Article
What is Alzheimers
By Michael Murphy on July 11th, 2008(viewed 2811 times).






 

What is Alzheimers

 

Introduction

Alzheimer’s disease is a brain disorder named for German physician Alois Alzheimer, who first described it in 1906. Scientists have learned a great deal about Alzheimer’s disease in the century since Dr. Alzheimer first drew attention to it. Today we know that Alzheimer’s:

  • Is a progressive and fatal brain disease. As many as 5 million Americans are living with Alzheimer’s disease. Alzheimer's destroys brain cells, causing problems with memory, thinking and behavior severe enough to affect work, lifelong hobbies or social life. Alzheimer’s gets worse over time, and it is fatal. Today it is the sixth-leading cause of death in the United States. For more information, see Warning Signs and Stages of Alzheimer’s Disease.

 

  • Is the most common form of dementia, a general term for the loss of memory and other intellectual abilities serious enough to interfere with daily life. Vascular dementia, another common type of dementia, is caused by reduced blood flow to parts of the brain. In mixed dementia, Alzheimer’s and vascular dementia occur together. For more information about other causes of dementia, please see Related Dementias.
  • Has no current cure. But treatments for symptoms, combined with the right services and support, can make life better for the millions of Americans living with Alzheimer’s. We’ve learned most of what we know about Alzheimer’s in the last 15 years. There is an accelerating worldwide effort under way to find better ways to treat the disease, delay its onset, or prevent it from developing. Learn more about recent progress in Alzheimer science and research funded by the Alzheimer’s Association in the Research section.

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Alzheimer's and the brain

Just like the rest of our bodies, our brains change as we age. Most of us notice some slowed thinking and occasional problems remembering certain things. However, serious memory loss, confusion and other major changes in the way our minds work are not a normal part of aging. They may be a sign that brain cells are failing.

The brain has 100 billion nerve cells (neurons). Each nerve cell communicates with many others to form networks. Nerve cell networks have special jobs. Some are involved in thinking, learning and remembering. Others help us see, hear and smell. Still others tell our muscles when to move. To do their work, brain cells operate like tiny factories. They take in supplies, generate energy, construct equipment and get rid of waste. Cells also process and store information. Keeping everything running requires coordination as well as large amounts of fuel and oxygen. In Alzheimer’s disease, parts of the cell’s factory stop running well. Scientists are not sure exactly where the trouble starts. But just like a real factory, backups and breakdowns in one system cause problems in other areas. As damage spreads, cells lose their ability to do their jobs well. Eventually, they die. Learn more about Alzheimer's: Take the Brain Tour

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The role of plaques and tangles

Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques and tangles were among the abnormalities that Dr. Alois Alzheimer saw in the brain of Auguste D., although he called them different names.

  • Plaques build up between nerve cells. They contain deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd). Tangles are twisted fibers of another protein called tau (rhymes with “wow”).
  • Tangles form inside dying cells. Though most people develop some plaques and tangles as they age, those with Alzheimer’s tend to develop far more. The plaques and tangles tend to form in a predictable pattern, beginning in areas important in learning and memory and then spreading to other regions.

Scientists are not absolutely sure what role plaques and tangles play in Alzheimer’s disease. Most experts believe they somehow block communication among nerve cells and disrupt activities that cells need to survive.

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Early stage and younger onset

Early-stage is the early part of Alzheimer’s disease when problems with memory, thinking and concentration may begin to appear in a doctor’s interview or medical tests. Individuals in the early-stage typically need minimal assistance with simple daily routines. At the time of a diagnosis, an individual is not necessarily in the early stage of the disease; he or she may have progressed beyond the early stage.  The term younger-onset refers to Alzheimer's that occurs in a person under age 65. Younger-onset individuals may be employed or have children still living at home. Issues facing families include ensuring financial security, obtaining benefits and helping children cope with the disease. People who have younger-onset dementia may be in any stage of dementia – early, middle or late. Experts estimate that some 500,000 people in their 30s, 40s and 50s have Alzheimer's disease or a related dementia.

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History

At a scientific meeting in November 1906, German physician Alois Alzheimer presented the case of “Frau Auguste D.,” a 51-year-old woman brought to see him in 1901 by her family. Auguste had developed problems with memory, unfounded suspicions that her husband was unfaithful, and difficulty speaking and understanding what was said to her. Her symptoms rapidly grew worse, and within a few years she was bedridden. She died in Spring 1906, of overwhelming infections from bedsores and pneumonia. Dr. Alzheimer had never before seen anyone like Auguste D., and he gained the family’s permission to perform an autopsy. In Auguste’s brain, he saw dramatic shrinkage, especially of the cortex, the outer layer involved in memory, thinking, judgment and speech. Under the microscope, he also saw widespread fatty deposits in small blood vessels, dead and dying brain cells, and abnormal deposits in and around cells. The condition entered the medical literature in 1907, when Alzheimer published his observations about Auguste D. In 1910, Emil Kraepelin, a psychiatrist noted for his work in naming and classifying brain disorders, proposed that the disease be named after Alzheimer.

 http://www.alz.org/national/images/subpage_people_aguste.gif  Auguste D.

 http://www.alz.org/national/images/subpage_people_alois.gif  Dr. Alois Alzheimer

 

 

Introduction

A growing number of herbal remedies, vitamins and other dietary supplements are promoted as memory enhancers or treatments for Alzheimer’s disease and related diseases. Claims about the safety and effectiveness of these products, however, are based largely on testimonials, tradition and a rather small body of scientific research. The rigorous scientific research required by the U.S. Food and Drug Administration (FDA) for the approval of a prescription drug is not required by law for the marketing of dietary supplements.

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Concerns about alternative therapies

Although many of these remedies may be valid candidates for treatments, there are legitimate concerns about using these drugs as an alternative or in addition to physician-prescribed therapy:

  • Effectiveness and safety are unknown. The maker of a dietary supplement is not required to provide the FDA with the evidence on which it bases its claims for safety and effectiveness.
  • Purity is unknown. The FDA has no authority over supplement production. It is a manufacturer’s responsibility to develop and enforce its own guidelines for ensuring that its products are safe and contain the ingredients listed on the label in the specified amounts.
  • Bad reactions are not routinely monitored. Manufacturers are not required to report to the FDA any problems that consumers experience after taking their products. The agency does provide voluntary reporting channels for manufacturers, health care professionals, and consumers, and will issue warnings about product when there is cause for concern.
  • Dietary supplements can have serious interactions with prescribed medications. No supplement should be taken without first consulting a physician.

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Coenzyme Q10

Coenzyme Q10, or ubiquinone, is an antioxidant that occurs naturally in the body and is needed for normal cell reactions. This compound has not been studied for its effectiveness in treating Alzheimer’s.

A synthetic version of this compound, called idebenone, was tested for Alzheimer’s disease but did not show favorable results. Little is known about what dosage of coenzyme Q10 is considered safe, and there could be harmful effects if too much is taken.

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Coral calcium

“Coral” calcium supplements have been heavily marketed as a cure for Alzheimer’s disease, cancer and other serious illnesses. Coral calcium is a form of calcium carbonate claimed to be derived from the shells of formerly living organisms that once made up coral reefs. In June 2003, the Federal Trade Commission (FTC) and the Food and Drug Administration (FDA) filed a formal complaint against the promoters and distributors of coral calcium. The agencies state that they are aware of no competent and reliable scientific evidence supporting the exaggerated health claims and that such unsupported claims are unlawful. Coral calcium differs from ordinary calcium supplements only in that it contains traces of some additional minerals incorporated into the shells by the metabolic processes of the animals that formed them. It offers no extraordinary health benefits. Most experts recommend that individuals who need to take a calcium supplement for bone health take a purified preparation marketed by a reputable manufacturer. See also the FDA/FTC press release on the coral calcium complaint.

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Ginkgo biloba

Ginkgo biloba is a plant extract containing several compounds that may have positive effects on cells within the brain and the body. Ginkgo biloba is thought to have both antioxidant and anti-inflammatory properties, to protect cell membranes and to regulate neurotransmitter function. Ginkgo has been used for centuries in traditional Chinese medicine and currently is being used in Europe to alleviate cognitive symptoms associated with a number of neurological conditions.

In a study published in the Journal of the American Medical Association (October 22/29, 1997), Pierre L. Le Bars, M.D., Ph.D., of the New York Institute for Medical Research, and his colleagues observed in some participants a modest improvement in cognition, activities of daily living (such as eating and dressing) and social behavior. The researchers found no measurable difference in overall impairment.

Results from this study show that ginkgo may help some individuals with Alzheimer’s disease, but further research is needed to determine the exact mechanisms by which Ginkgo works in the body. Also, results from this study are considered preliminary because of the low number of participants, about 200 people.

Few side effects are associated with the use of Ginkgo, but it is known to reduce the ability of blood to clot, potentially leading to more serious conditions, such as internal bleeding. This risk may increase if Ginkgo biloba is taken in combination with other blood-thinning drugs, such as aspirin and warfarin.

Currently, a large federally funded multicenter trial with about 3,000 participants is investigating whether Ginkgo may help prevent or delay the onset of Alzheimer’s disease or vascular dementia.

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Huperzine A

Huperzine A (pronounced HOOP-ur-zeen) is a moss extract that has been used in traditional Chinese medicine for centuries. It has properties similar to those of cholinesterase inhibitors, one class of FDA-approved Alzheimer medications. As a result, it is promoted as a treatment for Alzheimer's disease.

Evidence from small studies shows that the effectiveness of huperzine A may be comparable to that of the approved drugs. In Spring 2004, the National Institute on Aging (NIA) launched the first large U.S. clinical trial of huperzine A as a treatment for mild to moderate Alzheimer’s disease.

Because currently available formulations of huperzine A are dietary supplements, they are unregulated and manufactured with no uniform standards. If used in combination with FDA-approved Alzheimer drugs, an individual could increase the risks of serious side effects.

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Omega-3 fatty acids

Omega-3s are a type of polyunsaturated fatty acid (PUFA). Research has linked certain types of omega-3s to a reduced risk of heart disease and stroke.

The U.S. Food and Drug Administration (FDA) permits supplements and foods to display labels with “a qualified health claim” for two omega-3s called docosahexaneoic acid (DHA) and eicosapentaenoic acid (EPA). The labels may state, “Supportive but not conclusive research shows that consumption of EPA and DHA omega-3 fatty acids may reduce the risk of coronary heart disease,” and then list the amount of DHA or EPA in the product. The FDA recommends taking no more than a combined total of 3 grams of DHA or EPA a day, with no more than 2 grams from supplements.

Research has also linked high intake of omega-3s to a possible reduction in risk of dementia or cognitive decline. The chief omega-3 in the brain is DHA, which is found in the fatty membranes that surround nerve cells, especially at the microscopic junctions where cells connect to one another.

A Jan. 25, 2006, literature review by the Cochrane Collaboration found that published research does not currently include any clinical trials large enough to recommend omega-3 supplements to prevent cognitive decline or dementia. But the reviewers found enough laboratory and epidemiological studies to conclude this should be a priority area for further research.

According to the review, results of at least two larger clinical trials are expected in 2008. The Cochrane Collaboration is an independent, nonprofit organization that makes objective assessments of available evidence on a variety of issues in treatment and health care.

Theories about why omega-3s might influence dementia risk include their benefit for the heart and blood vessels; anti-inflammatory effects; and support and protection of nerve cell membranes. There is also preliminary evidence that omega-3s may also be of some benefit in depression and bipolar disorder (manic depression).

A report in the April 2006 Nature described the first direct evidence for how omega-3s might have a helpful effect on nerve cells (neurons). Working with laboratory cell cultures, the researchers found that omega-3s stimulate growth of the branches that connect one cell to another. Rich branching creates a dense “neuron forest,” which provides the basis of the brain’s capacity to process, store and retrieve information.

See also the 2004 FDA press release announcing extension of the qualified health claim for omega-3s and coronary heart disease from supplements to foods.

 

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Phosphatidylserine

Phosphatidylserine (pronounced FOS-fuh-TIE-dil-sair-een) is a kind of lipid, or fat, that is the primary component the membranes that surround nerve cells. In Alzheimer’s disease and similar disorders, nerve cells degenerate for reasons that are not yet understood. The theory behind treatment with phosphatidylserine is its use may shore up the cell membrane and possibly protect cells from degenerating.

The first clinical trials with phosphatidylserine were conducted with a form derived from the brain cells of cows. Some of these trials had promising results. However, most trials were with small samples of participants.

This line of investigation came to an end in the 1990s over concerns about mad cow disease. There have been some animal studies since then to see whether phosphatidylserine derived from soy may be a potential treatment. A report was published in 2000 about a clinical trial with 18 participants with age-associated memory impairment who were treated with phosphatidylserine. The authors concluded that the results were encouraging but that there would need to be large carefully controlled trials to determine if this could be a viable treatment.

 

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