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

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

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

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

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

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
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
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

Conclusion

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.

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Editor's Note:

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Visit www.amazon.com – a great way to find competitive deals on supplements offered by many different manufacturers.

Visit www.hfn-usa.com – when commitment to quality and freshness is important, this factory direct solution is preferred by many of our readers.

This article is not intended to diagnose, treat, cure, or prevent any disease. Always consult with a physician before embarking on a dietary supplement program.

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