Clear Your Brain of the Toxic Gunk that Causes Alzheimer’s Disease!

Many of us have heard friends complain—in jest—that they think they’re getting Alzheimer’s disease. Or maybe you’ve made that comment yourself after forgetting an appointment or locking your keys in the car. But it’s nothing to joke about, and actually, unless you’re a caregiver and/or have someone close to you with the disease, most people have no idea that Alzheimer’s disease entails a lot more than forgetfulness. Alzheimer’s disease literally kills the brain, wiping out the ability to use language, add a simple column of numbers, read the newspaper, control thoughts, and eventually recognize close friends and family.

Initially, the only symptom of Alzheimer’s may be mild forgetfulness, like forgetting what you went into a room for, what you ate for lunch, or where you put your hat. In later stages, behavioral and personality changes such as aggressive acts or aimless wandering may accompany the cognitive decline. Eventually, patients are bedridden and require total care.

Whether you know someone with Alzheimer’s or not, please keep on reading this report . . . because:

1) We want to tell you about nine nutraceuticals that have been shown to clear amyloid—the toxic gunk that causes Alzheimer’s—out of your brain.

2) These herbs and nutrients can help prevent Alzheimer’s disease from grabbing hold of your brain.

3) These nutraceuticals produce a cognitive-enhancing effect that can support your memory NOW.

4) Sooner or later, you will know someone with Alzheimer’s disease.

5) 14 million Baby Boomers are predicted to succumb to this disease in the
next decade.

After years of research, most scientists now believe that amyloid plaques and neurofibrillary tangles—within the brain—are the hallmarks of Alzheimer’s disease, and that they contribute to the degradation of the neurons in the brain and the subsequent symptoms of the disease.

What is amyloid protein?

Amyloid is a microscopic protein fragment of a larger protein called amyloid precursor or protein (APP) that is normally found throughout the body. In Alzheimer’s disease, this protein is processed improperly,
creating a substance called beta-amyloid, which is toxic to brain cells. In a healthy brain, these protein fragments would be broken down and eliminated. But in Alzheimer’s disease the fragments accumulate to form insoluble plaques.

What are neurofibrillary tangles?

These bundles of twisted filaments are the other structural indicator of Alzheimer’s disease. Neurofibrillary tangles are made up of tau protein. In healthy neurons, tau forms part of a structure called a microtubule, which helps transport nutrients and other important substances from one part of the nerve cell to another. In Alzheimer’s disease, however, the tau protein is abnormal and the microtubule structures collapse, which leads to the death of brain cells.

How do you know it’s Alzheimer’s?*
*Alzheimer’s disease is more than forgetting where you put the car keys, or walking into a room and wondering what you went in there for.

Here’s a guideline to help you access your concerns.
Does the person you are concerned about:

  1. Repeat things or ask the same questions over and over?
  2. Seem more forgetful, or have trouble with short term memory?
  3. Need reminders to do things like chores, grocery shop, eat, take
  4. nutritional supplements, etc.?
  5. Forget appointments, family occasions, or holidays?
  6. Feel “blue,” or cry more often than in the past?
  7. Have trouble doing calculations, managing finances, or balancing the checkbook?
  8. Show a loss of interest in activities such as hobbies, reading, attending religious services, or other social activities?
  9. Need help preparing a meal, dressing, bathing, or using the bathroom?
  10. Become irritable, agitated, suspicious, or hear or believe things that are not real?
  11. Get lost while driving or drive unsafely?
  12. Have trouble finding the right words, finishing sentences, or naming people or things?

*Adapted from Mundt JC, Freed DM, Griest JH. Lay person-based screening for early detection of Alzheimer’s disease: development and validation of an instrument. J Gerontol Psychol Sci Sco. 2000, 55B: 163-170.


Rosemary is one of the top ten herbs in your spice rack that does a
lot more than flavor your chicken and roasted potatoes. It may actually help protect you from getting Alzheimer’s disease, cancer, and
heart disease.

Aside from cooking, rosemary has a long folk use as a brain stimulant, a remedy for heart trouble, an antiseptic, an insect repellent, and a food preservative.

In ancient Greece, students wore sprigs of rosemary in their hair to fortify the brain and refresh the memory. It was burned regularly in French hospital wards until the twentieth century to purify the air and prevent the spread of infection. Now, research studies are showing that rosemary contains more than two dozen antioxidants that may prevent some of the most dreaded diseases of the 20th century. Several new studies have indicated that rosmarinic acid—an antioxidant found in rosemary—that is also antiviral, antibacterial, and anti-inflammatory, protects brain cells from beta-amyloid toxicity.15

A recent study at the University of Naples, Italy, demonstrated the neuroprotective effect of rosmarinic acid on the brain cells of laboratory animals that were exposed to the toxic effects of beta-amyloid protein. Previous evidence suggests that oxidative damage caused by highly reactive oxygen molecules in the body plays a role in Alzheimer’s. And in this study, rosmarinic acid was found to reduce reactive oxygen species (ROS) formation, in addition to lipid peroxidation, DNA damage, and tau phosphorylation—all factors involved in Alzheimer’s disease. The researchers concluded that the extract might be effective in patients suffering from mild to moderate Alzheimer’s disease.

In addition to preventing the toxicity of beta-amyloid to brain cells, rosmarinic acid has also been found to both inhibit the formation of beta-amyloid AND destabilize and dissolve beta-amyloid fibrils that have already formed. These results were so impressive that the researchers concluded that rosmarinic acid “could be a key molecule for the development of therapeutics for Alzheimer’s disease.”15
Another recent study also showed that rosmarinic acid exerts a calming effect on the mind while supporting short and long term memory.16

This is an added bonus for anybody.

According to James Duke, Ph.D., renowned authority on healing herbs and author of The Green Pharmacy, in addition to its ability to alleviate the damaging effect that beta-amyloid protein has on brain cells, rosemary extract also helps prevent the breakdown of acetylcholine. So if you want a good memory, remember to take your rosemary!

The pending epidemic

If you don’t know someone suffering from Alzheimer’s consider yourself lucky. Very lucky . . . because according to a 1992 Gallup poll commissioned by the Alzheimer’s Association, one in 10 Americans said they had a family member with Alzheimer’s disease, and one in three knew someone with the disease. In fact, four million families are affected by the disease,2 and the numbers keep rising.

According to a statement made in 2003 by Sheldon Goldberg, past president of the Alzheimer’s Association, “We have 10 years at most to prevent a disaster. If we miss that chance, Alzheimer’s will bankrupt family, state, and federal budgets as up to 14 million Baby Boomers succumb to the disease.”

But it’s not all doom and gloom. Luckily there is something you can do NOW to prevent this crippling disease from taking hold of your brain . . . and to help those who already have the disease.

What happens to the brain of a person with Alzheimer’s?

The brain is made up of 100 billion neurons. In the Alzheimer’s brain, neurofibrillary tangles and amyloid plaques disable the cell’s ability to communicate. These plaques contain beta-amyloid, a protein that releases free radicals, or highly reactive molecules that can cause damage to cells through a process called oxidation. These free radicals are believed to lower levels of acetylcholine (a brain chemical that helps transmit impulses in the nervous system) and damage brain tissue, bringing on the symptoms of Alzheimer’s disease.

This insidious neurodegenerative disorder starts with the accumulation of beta-amyloid deposits, triggering inflammation,35 and then goes on to include:

  • cognitive decline,
  • a pronounced “shrinking” of the brain (In normal aging, the brain will suffer only slight atrophy.),
  • loss of nerve cells that are vital to
  • memory and other mental abilities,
  • reduced amounts of neurotransmitter chemicals (especially acetylcholine)
  • that serve a key function in relaying messages among billions of nerve cells in the brain, and
  • neurofibrillary tangles—bundles of twisted filaments which prevent neurons from sending and receiving messages.

Acetylcholine—your brain’s messenger molecule

This messenger molecule is the most abundant and essential neurotransmitter in the brain that is responsible for numerous functions, including many related to cognition and memory. Acetylcholine is released into the synapse, or space between two nerve cells, where it stimulates the transfer of nerve impulses from one nerve cell to another. After the nerve impulse is transmitted, acetylcholinesterase—an enzyme that is found in nerve endings—breaks down acetylcholine into choline and acetate, and the nerve signal ends.

Loss of acetylcholine function is a primary feature of several types of brain dysfunction, including Alzheimer’s disease. In Alzheimer’s disease and senile dementia, acetylcholine is destroyed too quickly, and consequently the nerve impulse is either too weak to be received or it is incompletely transmitted between nerve cells. A shortage of acetylcholine is considered the most common cause of memory loss, decreased learning ability, and intelligence. Eventually, the greatest amount of damage in the Alzheimer’s brain is in the cells using acetylcholine.4

A growing body of evidence suggests that there are a number of therapeutic nutraceuticals that are showing great promise in:

  • reducing and removing beta-amyloid deposits in the brain,
  • helping support the regeneration of brain neural networks,
  • repairing damage that has already occurred,
  • providing potent antioxidant protection and mind-boosting capabilities, and
  • improving mental functions in people with Alzheimer’s disease.

Alzheimer’s disease is increasing so fast that more than 22 million people worldwide will be affected by 2025, experts have warned.


Scientists believe that aging and many diseases, including arthritis, cancer, Alzheimer’s, and atherosclerosis are the result of oxidative stress and the accumulation of free radicals. Ginkgo biloba extract’s antioxidant properties neutralize the free radicals that can damage proteins within the cell, enzymes, or the fragile lipid membranes that surround and protect the cell.

Brain cells are composed mainly of fat, which is particularly vulnerable to free radical damage. Individuals who sustain free radical damage over a long period of time may experience deterioration in their mental capacity. Ginkgo has been proven to protect the delicate brain cells from this devastating damage, and to improve blood flow to the brain, which is also important for healthy cognitive function.

Since numerous studies have shown that ginkgo biloba extract has a beneficial effect on Alzheimer’s disease, its effect on the exposure of brain cells to beta-amyloid protein has also been investigated, and the results are very promising. A study published in the May 2004 issue of the Journal of Neuroinflammation reported that brain cells pre-treated with ginkgo extract and then exposed to beta-amyloid protein were resistant to the toxic effects of beta-amyloid and survived without damage.17

A study at Georgetown University Medical Center, Washington, D.C., found that nerve cells exposed to beta-amyloid displayed free radical production, and cellular death. On the other hand, after they had been pre-treated with ginkgo biloba extract, free radical production, and cellular damage and death were all inhibited.18

Likewise, a study at the University of Southern Mississippi found that brain cells treated with ginkgo biloba extract were resistant to the damaging effects of beta-amyloid.19


Also called panax ginseng, red ginseng is an adaptogen—an herb used to help individuals cope with physical and emotional stress—and is the most commonly used Asian ginseng. Thousands of studies have demonstrated that ginseng supports a myriad of health concerns ranging from maintaining normal glucose levels to stimulating immune function. Red ginseng extract has also been found to benefit cognitive function. Two ginseng phytochemicals in particular—ginsenosides Rb1 and Rg1—have demonstrated the ability to improve memory in Alzheimer’s disease-model mice, both in vivo and in vitro.20

Recent Japanese studies even showed that in addition to improving memory, the ginseng extracts were able to regenerate brain axons and synapses in laboratory animals. This is highly significant because these brain cells are typically destroyed by Alzheimer’s.2324

An exciting new study performed at the College of Pharmacy, Chung-Ang University, Seoul, Korea, found that red ginseng extract was able to reduce the inflammation of in vitro brain cells exposed to beta-amyloid protein. In a normal brain, cells called microglia are phagocytic, or capable of engulfing foreign and toxic particles—like beta-amyloid—that cause inflammation. In this study, the ginseng extract promoted the microglial phagocytosis of the beta-amyloid, leading the researchers to believe that it has therapeutic potential in the treatment of Alzheimer’s.2526

A study at the China Academy of Traditional Chinese Medicine, Beijing, focused on the effects of a combination of ginseng and ginkgo extracts on the brain neurotransmitter acetylcholine in laboratory animals, whose brains had been injected with beta-amyloid. Therapeutic strategies in Alzheimer’s disease are largely aimed at increasing available acetylcholine.

In this study, the animals were given the ginseng and ginkgo extracts every day for a month, and in the end, the extracts significantly increased the amount of acetylcholine in the animals’ brains, allowing for good cognitive function.27

Frequently asked questions

Q. What’s the difference between Alzheimer’s and dementia?

Every case of dementia is caused by a disease, and although Alzheimer’s is one of those diseases, it is the most common form of dementia. Other forms of dementia result from stroke; various infections and diseases, including Parkinson’s disease; head injuries; drugs; nutritional deficiencies, and age associated mental decline.

Q. Is there any way to determine if you have amyloid plaque building up in your brain?

Researchers suspect that abnormally high levels of beta-amyloid begin accumulating in the brains of Alzheimer’s patients long before symptoms appear. So far, there hasn’t been a reliable test, but in a study at the University of Pennsylvania, scientists developed a new compound designed to cross the blood-brain barrier, which attaches to amyloid deposits and then sends out harmless radioactive signals that can be detected with a PET scan—brain-imaging technology known as positron-emission tomography. The study found preliminary evidence that the new compound or “tracer” may also be effective at allowing the researchers to use PET scans to discriminate between amyloid levels one would expect to see in Alzheimer’s disease versus non-Alzheimer’s disease patients. Most likely, a test for determining actual amyloid plaque build-up will be available in the next decade, and will be prohibitively costly for people without medical insurance.49

Q. Does amyloid plaque appear in any diseases other than Alzheimer’s?

A relationship between Down Syndrome and Alzheimer’s disease has been discussed for many years. Almost all persons with Down Syndrome show evidence of Alzheimer’s disease-like brain plaques after age 35. 50

Q. Is amyloid plaque similar to the plaque that clogs arteries?

Well, they are both sticky and cause inflammation (or are caused by inflammation—a situation similar to “what came first, the chicken or the egg?”). But arterial plaque doesn’t kill cells the way amyloid plaque kills brain cells. There is, however, a correlation between high cholesterol and amyloid plaque. Brain cells make their own cholesterol, and excess cholesterol in brain cells boosts the conversion of amyloid precursor protein to both alpha- and beta-amyloid protein. Alpha- and beta-amyloid are very similar, but beta-amyloid forms the toxic plaques that kill brain cells and alpha-amyloid does not. Excess cholesterol in the brain may shift the balance from alpha- to beta-amyloid. The result is relatively more beta-amyloid than alpha, and thus more plaques.51

Q. Who is at risk for Alzheimer’s?

There are a number of risk factors:

  • Increasing age and family history of dementia are the most consistent risk factors for Alzheimer’s disease. By age 80, people with Alzheimer’s disease in both parents had a 54% risk, 1.5 times the risk of Alzheimer’s in people with just one affected parent, and five times the risk of people with two unaffected parents. A parent or a sibling with Alzheimer’s disease doubles the risk for developing Alzheimer’s disease.
  • Mild cognitive impairment is a strong early predictor of Alzheimer’s disease. According to a new study in Neurology, diabetes may also impair the function of the brain and hasten the process of senile dementia. Researchers found that diabetes nearly doubles the risk of developing both vascular dementia and Alzheimer’s disease, according to the Rotterdam Study, a large prospective analysis that tracked dysglycemia and dementia in more than 6,000 individuals over age 55. Diagnosis of diabetes was based on World Health Organization criteria using a glucose tolerance test.52

A related editorial referred to Alzheimer’s as a possible “brain-type diabetes.” Besides damaging important blood vessel networks and increasing the risk of small “silent” strokes deep inside the brain, dysglycemia may be directly involved in the development of the neurofibrillary tangles, the clumping of nerves and fiber tissue inside the brain characteristic of Alzheimer’s.

Diabetes also disrupts insulin signaling to other cells in the body. This altered signaling may increase the activity of a neuronal enzyme that stimulates tau proteins to build up, a key trigger mechanism cited as one of the earliest signs of Alzheimer’s.

A serious head injury is also a strong risk factor for the disease. Inflammation in the brain can lead to the death of cells, which contributes to the disease.

There are several genetic factors that specifically link to Alzheimer’s disease:

  1. Mutations at specific genetic loci on chromosomes.891012
  2. E4 allele of apolipoprotein E gene. (This roughly triples the risk of Alzheimer’s disease, and the risk is greater for women than for men.)
  3. Family history of trisomy 21. (Early onset of Alzheimer’s prior to age 60 occurs in only about 5% of cases and is due to inherited mutations that are autosomal-dominant and occur at specific genetic loci on chromosomes.11)
  4. The important thing to remember is that no one is immune from getting Alzheimer’s disease, and even if you have a family history or other predisposition for getting the disease, it doesn’t mean you will.


Turmeric does a lot more than add flavor and color to mustards and curries. It is a member of the ginger family and contains a class of polyphenolic compounds called curcuminoids. Research on these compounds has focused primarily on the one for which the group is named—curcumin. Used extensively in Indian cooking, turmeric is valued in ancient Indian Ayurvedic medicine because it has antioxidant, anti-inflammatory, anti-carcinogenic, anti-hepatotoxic, and antimicrobial effects.

This may help to explain why the incidence of Alzheimer’s disease is much lower in India than in the West.

In fact, according to an on-line BBC article called “Curry May Slow Alzheimer’s” (Nov. 21, 2001),32 previous studies have found that Alzheimer’s affects just 1% of people over the age of 65 living in some Indian villages.

Curcumin got a lot of press coverage a couple of years ago when researchers at the University of California at Los Angeles announced that it reduced Alzheimer’s-like brain changes in mice that were injected with beta-amyloid to create conditions like those that exist in patients with the disease. They found that curcumin helped to clear amyloid from the brain and that its relative lack of side effects and combined anti-inflammatory and antioxidant properties could be beneficial to Alzheimer’s patients.

In the study, scientists raised two groups of mice; one that was fed a diet high in curcumin and the other a regular diet. When fed to aged mice with advanced plaque deposits similar to Alzheimer’s disease, the curcumin reduced the amount of plaque. When the curcumin was given to the mice with the Alzheimer’s-like condition, it attached to the plaques, hampering further development of plaque and, again, reduced plaque levels.

Not only was there less evidence of plaque buildup in the curcumin-fed rats, they also outperformed rats on normal diets when carrying out maze-based memory tests. Curcumin also appeared to reduce Alzheimer’s-related inflammation in the brain tissue.

Also, in other experiments, the researchers showed that curcumin reduced plaque better than the over-the-counter painkillers naproxen and ibuprofen. Some studies have shown that people taking these common anti-inflammatories have a decreased risk of developing Alzheimer’s disease.33

“The prospect of finding a safe and effective new approach to both prevention and treatment of Alzheimer’s disease is tremendously exciting,” Gregory Cole, M.D., a professor of medicine and neurology at the David Geffen School of Medicine at UCLA, said in a news release after the study was released.34


Ashwagandha, also known as Withania somnifera, holds a place in Ayurvedic pharmacology similar to ginseng in Chinese medicine. It is a superb rejuvenative herb and powerful adaptogen. It also helps increase
energy, endurance, and libido while strengthening the immune system. In addition to its anti-inflammatory, anti-stress, and rejuvenating properties, researchers have recently discovered that ashwagandha is also a potent antioxidant with mind-boosting properties.

Ashwagandha contains flavonoids and many active ingredients of the withanolide class. Withanolides are believed to account for the multiple medicinal applications of ashwagandha. Ashwagandha is used in India to treat mental deficits in geriatric patients, including amnesia. Researchers from the University of Leipzig in Germany wanted to find out which neurotransmitters were influenced by ashwagandha. After injecting withanolides into laboratory animals, they examined slices of the animals’ brains and found an increase in acetylcholine receptor activity.

According to the researchers, this helps explain the cognition-enhancing and memory-improving effects of extracts from ashwagandha observed in animals and humans.44

Supports Normal Brain Function
Several years ago, two Japanese studies found that ashwagandha stimulates the growth of axons and dendrites in human neuroblastoma cells, and in rat neurons.45 This is significant because the extension of dendrites and axons—which bring information to and from the brain—may compensate for and repair damaged neuronal circuits in the aging brain.48

In two very recent studies at the Institute of Natural Medicine, Toyama Medical and Pharmaceutical University, Sugitani, Japan, the same Japanese researchers found an improvement in the memory of laboratory animals that had been injected with beta-amyloid. The ashwagandha also prevented a loss of axons, dendrites and synapses—all vital to normal brain function.45

Even more remarkable, in another study, animals whose brains had been severely damaged by beta-amyloid injections, the oral administration of withanolide-A derived from ashwagandha regenerated almost completely the damaged brain connections. In fact, the author’s concluded that, “Withanolide-A is therefore an important candidate for the therapeutic treatment of neurodegenerative diseases, as it is able to reconstruct neuronal networks.”
Thus, the active components of ashwagandha may actually be able to reverse damage caused beta-amyloid and regenerate vital neural connections.47

Q. I’ve heard that people with fewer years of formal education are at higher risk for getting Alzheimer’s. Am I less likely to get it because I have an advanced degree?

According to Rosebud Roberts, M.B.Ch.B., a Mayo Clinic epidemiologist, and lead investigator in a study correlating age and lack of education with the risk of developing Alzheimer’s disease, “People with more years of education may experience a loss of cognitive ability, but they can compensate better and thus they don’t demonstrate the symptoms of mild cognitive impairment. It’s as though their education protects them from exhibiting the effects of mild cognitive impairment.”

In the study, the prevalence of mild cognitive impairment also varied according to years of education, ranging from:

  • 25 percent in those with up to eight years of education,
  • 14 percent in those with nine to 12 years,
  • 9 percent in those with 13 to 16 years, and
  • 8.5 percent in those with greater than 16 years.53


Huperzine, an alkaloid extracted from a Chinese moss, Huperzia serrata, has a long history of use in traditional chinese medicine. It is showing great promise as a therapeutic treatment for Alzheimer’s disease and other memory loss disorders, and has been approved as a drug in China to treat Alzheimer’s disease and other age-associated memory impairments. In fact, clinical trials in China have demonstrated that huperzine significantly relieves memory deficits in the elderly due to Alzheimer’s disease and vascular dementia, without the side effects that usually accompany pharmaceutical acetylcholinesterase inhibitors.

Both animal studies and clinical trials indicate that huperzine possesses the ability to protect cells against hydrogen peroxide, beta-amyloid protein, glutamate, ischemia (inadequate blood flow to the brain), and cellular death.30

Huperzine protects against free radicals

In addition to its anticholinesterase effects, huperzine was found to protect against free radical induced cell toxicity in lab tests.13
This is significant because many modern diseases are believed to be the result of free radical damage.

Reverses effects of amnesia

Scopolamine is a class of amnesiac drugs with choline blocking ability that causes amnesia and memory loss. A study performed on young and old monkeys given the drug showed that huperzine reversed the deficits in performance and memory that result from scopolamine, suggesting that huperzine may benefit cognitive impairments in patients with Alzheimer’s disease and other memory disorders.14

Adolescent students also benefit from Huperzine

In a study to determine the effects of huperzine on memory and learning in adolescents, Chinese researchers selected 34 matched pairs of normal middle school students whose only complaints were of poor memory and difficulty in learning.

In a double-blind trial, one member of each pair was given 100 mcg of huperzine twice daily for four weeks, while the other member received the placebo. The students’ memory quotients were measured before and after the trial, and their academic performance in their Chinese, English, and mathematics lessons was also monitored.

At the end of the study, the huperzine group scored significantly higher than the control group on standard memory tests. They also did significantly better in their Chinese and English lessons, but not in math. No side effects of any kind were noted.35

Protects cells from toxic effects of beta-amyloid

In a recent study at the Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, animal brain cells that were pre-treated with huperzine for just two hours before being exposed to a solution containing beta-amyloid showed less cellular stress than the untreated cells.

This study was particularly important because it discovered new evidence of just how toxic beta-amyloid is to brain cells. After exposure to beta-amyloid for various periods of time, the cells exhibited a rapid decline of ATP (adenosine triphosphate)—the major energy currency of cells. As a result, mitochondrial membrane homeostasis and integrity were disrupted, so the cells weren’t able to transport proteins, their energy metabolism was greatly decreased, and they suffered severe oxidative stress and death. The huperzine, however, protected the cells from the toxic effects of beta-amyloid.31

Huperzine also inhibits the activity of acetylcholinesterase, so the breakdown of acetylcholine is slowed and the strength and duration of the nerve impulse is improved. Fortunately, based on scientific studies in both human and animal models, we now know that huperzine makes more acetylcholine available for better brain functioning,
and that it is a promising supplement for reversing and/or slowing down Alzheimer’s disease and other brain disorders.


Ferulic acid is a phytochemical with anti-inflammatory and antioxidant properties that is found in foods such as brown rice, wheat, oats, coffee, apples, artichokes, peanuts, oranges, and pineapple. Ferulic acid has a chemical structure that is very similar to that of curcumin.

A number of in vitro studies done in the past few years in Japan,37 Korea,41 and the United States,40 all found that it protects neuronal cells from the damaging effects of beta-amyloid.

Two other studies also showed that pre-treatment with ferulic acid protected laboratory animals that had been injected with beta-amyloid from learning and memory deficits. In a study at the Institute of Natural Medicine, Hallym University, Chunchon, South Korea, mice were allowed free access to drinking water containing ferulic acid for four weeks, before being injected with beta-amyloid. The control mice, which were injected with the beta-amyloid but did not have access to ferulic acid, exhibited impaired performance on memory and behavior tests, whereas, the mice treated with ferulic acid were protected from the decrease in performance skills.

The scientists concluded that these results demonstrate that long-term administration of ferulic acid induces resistance to beta-amyloid toxicity in the brain, and suggest that it may be a useful preventive against Alzheimer’s disease.4142

Myricetin is a flavonoid that is commonly found in foods such as berries, vegetables, teas, wine, and herbs. Research has shown that myricetin has antioxidant and anti-inflammatory properties, and now, although the exact mechanism is unclear, scientists at the Kanazawa University School of Medical Science in Japan have found that myricetin also has the ability to inhibit the accumulation of beta-amyloid protein.37

Additionally, these researchers also found that like rosmarinic acid and curcumin, myricetin was extremely effective in not only preventing the build up of beta-amyloid deposits in the brain, but that it could also dissolve beta-amyloid deposits that had previously formed.

This type of therapeutic strategy is of great interest to researchers trying to develop a means of not only preventing the formation of amyloid plaques, but also removing preformed amyloid deposits.

Vinpocetine, derived from the periwinkle plant Vinca minor, is also showing a number of neuroprotective properties that may help in the treatment of Alzheimer’s and other neurodegenerative disorders in which oxidative stress is involved. It is an antioxidant and vasodilator, increasing blood flow to the brain,28 and researchers from the University of Coimbra in Portugal found that it helps prevent oxidative stress in cells treated with beta-amyloid.29


No one understands exactly why we are experiencing an epidemic of Alzheimer’s disease, other than the fact that people are living longer. What we do know is this: In less than 10 years, about 14 million Baby Boomers will be affected by the disease, with annual costs of up to 700 billion dollars.

Don’t wait until it’s too late for you and your family. Act now by protecting yourself with amyloid-busting nutraceuticals. It takes years, probably even decades, for the amyloid deposits to wreak havoc on the brain. We know from the excellent research being done on these nine nutraceuticals that we can help stop Alzheimer’s in its tracks before extensive damage is done. We also know that these amyloid busters can reverse some of the damage that has already been done.

So, play it safe. Protect your brain NOW, so you can appreciate life to its fullest later.


  1. Adapted from a fact sheet published by the Alzheimer’s Association, Experimental Alzheimer drugs targeting beta-amyloid and the “amyloid hypothesis.” ©2005 Alzheimer’s Association. All rights reserved. This is an official publication of the Alzheimer’s Association but may be distributed by unaffiliated organizations and individuals. Such distribution does not constitute an endorsement of these parties or their activities by the Alzheimer’s Association.
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  6. Adapted from a fact sheet published by the Alzheimer’s Association, Experimental Alzheimer drugs targeting beta-amyloid and the “amyloid hypothesis.” ©2005 Alzheimer’s Association. All rights reserved. This is an official publication of the Alzheimer’s Association but may be distributed by unaffiliated organizations and individuals. Such distribution does not constitute an endorsement of these parties or their activities by the Alzheimer’s Association.
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  15. Iuvone T, De Filippis D, Esposito G, D’Amico A, Izzo AA. The spice sage and its active ingredient rosmarinic acid protect PC12 cells from amyloid-{beta} peptide-induced neurotoxicity. J Pharmacol Exp Ther. 2006 Feb 22; [Epub ahead of print].
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