Here is the full list of pages on alzheimers.phoolish.org

Here is the full list of pages on alzheimers.phoolish.org

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50. Wanted: Volunteers for a New Study on Genes and Alzheimer's
49. Symptoms of Depression Linked to Onset of Alzheimer's
48. The Delicate Balance of End-of-Life Care
47. Weight Loss May Be an Early Sign of Alzheimer’s
46. Signs of Alzheimer's May Be Present 10 Years Before Diagnosis
45. Signs of Alzheimer's May Be Present 10 Years Before Diagnosis
44. Fisher Center Scientists Probe the Root Cause of Alzheimer's
43. Immune System Problem Linked to Alzheimer's
42. Alzheimer's May Pose Special Challenges for Latinos
41. Nerve "Traffic Jam" Marks Early Alzheimer's
40. Doctors Identify Possible New "Alzheimer's Gene"
39. Weight Loss May Signal Early Alzheimer's
38. Researchers Zero In on Alzheimer's Genes
37. Scrambled Brain Signals Point to Alzheimer's Defects
36. PET Brain Scans Now Covered by Medicare
35. “Good” Cholesterol May Help Keep Alzheimer's at Bay
34. Blood Pressure Drop May Herald Alzheimer's
33. Alzheimer's Brain Scans to be Covered by Medicare
32. Good Genes, Bad Genes: The Pros and Cons of Alzheimer’s Screening
31. Cancer-Alzheimer's Link to Be Explored
30. Estrogen Alone May Raise Dementia Risk
29. Hormone Replacement Therapies Carry Alzheimer's Risk
28. In Alzheimer's, Nature and Nurture Play Dueling Roles
27. Strokes May Increase Alzheimer's Risk
26. Emotional Distress May Up Alzheimer's Risk
25. MRI Scans Show Promise for Early Detection of Memory Loss
24. Infections Linked to Alzheimer's Disease
23. Should You Be Screened for Alzheimer's?
22. Ronald Reagan's Recent Birthday Underscores Urgency of Alzheimer's Research and Public's Need for Accurate, Up-to-Date Information
21. Alzheimer’s Affects a Growing Segment of Elderly Population
20. New Gene Linked to Alzheimer’s
19. Cold Sore Virus Might Play A Role in Alzheimer’s
18. Experimental Brain Scan Technique Detects Early Alzheimer’s
17. Protein “Fingerprint” May One Day Lead to an Alzheimer’s Test
16. Aging Cats Can Succumb to Dementia
15. Shedding Pounds May Be An Early Indicator of Alzheimer’s Disease
14. Memory Deficits Linked to Brain Loss
13. Stress May Hasten Progression of Alzheimer’s Disease
12. Alzheimer's Treatment
11. Alzheimer's Diagnosis
10. 10 warning signs of Alzheimer's
09. Alzheimer's Symptoms
08. Alzheimer's Information
07. Alzheimer’s Affects a Growing Segment of Elderly Population
06. New Gene Linked to Alzheimer’s
05. Therapy Pets Prove Soothing to People with Alzheimer’s
04. In Search of an Alzheimer’s Cure
03. More Than 5 Millions Americans Are Living with Alzheimer’s
02. Hope for an Alzheimer’s Vaccine
01. All About Alzheimer's disease


95. Preventing Dementia and Alzheimer's
94. UCI researchers identify first compound to block progression of Alzheimer’s disease
93. Putting Ginkgo to the Test
92. Antioxidants decrease disease in an insect model of Alzheimer’s disease
91. Ronald Reagan's Alzheimer's Letter
90. Accelerated Disease of the Aged in Alzheimers
89. AD Alzheimer disease
88. Alzheimer and Balance
87. Help with Alzheimer
86. Health and Alzheimer Disease
85. Fighting Alzheimers disease
84. Economy and Alzheimer
83. Down with Alzheimer
82. Down with Alzheimer Disease
81. Diagnosis of Alzheimer
80. Diabetes and Alzheimer
79. Developing Alzheimer Disease
78. CNS and the Alzheimer
77. Causes of Alzheimer
76. Caring for a loved one with Alzheimer disease
75. Caring for a loved one with Alzheimer
74. Care Provider and the Alzheimer
73. Care giving for Alzheimer Patients
72. Battling the Disease Alzheimer
71. Alzheimer the Series of Disorders
70. Alzheimer the Brain Killer
69. Alzheimer Reducing Risks
68. Alzheimer Disease and the Central Nervous System
67. Alzheimer and Symptoms
66. Alzheimer and Pain
65. Alzheimer and Down syndrome
64. Alzheimer and Dementia
63. Dope Hope For Alzheimer's
62. The Latest on Hormone Therapy and Alzheimer's
61. Diabetes May Increase Your Risk of Alzheimer's
60. Gene Influences When Alzheimer’s Symptoms Appear
59. A Simple Word Test May Aid Doctors in Alzheimer’s Care
58. Study Links a Common B Vitamin to Poor Memory in Seniors
57. Alzheimer's: A Growing Epidemic
56. Hormone Replacement Therapy May Up Your Alzheimer's Risk
55. Another Person Develops Dementia Every Seven Seconds
54. Immune Therapy Helps "Untangle" Alzheimer's Disease
53. Alzheimer's May Hit Minorities Especially Hard
52. Gene May Play a Role in Alzheimer's and Parkinson's Onset
51. A Lab Test for Alzheimer's

Preventing Dementia and Alzheimer's

Dementia is the loss of mental abilities and most commonly occurs late in life. Of all persons over age 65, 5-8% are demented. This percentage increases considerably with age. Twenty-five to 50% of people over 85 are affected. The most common form of dementia, Alzheimers disease, accounts for 50-75% of all cases of dementia.
Fish

Tucking into more fresh tuna, trout, sardines, mackerel, anchovies and salmon could help you reduce the risk of dementia and Alzheimers. It is well-known that oil-rich fish paves the way to a healthy heart. But recent studies are showing that oily fish has a beneficial effect on the brain.

Eating fish just once a week reduces the risk of developing Alzheimers by 60%, according to a recent study by Dr. Martha Morris and her colleagues of the Rush Presbyterian St. Lukes Medical Center in Chicago. They followed 815 people, aged 65 to 94 years, for seven years and found that the dietary intake of fish was strongly linked to Alzheimers risk.

They found that the strongest link was the amount of DHA, a form of omega 3 fat found in fish. And those who consumed the most total omega 3's (from fish, vegetable oils and nuts combined) had 70% less risk. The more a persons DHA, the lower their risk of developing Alzheimers.

With the right nutrition and the right attitude, age-related memory loss can be prevented.

A study led by Dr. Robert Friedland, a neurologist at Case Western Reserve University School of Medicine in Cleveland, combined mental, physical and even social activities in adults, and compared activity levels with the rate of Alzheimer's disease. Friedland's team measured changes in 26 activity levels in 193 patients with likely or possible Alzheimer's and 358 healthy people. Some activities were physical, like exercise and gardening; some were passive, like television viewing and going to church; others were intellectual, including reading and writing letters. In addition to the variety of activities people pursued with age, the researchers also were interested in how intensely subjects stayed involved between ages 20 and 60.

Compared with Alzheimer's patients, people with healthy brains had been involved in a broader variety of activities during adulthood, the researchers say. Those whose activity levels fell below the average had nearly a four-fold increase in the risk of the disease, even after accounting for other Alzheimer's risk factors like age and education level.

What's more, people who spent more time pursuing the 26 activities as they got older appeared to gain significant protection from brain changes linked to Alzheimer's.

In fact, Alzheimer's patients, or their caretakers, reporting doing less of every activity than healthy subjects except one, television watching, says Friedland. TV represents an activity which is often not intellectual, and is not physical except changing the channels.

Nutrition expert Patrick Holford, author of The Alzheimers Prevention Plan, offers tips to keep your memory and mind sharp:

* Eat fish and seeds high in essential omega 3 fats. Sprinkle flaxseeds on your cereal. Snack on pumpkin seeds, also rich in omega 3 fats.
* Eat eggs, high in phospholipids. The best eggs are omega 3-rich eggs, from chickens fed flaxseeds because you also get omega 3 fats. Lecithin, which you can buy in health food stores in either capsules or granules, are also high in phospholipids. Sprinkle a dessertspoon on your cereal.
* Eat slow-release carbohydrates such as oat-based cereals, oat cakes, whole-wheat pasta and brown basmati rice.
* Eat vitamin-, mineral- and antioxidant-rich food like berries, and dark green leafy and root vegetables.
* Avoid hydrogenated fats found in junk food and burnt fats like fried food, sugar and excess caffeine and alcohol.
* Take a high-strength multivitamin, with vitamin E, C and at least 20mg of vitamin B6, 10mcg of B12 and 250mcg of folic acid.
* Test your homocysteine level. (Elevated levels of the amino acid homocysteine in the blood can lead to a higher risk of dementia, including Alzheimer's-related dementia.)
* Use your brain. Keep learning throughout your life.
* Keep physical. Ideally, take up an exercise that helps develop yogic breathing, such as yoga, tai chi or psycho-calisthenics. Dancing to the music helps to improve memory.
* Make sure you get enough light. Spend some time outdoors most days.

UCI researchers identify first compound to block progression of Alzheimer’s disease

Compound reduces hallmark lesions of the disease in mice, improving cognitive function

Irvine, Calif., March 1, 2006

Researchers at UC Irvine have found that a new compound not only relieves the cognitive symptoms of Alzheimer’s disease, but also reduces the two types of brain lesions that are hallmarks of this devastating disease, thereby blocking its progression.

In a study with genetically modified mice, a team of UCI researchers led by Frank LaFerla, professor of neurobiology and behavior, found that a compound known as AF267B, developed by paper co-author Abraham Fisher of the Israel Institute for Biological Research, reduced both plaque lesions and tangles in brain regions associated with learning and memory. Although drugs exist on the market today to treat the symptoms of Alzheimer’s, AF267B represents the first disease-modifying compound, meaning it appears to affect the underlying cause and reduces the two signature lesions, plaques and tangles.

The researchers report their findings in the March 2 issue of Neuron.

“AF267B could be a tremendous step forward in the treatment of Alzheimer’s disease,” said LaFerla, who serves as co-director of the UCI Institute for Brain Aging and Dementia. “Not only does it appear to work on the pathology of Alzheimer’s and ease its symptoms, it crosses the blood-brain barrier, which means it does not have to be directly administered to the brain, a significant advantage for a pharmaceutical product. Although we cannot determine what the effects of AF267B will be in humans until clinical trials are complete, we are very excited by the results our study has yielded.”

According to LaFerla, AF267B works by mimicking the effects of the neurotransmitter acetylcholine, a chemical in the brain essential for learning and memory. Neurotransmitters act as carriers for messages between brain cells and bind to receptors on the cells’ surfaces. Acetylcholine generally binds to specific receptors in the brain, including the M1 receptor, a potentially novel therapeutic target for Alzheimer’s disease.

Scientists have known for years that there is a major loss of the neurons that produce acetylcholine in the brains of Alzheimer’s patients. Compounds classified as M1 agonists - meaning that they mimic the effects of acetylcholine and bind to M1 receptors – are regarded as one hope for counteracting or compensating for the loss of acetylcholine. Unfortunately, previous M1 agonists had been tested but failed in clinical trials.

AF267B, however, appears to have overcome the problems seen with earlier generations of M1 agonists. In this study, the researchers found that the administration of AF267B reduced the amount of plaques and tangles in the hippocampus and the cortex of the mice, and improved cognitive performance. When the compound binds to the M1 receptor in those regions of the brain, the levels of an enzyme known as alpha secretase are increased. This enzyme prevents the production of beta-amyloid, which, according to a theory known as the amyloid cascade hypothesis, also would block the eventual accumulation of tangles.

“These findings are highly important because they offer a new understanding of the importance of cholinergic activation of cells in the hippocampus and cerebral cortex that are essential for creating and preserving memories,” said James L. McGaugh, research professor of neurobiology and behavior and a member of the National Academy of Sciences who pioneered the study of drug and stress-hormone influences on memory. “The evidence suggests the exciting prospect of possibly preventing the development of this devastating disease.”

TorreyPines Therapeutics, a biopharmaceutical company in San Diego, is conducting clinical studies to determine whether the compound is safe for use. In early tests, the compound was well tolerated at tested doses in a group of young, healthy males.

Alzheimer’s disease is marked by the accumulation of two types of brain lesions – beta-amyloid plaques and neurofibrillary tangles. The disease is a progressive neurodegenerative disorder, affecting 4.5 million to 5 million adults in the United States. If no effective therapies are developed, it is estimated that 13 million Americans will be afflicted with the disease by 2050. It is the third most expensive disease to treat and the third leading cause of death, behind cancer and coronary heart disease.

In recent years, LaFerla has been at the forefront of Alzheimer’s research and has made a number of significant strides in understanding the molecular development of the disease. In addition to finding that early treatment of beta-amyloid plaques can halt the progression of Alzheimer’s, he and other members of his research team created the genetically-altered mouse that was used in this study. His work also determined that chronic nicotine exposure worsens some Alzheimer-related brain abnormalities, contradicting the common belief that nicotine can actually be used to treat the disease.

This study was funded primarily by a grant from the National Institute on Aging and the Alzheimer’s Association.

About the Study: LaFerla and his associates, including the study’s first author Antonella Caccamo, a UCI staff research associate, tested AF267B on both normal mice and on special Alzheimer’s mice engineered by the LaFerla lab, which manifest several features of Alzheimer’s including plaques and tangles. The mice were injected with AF267B or with a compound called dicyclomine, which is an M1 antagonist and performs exactly the opposite function of an M1 agonist. Dicyclomine was used as proof of concept; if M1 agonists help improve cognitive function and reverse memory decline, then an M1 antagonist should have the opposite effect.

After eight weeks of daily AF267B administration and four weeks of daily dicyclomine injections, the mice were tested using two different behavioral tasks. In the Morris water maze, mice are tested for spatial reference, a task dependent on the hippocampus and the cortex. In the test, the mice were placed in a maze in a water tank and encouraged repeatedly to locate a hidden platform in the tank by making spatial association in the room to facilitate their search. After the platform was removed, the researchers monitored in subsequent trials how many times the mice would cross over the space where the platform used to be – an indication of how well they remembered its location.

Although AF267B had no effect on the normal mice who were not afflicted with the plaques or tangles, the tests clearly showed that the Alzheimer’s transgenic mice treated with this compound better remembered the platform’s location compared to the control group of transgenic mice that received placebo. Strikingly, all the mice, both normal and transgenic, did not remember the platform’s location when injected with dicyclomine, proving that an M1 antagonist does seem to have an adverse effect on memory. Neuropathological examination of the mice also showed that there were fewer plaques and tangles in the brains of the transgenic mice treated with AF267B than in the brains of the transgenic mice that received placebo. All the mice injected with dicyclomine showed more diffuse plaques and tangles.

LaFerla and his team also used a test related to contextual information and unpleasant stimuli, memories processed by the amygdala. The mice were placed inside a dark box to familiarize themselves with that context. After a few seconds, a light went on and a door was opened to a second, darker compartment. As mice prefer to stay in the dark, they moved to the dark compartment where they were given a mild foot shock. At a later time, the mice were replaced in the starting compartment and tested to see how long they would avoid the dark, shock-associated compartment, a sign of whether they remembered the unpleasant stimulus.

Whereas the normal mice avoided the shock compartment, all the Alzheimer’s mice, including those that had been treated with AF267B, showed impaired memory for this task. A neuropathological examination of their brains showed no reduction of the plaques or tangles in the amygdala. However, the administration of dicyclomine reduced memory function in both normal and transgenic mice.

According to LaFerla, this is because in the amygdala there is less production of the alpha secretase enzyme, which when active prevents the formation of beta-amyloid. Thus, the levels of this enzyme could not be increased by AF267B in the amygdala and the production of beta-amyloid could not be prevented.

LaFerla’s research has shown previously that the accumulation of beta-amyloid within neurons is the trigger for the onset of memory decline in Alzheimer’s. His team also has shown that removing plaques from the brain can lead to a clearance of the tangle pathology, supporting a theory known as the “amyloid cascade hypothesis.” According to this hypothesis, it is the buildup of beta-amyloid in the brain that triggers the development of Alzheimer’s in people.

About the University of California, Irvine: The University of California, Irvine is a top-ranked university dedicated to research, scholarship and community service. Founded in 1965, UCI is among the fastest-growing University of California campuses, with more than 24,000 undergraduate and graduate students and about 1,400 faculty members. The second-largest employer in dynamic Orange County, UCI contributes an annual economic impact of $3.3 billion. For more UCI news, visit www.today.uci.edu.

Putting Ginkgo to the Test

We don't know yet whether ginkgo biloba prevents or treats Alzheimer's disease. Why not?

In the premiere issue of Memory Loss & the Brain, we took a critical look at research on the alleged memory-enhancing effects of ginkgo biloba. Extracts made from the leaves of the ginkgo biloba tree are also under investigation as a treatment for Alzheimer's disease -a debilitating illness marked by impairments in memory, thought, and emotion. But in dozens of published studies, including a major trial in the prestigious Journal of the American Medical Association (JAMA), the evidence doesn't support ginkgo as a treatment for Alzheimer's disease or for boosting memory power in otherwise healthy people.

Artwork © Corbis



Why the big black hole of uncertainty? It all comes down to the quality of the studies conducted so far. By understanding what makes a drug study tick, you can get some insight into what counts as convincing evidence in medical research-and why ginkgo biloba hasn't yet moved from the dietary supplement racks to the prescription pads of U.S. doctors.

What's a good study?

Scientists conduct small pilot studies, involving less than a dozen people, to investigate interesting research questions. If results show that the research is on the right track, the researchers may undertake larger "clinical trials" to evaluate whether a new drug or treatment is safe and effective. At a minimum, these clinical trials must have three features:

1. Steps to minimize bias
These features of the study help to minimize influences on the test results not directly related to the chemical actions of the drug itself:

# Placebo control: In the best clinical trials, subjects are divided into at least two groups. One receives the test drug; the other receives an inactive placebo pill. It's done this way because people tend to report improvement in their symptoms following any kind of treatment-even an inactive compound, such as a sugar pill). The placebo group provides a way to distinguish actual drug effects from the "placebo effect." (In some studies, the group receiving the test drug is compared against one or more groups receiving currently-marketed drugs, instead of or in addition to, comparing against the placebo group.)

# Randomization: This means that researchers assign people in the study to the drug treatment or placebo group at random, decreasing the chance that people will cluster in patterns that may influence the results. For example, assigning the most healthy individuals to the treatment group could make the drug look more effective than it really is.

# Double blinding. This insures that neither the patients nor the researchers know who received the drug until the final results are tallied. Otherwise, the knowledge of who did and didn't get the drug could influence the scientists or the study participants.

2. Careful selection of subjects
In a well-done clinical trial, all the participants are screened carefully for the disease that the drug is supposed to treat. This sounds obvious, but a lot of health problems have similar symptoms. For example, both early Alzheimer's disease and depression can both cause memory impairments.

3. Measuring what matters
In any drug trial, researchers have to choose an appropriate way to measure the effect of the drug. In trials for Alzheimer's drugs, for instance, participants undergo standard tests to determine if the drug reduces memory impairment and other symptoms. The best clinical trials also check for "clinical significance," or whether the treatment made a meaningful difference in patients' lives. If patients taking a new Alzheimer's drug show a small improvement in a laboratory test of memory, this is all well and good. But does this improved test score translate into a decrease in forgetfulness or confusion in everyday life-a meaningful benefit? Typically, a doctor determines this during individual meetings with patients. Information from family members is also included in many studies.

Past imperfect

Not many studies of ginkgo have met these standards. A few years ago, several researchers in Oregon reviewed all the studies they could find of ginkgo biloba as a treatment for dementia, focusing on those studies involving people with Alzheimer's disease (the leading cause of dementia). Out of 50 studies, only four met the minimum standards for a clinical trial of a drug for Alzheimer's.

Together, the four studies included 212 subjects treated with ginkgo and 212 subjects given a placebo. The Oregon researchers concluded that daily treatment with 120 to 240 mg of ginkgo for three to six months brought about a small improvement in test scores, but it did not appear that the change was clinically significant.

There were other problems, too. Past studies of ginkgo and dementia (Alzheimer's and other types) were often conducted by a single scientist, or team of scientists, on patients recruited in one location. These "single-site" studies cannot be trusted as much as those conducted at different locations around the country, explains Lon Schneider, MD, a professor of psychiatry, neurology, and gerontology at the University of Southern California in Los Angeles. Single-site studies "are hugely subject to bias, because at one site the investigator is holding all the cards," Schneider says. "These are never as compelling as multicenter studies." In multi-center trials, any errors or bias contributed by a particular research group has less of an impact.

Another weakness has been the reliance on small groups of research subjects. In the clinical trials to test current Alzheimer's drugs, hundreds of research subjects were involved. When a study involving a dozen or two subjects claims to show that ginkgo helps people with dementia, people like Schneider get suspicious. Was the improvement in one or two people misreported or mismeasured, which then bumped up the average? "You can show improvement with 20 people only when there is an exaggeratedly large and unrealistic effect," he adds. More typically, hundreds of participants are required just to distinguish drug effects from those of the placebo.

The JAMA study: almost but not quite

One recent study of gingko for Alzheimer's avoided some of these pitfalls-the study published in JAMA in 1997. Hundreds of patients with early Alzheimer's took 120 mg of ginkgo per day for a full year, and were tested periodically. The study suggested that ginkgo delayed the progression of the symptoms for up to six months. These widely-publicized findings influenced many people to take ginkgo in hopes of preventing or treating Alzheimer's disease.

But when other researchers took a close look, they found flaws-some fairly serious. For one thing, some of the people in the placebo group did not worsen as much as they should have without treatment. "It was not as it ought to be, and it leaves you wondering if these are truly patients with dementia," observes Paul Solomon, Ph.D., a professor of psychology at Williams College in Massachusetts. Also, the change in mental skills detected by the study was small-about 25 percent of what would be expected in a patient treated with existing Alzheimer's drugs, Solomon says.

Clinical significance

The real kicker was the fact that researchers could not tell the difference between treated subjects and those on placebo. In other words, the study could not prove that the effect of ginkgo on these people was clinically significant. Based on information provided by caregivers and family members, the researchers did document a difference, although it was relatively small: for every seven people treated with ginkgo, caregivers and family members detected improvement in one person on ginkgo.

"The outcome measure that is required in the United States is that observers who are blinded can notice a difference in the patients, and no one could notice any difference," Solomon notes. "If that study was submitted to the FDA to have a drug approved, it would not be acceptable."

The next wave

Despite all the flaws of past studies, the evidence was good enough to launch two new and improved studies of ginkgo for dementia in the United States. In 1999, the National Institutes of Health (NIH) in Bethesda, Maryland, started a $15 million multicenter study to determine if treatment with ginkgo either prevents or delays the onset of Alzheimer's in older people at risk of the disease. The six-year study will involve 2,000 people recruited at four locations around the country.

Another large study of ginkgo for dementia concluded this year. The study is led by Schneider and financed by Dr. Willmar Schwabe Pharmaceuticals, a company based in Germany. Schwabe is also supplying the daily doses of ginkgo 240 mg/day) for the NIH study. The Schwabe trial is a "regulatory quality" study on the level of the trials on which the FDA approved current Alzheimer's drugs, Schneider says. It involved about 500 people with Alzheimer's disease at dozens of different centers who were given 120 or 240 mg of either ginkgo or a placebo and followed for six months. The study concluded earlier this year, and the first results may be announced this summer.

Leaping over the counter

Today, U.S. manufacturers of over-the-counter ginkgo supplements can make general claims that the herb "helps memory" or "improves concentration." The brass ring for a pharmaceutical giant like Schwabe would be to get approval by the FDA to make so-called "health claims," such as "Delays progression of Alzheimer's disease."

The NIH and Schwabe studies may not provide the final word on ginkgo and dementia. Clinical trials are so complex and difficult, it's unusual for a single study, however well-conducted, to settle a medical controversy like the one swirling around ginkgo biloba. Often it takes many years for evidence to pile high enough for experts to reach a consensus. In the meantime, Alzheimer's treatment will continue to rely on what works: skilled and compassionate caregivers and the handful of medications that won a place in physician's formulary by playing by the rules of evidence.

Further Reading:

The Physician's Desk Reference for Nutritional Supplements, by Sheldon Saul Hendler Ph.D., M.D., and David Rorvik. (Montvale, NJ: The Medical Economics Company, Inc., 2001, 700 pp., $59.95). This frank and science-based book reviews the scientific evidence for ginkgo biloba and other herbal remedies.

The US governments Food and Drug Administration (FDA) maintains a website with information on drugs and supplements, as well as information about what claims a specific product may make: http://www.fda.gov.

To learn more about proven therapies for Alzheimer's Disease as well as research on new ones, contact the Alzheimer's Disease Education and Referral (ADEAR) center. It can answer questions about the disease, provide free brochures, and offer referrals to patients and caregivers. Tel: 800-438-4380, or visit the website: http://www.alzheimers.org.

The study by Oregon researchers that reviewed existing gingko studies:

B. Oken and others, "The efficacy of ginkgo biloba on cognitive function in Alzheimer disease," in Archives of Neurology, November 1998, vo. 55, no. 11, pp. 1409-1415.

A few of the many conflicting studies testing the effects of ginkgo on Alzheimer's disease and dementia, including the JAMA article cited in the text:

"A placebo-controlled, double-blind, randomized trial of an extract of ginkgo biloba for dementia," by the North American EGb Study Group, in Journal of the American Medical Association, October 1997, vol. 278, no. 16, pp. 1327-1332.

"The efficacy of ginkgo for elderly people with dementia and age-associated memory impairment: new results of a randomized clinical trial," by M. van Dongen and others, in Journal of the American Geriatric Society, October 2000, vol. 48, no. 10, pp. 1183-1194.

"A 26-week analysis of a double-blind, placebo-controlled trial of the ginkgo biloba extract EGb 761 in dementia," by P. Le Bars and others, in Dementia and Geriatric Cognitive Disorders, July-August 2000, vol. 11, no. 4, pp. 230-237.

Antioxidants decrease disease in an insect model of Alzheimer’s disease

Alzheimer’s disease (AD) is one of a number of neurodegenerative disorders in which brain cells damaged by naturally occurring chemicals known as reactive oxygen species (ROS) have been observed. However, whether this oxidative damage causes neurodegeneration or is a consequence of it has not been previously determined. A study appearing online on December 14, in advance of publication in the January print issue of the Journal of Clinical Investigation, indicates that oxidative damage is a factor contributing to neurodegeneration in a Drosophila model of neurodegenerative disorders such as AD.

Mel Feany and colleagues from Brigham and Women’s Hospital and Harvard Medical School assessed neuron cell death in Drosophila expressing a neurodegenerative disease–associated form of the human protein tau. The number of dying neurons was increased if these insects were also genetically modified to have high levels of ROS. By contrast, if the insects were treated with the antioxidant vitamin E they had decreased numbers of dying neurons. This demonstration that oxidative stress contributes to neurodegeneration in this model of AD suggests that targeting antioxidant pathways might provide a new approach for treating individuals with AD and other related neurodegenerative disorders.

Source: Journal of Clinical Investigation

Ronald Reagan's Alzheimer's Letter

My fellow Americans, I have recently been told that I am one of the millions of Americans who will be afflicted with Alzheimer's disease.

Upon learning this news, Nancy and I had to decide whether as private citizens we would keep this a private matter or whether we would make this news known in a public way.

In the past, Nancy suffered from breast cancer and I had cancer surgeries. We found through our open disclosures we were able to raise public awareness. We were happy that as a result many more people underwent testing. They were treated in early stages and able to return to normal, healthy lives.

So now we feel it is important to share it with you. In opening our hearts, we hope this might promote greater awareness of this condition. Perhaps it will encourage a clear understanding of the individuals and families who are affected by it.

At the moment, I feel just fine. I intend to live the remainder of the years God gives me on this earth doing the things I have always done. I will continue to share life's journey with my beloved Nancy and my family. I plan to enjoy the great outdoors and stay in touch with my friends and supporters.

Unfortunately, as Alzheimer's disease progresses, the family often bears a heavy burden. I only wish there was some way I could spare Nancy from this painful experience. When the time comes, I am confident that with your help she will face it with faith and courage.

In closing, let me thank you, the American people, for giving me the great honor of allowing me to serve as your president. When the Lord calls me home, whenever that may be, I will leave the greatest love for this country of ours and eternal optimism for its future.

I now begin the journey that will lead me into the sunset of my life. I know that for America there will always be a bright dawn ahead.

Thank you, my friends.

Sincerely,

Ronald Reagan

Accelerated Disease of the Aged in Alzheimers

Due to economical, social, healthcare, education, and other factors the diseases in our older generation are accelerating. Older people may lack education that helps them to spot signs at early stages, which can help geriatrists find cures to various diseases. In addition, as one grows older they tend to avoid socialization. The lack of socialism has caused acceleration of disease. Healthcare is deficient, which has also caused major problems for the older generation, as well as the younger societians.

With so many continuing problems experts of specialize in healthcare for senior citizens is finding solutions, yet these answers is not enough to stop the acceleration of diseases.

alzheimers is a form of dementias, which can escalate to progeroid syndrome. The condition will cause aging signs to increase dramatically, which shortens the expectancy of life. We see this type of disease in our younger generation as well. Children who bald early, or have hunches in the back has encountered accelerated aging conditions.

The condition moves to form Hutchinson - Gilford syndrome, or progeria. Werners syndrome may also develop early. In addition, various other diseases may follow, including Down syndrome. This is where alzheimers come in, since it is a general condition known as the sister of progeroid syndrome. Downs starts the aging process to accelerate swiftly. The condition affects glucose, which is the sugar source of energy that promotes proteins, fats, and carbohydrates. Blood vessels are affected as well, which starts another disease that leads to intolerance. Gradually the disease begins affecting the entire body, which can develop into cancer. In addition, the disease can escalate to degenerative bone illnesses. Once the bones are hit, thus the body diminishes rapidly. As well, Down syndrome can cause hair loss, which is another symptom of acceleration of aging. Moreover, the disease can cause death prematurely. Down syndrome is damning, since it will target CNS (Central Nervous System), which leads to retardation. The brain starts to deteriorate, which causes alzheimers disease to develop, as well as dementia.

How to fight back

To ward off these diseases early detections must be considered. Most diseases will send signals at the early stages to warn you. If you notice any symptoms emerging, seek medical treatment immediately. Even if the condition is minor, the doctor can move to action to prevent further problems.

The best thing we have in life is the ability to communicate. Use the gift we have, and speak with your physician regularly. Staying informed is another gift, which we have a wide array of information to help us learn. Learning is a beautiful gift and condition that we use to grow healthy. Use it to your advantage.

Statistics has not only shown, but has also proven that those who effectively communicate with their healthcare experts, discussing their condition with the professional medical experts, thus statistics have shown that these people live longer and healthier. Effectively communication however is not only speaking, but it is also the act of joining in the actions to better your health. This moves us back to learning.

When you are informed, you have knowledge that drives you to a well-versed solution. The strategies to take to prevent the diseases include, talking, taking action, partaking, listening, learning (specifically about your condition and overall health), visit your physician at regular intervals, and taking steps with your doctor to prevent disease.

Studies has shown that elders with alzheimers disease also has sister diseases, which counteract the other. To avoid such complications one must consider primary healthcare, and know when to contact the doctor when symptoms emerge. Record keeping can help you continue to monitor your health, which is an outstanding method to reduce disease.