Information about Alzheimers Disease.

Thank you for your well wishes!

i heard about that disease but never seen any anyone who is infected to that disease .only i can do is," wish u good luck for ur grandmother " .

SORRY ITEM WAS TOO LONG HERE IS THE REST OF IT.......
Inflammation. There is evidence that inflammation in the brain may contribute to AD damage. Some studies have suggested that drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs) might help slow the progression of AD, but clinical trials thus far have not demonstrated a benefit from these drugs. A clinical trial studying two of these drugs, rofecoxib (Vioxx) and naproxen (Aleve) showed that they did not delay the progression of AD in people who already have the disease. Another trial, testing whether the NSAIDs celecoxib (Celebrex) and naproxen could prevent AD in healthy older people at risk of the disease was suspended due to concerns over possible cardiovascular risk. Researchers are continuing to look for ways to test how other anti-inflammatory drugs might affect the development or progression of AD.

Antioxidants. Several years ago, a clinical trial showed that vitamin E slowed the progress of some consequences of AD by about 7 months. Additional studies are investigating whether antioxidants—vitamins E and C—can slow AD. Another clinical trial is examining whether vitamin E and/or selenium supplements can prevent AD or cognitive decline, and additional studies on other antioxidants are ongoing or being planned, including a study of the antioxidant treatments—vitamins E, C, alpha-lipoic acid, and coenzyme Q—in patients with mild to moderate AD.

Ginkgo biloba. Early studies suggested that extracts from the leaves of the ginkgo biloba tree may be of some help in treating AD symptoms. There is no evidence yet that ginkgo biloba will cure or prevent AD, but scientists now are trying to find out in a clinical trial whether ginkgo biloba can delay cognitive decline or prevent dementia in older people.

Estrogen. Some studies have suggested that estrogen used by women to treat the symptoms of menopause also protects the brain. Experts also wondered whether using estrogen could reduce the risk of AD or slow the disease. Clinical trials to test estrogen, however, have not shown that estrogen can slow the progression of already diagnosed AD. And one study found that women over the age of 65 who used estrogen with a progestin were at greater risk of dementia, including AD, and that older women using only estrogen could also increase their chance of developing dementia.

Scientists believe that more research is needed to find out if estrogen may play some role in AD. They would like to know whether starting estrogen therapy around the time of menopause, rather than at age 65 or older, will protect memory or prevent AD.

Participating in Clinical Trials

People with AD, those with MCI, or those with a family history of AD, who want to help scientists test possible treatments may be able to take part in clinical trials. Healthy people also can help scientists learn more about the brain and AD. The NIA maintains the AD Clinical Trials Database, which lists AD clinical trials sponsored by the Federal government and private companies. To find out more about these studies, contact the NIA’s ADEAR Center at 1-800-438-4380 or visit the ADEAR Center website at www.nia.nih.gov/Alzheimer... . You also can sign up for e-mail alerts on new clinical trials as they are added to the database. Additional clinical trials information is available at www.clinicaltrials.gov.

Many of these studies are being done at NIA-supported Alzheimer’s Disease Centers located throughout the United States. These centers carry out a wide range of research, including studies of the causes, diagnosis, treatment, and management of AD. To get a list of these centers, contact the ADEAR Center.
Advancing Our Understanding

Scientists have come a long way in their understanding of AD. Findings from years of research have begun to clarify differences between normal age-related memory changes, MCI, and AD. Scientists also have made great progress in defining the changes that take place in the AD brain, which allows them to pinpoint possible targets for treatment.
These advances are the foundation for the NIH Alzheimer’s Disease Prevention Initiative, which is designed to:

* understand why AD occurs and who is at greatest risk of developing it,
* improve the accuracy of diagnosis and the ability to identify those at risk,
* discover, develop, and test new treatments, and

discover treatments for behavioral problems in patients with AD.
Is There Help for Caregivers?

Most often, spouses and other family members provide the day-to-day care for people with AD. As the disease gets worse, people often need more and more care. This can be hard for caregivers and can affect their physical and mental health, family life, job, and finances.

The Alzheimer’s Association has chapters nationwide that provide educational programs and support groups for caregivers and family members of people with AD. Contact information for the Alzheimer’s Association is listed at the end of this fact sheet.

For More Information

To learn about support groups, services, research centers, getting involved in studies, and publications about AD, contact the following:

Alzheimer’s Disease Education and Referral (ADEAR) Center
P.O. Box 8250
Silver Spring, MD 20907-8250
1-800-438-4380
www.alzheimers.nia.nih.gov
This service of the NIA offers information and publications on diagnosis, treatment, patient care, caregiver needs, Long-term Care, education and training, and research related to AD. Staff answer telephone, e-mail, and written requests and make referrals to local and national resources.

Alzheimer’s Association
225 N. Michigan Avenue, Suite 1700
Chicago, IL 60611-7633
1-800-272-3900
www.alz.org

related resource: risk management

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A Disease of the Brain

AD is a brain disorder that occurs gradually. It starts with mild memory loss, changes in personality and behavior, and a decline in thinking abilities (cognition). It progresses to loss of speech and movement, then total incapacitation and eventually death. It is normal for memory to decline and the ability to absorb complex information to slow as people get older, but AD is not a part of normal aging.

Researchers aren't exactly sure what causes AD, but they do know that people with the disease have an abundance of two abnormal structures in the brain: plaques and tangles. Plaques are dense, sticky substances made up of accumulations of a protein called beta-amyloid. Tangles are twisted fibers caused by changes in a protein called tau. The beta-amyloid plaques reside in the spaces between the billions of nerve cells, or neurons, in the brain, and the neurofibrillary tangles clump together inside the neurons. Plaques and tangles block the normal transport of the electrical messages between the neurons that enable us to think, remember, talk and move. As AD progresses, nerve cells die, the brain shrinks, and the ability to function deteriorates.


Treating the Disease

Scientists continue to search for treatments to slow the progress of AD and to hold the disease off as long as possible. "If you could delay the onset of symptoms by five years, the total number of new cases projected into the future would be cut in half," says Steven Ferris, Ph.D., director of the Alzheimer's Disease Center at the New York University School of Medicine. "Within the next five to 10 years, we will at least be able to slow down the disease in people who already have symptoms and do a much better job at identifying people at high risk of getting Alzheimer's who do not yet have symptoms," Ferris predicts. And once new treatments come along to slow down the disease, those treatments may be given to people at high risk, he adds, so a growing number of people will live longer but not long enough to get AD.


Diagnosing Alzheimer's

Scientists are uncovering clues to better diagnose the disease and to determine who is at risk. "It is my hope that in time for the baby boomers, there will be both a prognostic test, as well as at least one therapeutic strategy," says Sunderland. "Both prognostic and therapeutic options are needed. If you had a preventative drug that potentially had toxicity associated with it, you wouldn't want to give it to everybody--only the subpopulation at greatest risk."

Today, AD can be diagnosed conclusively only by examining the brain after death. But physicians can make a probable diagnosis on living patients by taking a complete medical history, administering neurological and psychological tests, and doing a physical exam, blood and urine laboratory tests, and a brain-imaging scan. Once symptoms begin, the disease can be diagnosed with up to 90 percent accuracy by experienced physicians, according to the NIA.

But do people start getting AD before symptoms show themselves? "That's the big question in Alzheimer's disease: When does it really begin?" says Sunderland. No one knows for sure, he says, but research "suggests that the illness may predate clinical symptoms by years and maybe decades."

Advances in neuroimaging--taking pictures of the brain to measure its structure and activity--may allow researchers to see the accumulation of plaques and tangles at various points in time. Neuroimaging may one day prove useful in monitoring the progression of the disease and assessing people's responses to drug treatment.

Another early indication of AD could be found in a person's spinal fluid, which, like the brain, carries beta-amyloid and tau proteins. In a study at the NIMH, Sunderland's team of researchers was able to diagnose AD in most cases by measuring the levels of these proteins in spinal fluid. These measurements, or biomarkers, may help scientists identify people at risk for AD, says Sunderland. "By establishing a person's baseline and tracking levels over time, we might be able to interpret gradual changes as a sign that he or she is developing the disorder." Sunderland's study, which included physical examination of more than 200 participants and an analysis of over 50 similar studies, is reported in the April 23, 2003, issue of the Journal of the American Medical Association (JAMA). While work in this area is currently investigational in nature, spinal fluid testing may become a valuable routine diagnostic tool in the future.


Delaying the Disease

Some studies hint that a variety of existing drugs and supplements may be useful in delaying AD or stopping its progression. These studies are preliminary, and their findings would need to be demonstrated in adequately designed and conducted studies before their conclusions can be considered proven, says Katz.

Cholesterol-lowering drugs, anti-inflammatory drugs, antioxidants, and estrogen are some of the substances that have been studied, but study results have been conflicting. These studies don't prove causation, warns Thies of the Alzheimer's Association. "All they really tell us is it's a good place to start doing clinical trials." And researchers are doing just that.


The Heart and Head Connection

Studies have shown a link between known risk factors for heart disease--high blood pressure, high cholesterol levels, and diets high in saturated fats and trans fats--and an increased risk for AD. There is also evidence that an elevated level of homocysteine, an amino acid in the blood, presents a risk for both heart disease and AD. Further, taking cholesterol-lowering drugs (statins) is associated with a lower occurrence of AD.

"What is good for the heart may be good for the head," says Thies, and healthy lifestyle behaviors such as exercising, eating healthily, and managing blood pressure and cholesterol may be of value in protecting people from AD.

Large-scale clinical trials are being conducted to clarify the link between cardiovascular risk factors and AD. In addition to statins, substances being tested for slowing and preventing AD are folate (a form of B vitamin) and vitamins B6 and B12, which may lower homocysteine levels.
Anti-inflammatory Drugs

People who take large doses of non-steroidal anti-inflammatory drugs (NSAIDs), commonly used to reduce joint inflammation and pain, have a reduced likelihood of developing AD, according to some studies. NSAIDs, which include over-the-counter aspirin and ibuprofen, as well as some prescription drugs, such as Celebrex (celecoxib), may reduce the inflammation in the brain associated with AD.

None of the studies performed with the anti-inflammatory drugs to date are definitive, cautions Katz, and these drugs would need to be studied in scientifically rigorous trials before the effects of these drugs on AD could be accepted. One of these trials, the Alzheimer's Disease Anti-Inflammatory Prevention Trial (ADAPT), was launched in 2001 to test the effectiveness of some NSAIDs in preventing AD. The study of more than 2,500 healthy participants age 70 and over is sponsored by the NIA and is scheduled to run between five and seven years.


Antioxidants

Researchers are also looking at antioxidants to possibly prevent cognitive decline. Antioxidants, such as vitamin E, vitamin C and carotene, may help break down "free radicals"--cell-damaging compounds that are byproducts of normally functioning cells. The natural defenses of cells protect against these compounds, but these protective mechanisms decline as a person ages.

Some study results have suggested that antioxidants may protect against cell damage and lessen the likelihood of getting AD. But a four-year study of nearly 1,000 older people conducted at Columbia University found that consuming carotenes or vitamins C and E either through the diet or by supplements did not decrease the risk of developing AD. "This large-scale study is at variance with earlier indications that these supplements are effective as a treatment for Alzheimer's," says Thies. "This tells us that more work needs to be done before we completely understand the value of these agents." The results of this study are published in the February 2003 issue of Archives of Neurology.

"There are virtually shelf-fuls of compounds capable of acting in an antioxidant fashion," says Thies. One of these, Ginkgo biloba, used for thousands of years in Chinese herbal medicine, has been shown in a small study to result in a modest improvement in cognition, social behavior and performing activities of daily living, such as dressing and eating. A larger study (about 3,000 participants) funded by the National Institutes of Health (NIH) is currently investigating the effectiveness of Ginkgo in preventing or delaying cognitive decline in older adults.

The FDA cautions consumers that some supplements may interact with prescription and over-the-counter medicines and cause serious harm. Check with your doctor or health care provider before taking any dietary supplement, including herbs.
Estrogen

Several epidemiological studies have linked the female hormone estrogen to improved memory and possible delay or prevention of AD in women. But a large, long-term clinical trial sponsored by the NIH has provided evidence to the contrary. In the trial, part of the Women's Health Initiative Memory Study (WHIMS), women 65 and over taking estrogen combined with another hormone, progestin, had twice the rate of dementia, including AD, than those women not taking the hormones. The study, published in the May 28, 2003, issue of JAMA, also found that the hormone combination did not protect against the development of mild cognitive impairment, a form of mental decline less severe than dementia.


New Drug Development

New drugs are emerging from the basic science laboratories and moving toward testing in human trials. "The ones furthest along ar

related resources: risk analysis, long-term care

New Drug Development

New drugs are emerging from the basic science laboratories and moving toward testing in human trials. "The ones furthest along are based on the amyloid hypothesis," says Thies. The hypothesis is that AD starts with the accumulation of amyloid plaques, and that limiting this accumulation will change the progress of AD.

Scientists have isolated enzymes called secretases, which are thought to lead to the formation of beta-amyloid. Secretases are categorized as proteases, the same type of enzymes that are targeted by protease inhibitors to treat AIDS. Drugs called secretase inhibitors are being developed to block beta-amyloid formation, and some of these drugs are now being tested.

Another approach to plaque attack is to stimulate the body's immune system to destroy the beta-amyloid. Scientists developed a vaccine that put amyloid into the blood in the hopes of making antibodies to destroy the plaques. The vaccine was successful in transgenic mice--special mice that were injected with human genes that caused them to develop AD-like plaques. But when tested in a human trial, some people showed inflammation of the brain (encephalitis). Further vaccination was stopped, but study participants continue to be followed. Although this particular vaccine may be disappointing, many scientists believe that the strategy of fighting AD by stimulating the immune system still remains an important potential avenue to slow or prevent the disease.

"We are still searching for the sequence of events where we can intervene and cure the disease without causing harm," says Marcelle Morrison-Bogorad, Ph.D., associate director of the NIA's Neuroscience and Neuropsychology of Aging Program. Morrison-Bogorad notes that scientists may someday be able to inject a substance into the blood to draw amyloid from cerebral spinal fluid and the brain. "This can happen in transgenic mice--we don't know whether it happens in humans yet."
Risk Factors

The two biggest risk factors for getting AD are age and genetics, neither of which is in our control, says Thies. Scientists have identified several genes that play a role in early-onset AD, a rare form of the disease that strikes people as young as in their 30s. For late-onset AD, defined as showing symptoms after age 65, a gene that produces a protein called apolipoprotein E (ApoE) appears to play a role. The gene comes in several forms, or alleles. Having the ApoE4 allele increases the risk for getting AD, according to the NIA.

About 40 percent of people with AD have the ApoE4 allele, but inheriting it doesn't mean a person will definitely get AD. Some people with the gene never get the disease, and some without it do develop AD. Once researchers know more about how genetics affects AD, people could be genetically screened and then treated based on their genetic factors.

Some studies have shown that participating in mentally stimulating activities, such as reading books, doing crossword puzzles, or going to museums, may be associated with a reduced risk of AD. Researchers speculate that repetition might improve certain cognitive skills, making them less susceptible to brain damage.

This "use-it-or-lose-it" theory may have value, but further study is needed, says Morrison-Bogorad. AD may actually cause people to stop doing mentally challenging activities because the disease makes it harder to do them, she says. "It's impossible to tease out the cause and effect in these studies. We can only say it's correlative--not causal." Morrison-Bogorad does encourage mental activity. "It keeps you nimble--whether it helps prevent Alzheimer's, we don't know."

Linda Bren is a staff writer for FDA Consumer.

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For More Information

Alzheimer's Disease Education
and Referral (ADEAR) Center
National Institute on Aging
(800) 438-4380
www.alzheimers.org

Alzheimer's Association
(800) 272-3900
www.alz.org

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Eluding Alzheimer's

No cure or prevention for Alzheimer's disease exists yet, but experts offer some advice to help prolong mental health:

"The best thing people can do is to try to plan for their later years and try to remain as functional as possible," says William Thies, Ph.D., vice president of medical and scientific affairs at the Alzheimer's Association in Chicago. "And stay connected to the world, because the literature suggests that social isolation is a contributor to unhealthy aging."

Steven Ferris, Ph.D., director of the Alzheimer's Disease Center at the New York University School of Medicine, makes three recommendations:

* Stay mentally active. "The more you challenge the brain, the more you'll be able to maintain it," says Ferris. "When you're stimulating the brain, you're growing more interconnections and maybe even growing new neurons. The more brain cells and connections you have, the longer you'll be able to function well, even if you get Alzheimer's."
* Stay physically active. Physical exercise improves brain function as well as benefiting the rest of your body.
* Have a healthy diet and stay in good physical health. These are essential for maintaining good brain function.

Trey Sunderland, M.D., chief of the Geriatric Psychiatry Branch of the National Institute of Mental Health, encourages people to participate in Alzheimer's research studies so that they learn about the illness and are followed carefully for any incremental change that might occur in their health. "Our volunteers have found that they actually get reassured by being in a study," says Sunderland. "For the most part, we're telling them--in our long-term follow-up studies--that they continue to be normal."

It's really bad. I'd say she's delt with it for atleast 10 years if not more. She doesn't know who most family are anymore, including myself and my sister. She doesn't remember that her husband passed away years ago and her hygeine has gone out the window.

yes i want to also say thanxxxxxxxxxxxxxxx