain that result in massive atrophy of the brain’s neurotransmitters, nerves and neurons. From these stem the malfunctions that start with short term memory loss to severe impairment to memory and the loss of motor skills and other normal bodily functions.
An abnormally large repository of protein in the brain causes the massive atrophy. The conclusive detection of Alzheimer’s can only actually be done post mortem through an autopsy where the brain is studied and it shows a significant amount of shrinkage and a smoothening of the common brain wrinkles.
Even so, one need not wait for an autopsy to determine whether one is suffering from Alzheimer’s or not. With current Alzheimer’s information, one can have an 85 % to 90% accuracy in the diagnosis of the disease. No lab tests are performed.
Instead, there will be some cognitive tests and with a series of exercises and questions that are crossed checked against other conceivable sources of dementia. These tests, done to be able to diagnose Alzheimer’s, help also by letting the doctor know at which level of progression the sufferer may be at.
Individuals with the age of 65 and above are most probable to be at risk of Alzheimer’s.
Beatrice
I am choosing the best answer pretty randomly, because every single response has helped me tremendously. I wish I could pick all of you for the best answers. It helps to know a few things so I can find some common ground between the two of us. I cant thank all of you enough for your insight on such a heartbreaking disease. I’ll say it again anyway: Thank you.
He gave his name to the sickness despite the contribution his associate Emil Kraepelin made by isolating and identifying the symptoms of the disease. For years, Alzheimer’s disease could only be diagnosed with a high degree of accuracy post-mortem. Now researchers are learning more about what exactly is happening in the brain to cause the sickness and why those strange plaques and tangles develop in the first place.
Neurofibrillary tangles are one characteristic of Alzheimer’s disease. Brain damage occurs as a result of neurons being clogged with microscopic filaments, which are made up of an abnormal type of Tau protein. Normally functioning Tau protein sends chemical messages from neuron to neuron by bonding to microtubules, while the type of Tau protein found in an Alzheimer’s disease brain bonds with itself and goes nowhere.
Clogged neurons are no longer able to do their job and pass along the impulses they receive from the environment; therefore, disabled neurons are one cause of the cognitive impairment associated with Alzheimer’s disease. Brain damage due to neurofibrillary tangles is also found in associated diseases, such as Parkinson’s disease. Scientists aren’t sure why the Tau protein malfunctions and causes the tangles.
Some researchers believe that Tau malfunctions as a result of beta amyloid protein, which is what causes the second form of damage in an Alzheimer’s disease brain-plaques between neurons.
Senile plaque, which is considered to be the more detrimental of the two abnormalities in an Alzheimer’s disease brain, consists of large, abnormal, sticky patches containing beta amyloid protein. These patches block communication between neurons, causing the learning and memory problems consistent with the cognitive impairment associated with Alzheimer’s disease.
The more plaque there is in the brain, the worse the impairment becomes because plaque is thought to interfere with the functioning of acetylcholine, which transmits nerve impulses in the brain and body. The only FDA-approved medications used to treat Alzheimer’s are acetylcholinesterase inhibitors, which block the enzymes that eat away at acetylcholine. These medications work best, however, in the earliest stages of the disease before the amount of plaque in an Alzheimer’s disease brain has caused considerable damage.
Recent research has begun to clarify the possible cause-and-effect connection between plaques and tangles. A study that used proteins from the immune system of mice to get rid of the beta amyloid that causes plaque discovered that the proteins ate away at the tangles as well. Other medications used to lower levels of beta amyloid also worked on the tangles. Some researchers believe that plaques and tangles may themselves be the result of some other disease process in the brain, such as swollen axons.
In research done on mice that were genetically engineered to have a disease similar to Alzheimer’s, the swollen axons, which are important in communicating between neurons, caused a “traffic” jam of sorts that may, over time, lead to the neuronal degeneration, plaques and tangles apparent in the brains of Alzheimer’s patients. Researchers hope that, by focusing on the disease process in the brain of Alzheimer’s patients, they can one day find a cause and, ultimately, a cure for the sickness.
Lee
