| | | Amino Acid / Protein | L-Carnitine
 | In 19 male and 14 female subjects (mean ages 73.9 and 76.2 years, respectively) with Alzheimer's disease who were non-responders to acetylcholinesterase inhibitor therapy, subjects were given in addition to their donepezil at 5mg/day or rivastigmine at 3mg, BID, acetyl-L-carnitine at 2gm/day, BID. There was an improvement in responders from 38% with drug therapy alone to 50% with the addition of acetyl-L-carnitine. [Curr Med Res Opin. 2003;19(4): pp.350-353] |
Not recommended:
Glutamine
 | Glutamine accumulation has also been found in Alzheimer’s disease, Huntington’s disease and high levels of brain glutamine have been associated with a worse prognosis in Lou Gehrig’s disease. Likewise, recent studies have shown that high brain glutamine levels increase brain levels of free radicals and impair the ability of brain mitochondria to produce energy. When the brain produces low energy, excitotoxins, such as glutamate, become even more toxic. It has been shown that the reason for glutamine toxicity under these conditions is because it is converted to the excitotoxin - glutamate. Russell L. Blaylock, M.D. |
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Animal-based |
Fish Oil / Krill
 | Scientists have discovered the mechanism by which the omega-3 fatty acids found in fish oils can help protect the brain against the cognitive decline associated with Alzheimer's disease.
Docosahexaenoic acid (DHA), preformed in fish oil, reduces the levels of a protein known to cause damage in the brains of Alzheimer's patients. They also discovered that a derivative of the fatty acid called neuroprotectin D1 (NPD1) is formed in the human brain, and is essential in protecting against brain cell death. [Journal of Clinical Investigation September 8, 2005]
A number of epidemiological studies have shown that eating fatty fish provides a certain degree of protection against Alzheimer's and other dementia diseases - an effect often thought attributable to the omega-3 fatty acids it contains. Some studies also suggest that omega-3 can have a therapeutic effect on some psychiatric conditions.
Researchers at Karolinska Institutet and Uppsala University have now examined whether omega-3 supplementation has any effect on the psychiatric symptoms associated with Alzheimer's disease. Just under 200 patients with mild Alzheimer's were divided into two groups, one of which received omega-3, and one a placebo. The study lasted for one year.
There was no observable difference in therapeutic effect between the patients receiving the omega-3 and the placebo group. However, when the researchers took into account which of the patients carried the susceptibility gene APOE ?4 and which did not, an appreciable difference appeared. Carriers of the gene who had received active treatment responded positively to the omega-3 as regards agitation symptoms, while non-bearers of the gene showed an improvement in depressive symptoms. [International Journal of Geriatric Psychiatry, doi 10.1002/gps.1857 Published online 21 June 2007]
[Scotsman.com News April 6, 2008] Eat your omega-3's if you want to avoid getting Alzheimer's. In part, that's the moral of the story out of new research from Aberdeen University which has found that patients whose diets are high in omega-3 oils do better in mental tests than those who do not have the oils in their diet.
Calling the discovery a "major breakthrough" in the fight against Alzheimer's, the article in The Scotsman explains how the study was conducted using 58,000 Scots who suffer from the condition.
Lead researcher, Lawrence Whalley, professor of mental health at Aberdeen University, said: "Ten years ago this would have been science fiction. What we are touching on here is how nutrients can interact with specific genes in the body."
The red herring (excuse the pun) appears to be a crucial gene some individuals possess called APOE e4 that prevents the omega oils from having a healing or preventive effect. Unfortunately, those individuals must pursue other avenues of treatment.
Whalley said: "What emerges from this research is that if you don't have this gene, omega-3s can make a difference. The next big thing will be to identify what factors can influence how these genes can be switched on and off, and also what to do if you have the gene."
Maureen Thom, information manager for Alzheimer Scotland, said: "It's a very welcome and interesting piece of research, very thorough. I would like to see it developed and have results analyzed for a larger number of people. We do advise that everyone should try to stick to a healthy lifestyle and consume omega-3 oils as part of a healthy diet." |
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Botanical |
Coffee (Coffea genus)
 | Substantial evidence from epidemiological studies and fundamental research in animal models suggests that caffeine may be protective against the cognitive decline seen in dementia and Alzheimer's disease (AD). A special supplement to the Journal of Alzheimer's Disease, "Therapeutic Opportunities for Caffeine in Alzheimer's Disease and Other Neurodegenerative Diseases, 2010" sheds new light on this topic and presents key findings.
"Epidemiological studies first revealed an inverse association between the chronic consumption of caffeine and the incidence of Parkinson's disease," according to Mendonça and Cunha. "This was paralleled by animal studies of Parkinson's disease showing that caffeine prevented motor deficits as well as neurodegeneration "Later a few epidemiological studies showed that the consumption of moderate amounts of caffeine was inversely associated with the cognitive decline associated with aging as well as the incidence of Alzheimer's disease. Again, this was paralleled by animal studies showing that chronic caffeine administration prevented memory deterioration and neurodegeneration in animal models of aging and of Alzheimer's disease." |
Grape Seed Extract / Resveratrol
 | Although unmodified resveratrol appears to have a weak bioavailability, several studies have clearly demonstrated the in vivo neuroprotective properties of the red wine-derived polyphenol, strongly supporting the notion that natural metabolites of resveratrol may have biological activities. Furthermore, recent findings have shed light on the potential role of resveratrol in transcription- and degradation-dependent anti-amyloidogenic mechanisms, suggesting that natural metabolites or potent synthetic analogues of resveratrol have a therapeutic potential in Alzheimer's Disease. |
Chlorella / Algae Products
 | A study showed that among 50 people with Alzheimer’s, aged 70-90, taking 6gm daily of chlorella for 6 months, 68% experienced either a stabilization or improvement in cognitive functions. |
Pomegranate
 | Researchers from Loma Linda University in California (2006) believe that Alzheimer's may be caused by the buildup of plaque from deposits associated with brain cell death due to oxidation, called beta-amyloid deposits. Pomegranate juice, which is high in antioxidant polyphenols, may offer protection against the oxidative stress that causes beta-amyloid deposits.
The researchers studied two groups of transgenic mice that had been genetically engineered to express a protein that eventually leads to Alzheimer's disease. The mice -- aged between six and 12.5 months -- were split into two groups: The first group's diet was supplemented with plain water, and the second group's diet was supplemented with diluted pomegranate juice concentrate. The concentrate was diluted to resemble the strength of commercially sold pomegranate juices.
The researchers then tested the two groups' cognitive function by subjecting the mice to a water maze, which required the animals to swim various distances to find a submerged platform. The group given pomegranate juice negotiated the maze 35 percent faster than the water group, and also swam a more direct path to find the submerged platform compared to the water group.
The researchers then examined the amount of beta-amyloid deposits in the brain cortex of the mice, and found that the group supplemented with pomegranate juice had 50 percent less of the deposits than the non-supplemented mice.
"This study is the first to show beneficial effects (both behavioral and neuropathological) of pomegranate juice in an animal model of (Alzheimer's disease)," wrote lead researcher Richard Hartman. |
Huperzia serrata
Ginkgo Biloba
 | A Ginkgo biloba extract (EGb 761) was tested in Alzheimer's patients for one year at a daily dose of 120mg. Improvement was experienced in patients with primarily visual impairment, delayed worsening occurred in patients with predominant verbal deficits, and there was a stabilization of symptoms in patients with both types of impairment. [Pharmacopsychiatry 2003;36(Suppl 1): pp.S50-5] |
Marijuana
 | "Treatment with a synthetic compound similar to marijuana reduced inflammation in older rats in addition to making the animals "smarter," said Wenk, who is also a professor of neuroscience and molecular virology, immunology and medical genetics.
"The compound substantially improved the memories of the older rats," he said. "These animals were able to hold on to key details of a specific task. Untreated older rats, on the other hand, were not."
The colleagues treated young and old rats with WIN-55212-2 (WIN), a synthetic drug similar to marijuana. While the compound improved memory and helped to control inflammation, it is not a candidate for use in humans because it still contains substances that could trigger a high. [www.medicalnewstoday.com/] |
Cinnamon (Cinnamonum zeylanicum)
 | Michael Ovadia, from Tel Aviv University (Israel), and colleagues isolated CEppt, an extract found in cinnamon bark, and introduced the substance into the drinking water of mice that had been genetically altered to develop an aggressive form of Alzheimer's disease, and fruit flies that had been mutated with a human gene that also stimulated Alzheimer's disease and shortened their lifespan.
After four months, the researchers discovered that development of the disease had slowed remarkably and the animals' activity levels and longevity were comparable to that of their healthy counterparts. The extract inhibited the formation of toxic amyloid polypeptide oligomers and fibrils, which compose deposits of plaque found in the brains of Alzheimer's patients. In a test-tube study, CEppt was also found to break up amyloid fibers, similar to those seen in Alzheimer's patients.
Noting that CEppt caused a "reduction of plaques and improvement in cognitive behavior," the team concludes that: "Our results present a novel prophylactic approach for inhibition of toxic oligomeric A[beta] species formation in [Alzheimer's Disease] through the utilization of a compound that is currently in use in human diet."
A problem remains with the quantity of cinnamon one would need to consume to benefit from its anti-Alzheimer’s properties. “Raw cinnamon also contains substances harmful to the liver,” says Ovadia. “Whereas one may consume six to ten grams per day without damaging the liver, to reap the substance’s medicinal benefits, one would have to consume tens of grams per day at least, which starts to become dangerous. For this reason we developed a means of extracting the active substance from the cinnamon and separating it from the toxic substances.” [Frydman-Marom A, Levin A, Farfara D, Benromano T, Scherzer-Attali R, et al. (2011) Orally Administrated Cinnamon Extract Reduces ß-Amyloid Oligomerization and Corrects Cognitive Impairment in Alzheimer's Disease Animal Models. PLoS ONE 6(1): e16564. doi:10.1371/journal.pone.0016564]
This extract is not currently available for consumer use. |
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Diet |
Increased Fruit/Vegetable Consumption
 | News from the Telegraph U.K. says scientists have found that blueberries can increase your attention span in the short term and can maintain a healthy mind in the long term.
According to the report, they found that just one 200g blueberry smoothie was enough to increase powers of concentration by as much as 20 % over the day, and regular consumption of the fruit could lead to a rewiring of a part of the brain that is linked to memory.
The fruit, which is an anti-oxidant, has already been linked to lower heart disease and cancer rates as well as anti-aging. Antioxidants remove free radicals - chemicals that have the potential to cause damage to cells and tissues in the body.
Dr. Jeremy Spencer, a molecular nutritionist at the University of Reading who carried out the latest study, is quoted as saying he believes its affect on the mind has more to do with its ability to increase the blood flow to the brain, and that flavonoid rich foods, which also include chocolate, spinach and some fruit juices, can re-structure the brain and ward off memory loss associated with Alzheimer's. [reported at the British Science Festival, Sept 2009] |
Artificial Sweetener Avoidance
 | Aspartame use has been reported to trigger symptoms of Alzheimer's disease. |
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Drug |
Conventional Drugs / Information
 | Researchers found that clioquinol can almost stop the progression of Alzheimer’s disease. They believed that by absorbing the copper and zinc atoms that concentrate in the brains of Alzheimer's sufferers, clioquinol could stop the onset of dementia before it starts.
The finding came from a study conducted on 26 Alzheimer’s sufferers; half were given clioquinol while the other 13 were given a placebo. Researchers studied all 26 patients over a nine-month period of time and found that patients given the clioquinol retained more mental capacity than those who received the placebo. Research also showed patients who were given clioquinol had a 1.4 percent decrease in their mental capacity, whereas patients who were given the placebo had an 8.9 percent decrease in their mental capacity.
The study suggests that before dementia sets in in the brains of Alzheimer’s sufferers, clioquinol could prevent zinc from building up on the surface of the brain by absorbing the mineral’s atoms. The results of the study show that clioquinol could treat patients with Alzheimer’s twice as well as the latest Alzheimer’s drugs that are available.
Clioquinol has been around for 100 years and is currently used to treat athlete’s foot, ear infections and indigestion. [Archives of Neurology December, 2003;60(12):pp.1685-91]
In October 2003, the FDA finally approved memantine for the treatment of moderate to severe Alzheimer’s disease. Memantine is marketed in the US by Forest Laboratories under the trade name Namenda.
Memantine is an N-methyl- D-aspartate (NMDA) receptor antagonist that is neuroprotective by blocking glutamate, which can cause overstimulation of the nerves and become toxic to the nervous system. Memantine may benefit individuals with Alzheimer’s disease by improving cognition and overall functioning.
Jan 10, 2008. Newsmax reports that an "extraordinary new scientific study, which for the first time documents marked improvement in Alzheimer's disease within minutes of administration of a therapeutic molecule, has just been published in the Journal of Neuroinflammation."
Known as anti-TNF therapeutics, the drug used in the study is called Etanercept (trade name Enbrel) which is given by an injection into the spine. Improvement was said to have come came within minutes of the injection.
Sue Griffin, Ph.D., director of research at the Donald W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences (UAMS) in Little Rock and at the Geriatric Research and Clinical Center at the VA Hospital in Little Rock, said: "It is unprecedented that we can see cognitive and behavioral improvement in a patient with established dementia within minutes of therapeutic intervention."
To date other patients with mild to severe Alzheimer's have reportedly received the treatment and "all have shown sustained and marked improvement."
July 29, 2008 - For the first time, an experimental drug shows promise for halting the progression of Alzheimer's disease by taking a new approach: breaking up the protein tangles that clog victims' brains. The encouraging results from the drug called Rember, reported at a medical conference in Chicago, electrified a field battered by recent setbacks. The drug was developed by Singapore-based TauRx Therapeutics.
Even if bigger, more rigorous studies show it works, Rember is still several years away from being available, and experts warned against overexuberance. But they were excited. "These are the first very positive results I've seen" for stopping mental decline, said Marcelle Morrison-Bogorad, director of Alzheimer's research at the National Institute on Aging. "It's just fantastic."
The federal agency funded early research into the tangles, which are made of a protein called tau and develop inside nerve cells. For decades, scientists have focused on a different protein - beta-amyloid, which forms sticky clumps outside of the cells - but have yet to get a workable treatment. |
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Habits |
Aerobic Exercise
 | A study (October 2008) coming from Professor Art Kramer, of the US Beckman Institute at the University of Illinois, gives strong evidence that aerobic exercise can actually reverse mental decline.
According to a report in The Telegraph, research suggests that the benefits of regular workouts are seen not only in those undergoing the normal aging process but also in people suffering from Alzheimer's disease.
Indeed, says the report, the findings of one study suggested that people who exercised for just one hour three times a week over three months increased their brain size to that of someone three years younger.
Writing in the British Journal of Sports Medicine, Professor Kramer, who is quoted as saying he believes that around six months of physical activity would be enough to see a marked improvement in brain power, said: "We can safely argue that an active lifestyle with moderate amounts of aerobic activity will likely improve cognitive and brain function, and reverse the neural decay frequently observed in older adults. The effect of aerobic exercise training on cognitive function also seems to extend to older adults with dementia." |
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Mineral |
Lithium (low dose)
 | There are many research findings that strongly suggest that lithium will protect against potential Alzheimer's disease and slow the progression of existing cases. Researchers have reported that lithium inhibits beta-amyloid secretion, and also prevents damage caused by beta-amyloid protein once it's been formed. Beta-amyloid peptide is a signature protein involved in Alzheimer's disease: the more beta-amyloid protein, the worse the Alzheimer's becomes. Overactivation of a brain cell protein called tau protein also contributes to neuronal degeneration in Alzheimer's disease, as does the formation of neurofibrillary tangles Lithium inhibits both of these nerve-cell damaging problems. |
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Nutrient |
Lecithin / Choline / GPC
 | Study participants received 1200mg GPC daily for six months. On a variety of assessment scales for Alzheimer's disease (AD), GPC patients scored more favorably than patients from the control group, all of whom received placebo. The mental status of patients on GPC therapy improved, while those receiving the placebo worsened. These findings are comparable to the results obtained with the use of the prescription drugs Aricept (donepezil HCl) Exelon (rivastigmine tartrate) and Reminyl (galantamine hydrochloride) in the treatment of AD patients, and with fewer side effects. [Mech Ageing Dev 2001 Nov: 122(16): pp.2041-2055] |
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Oxygen / Oxidative Therapies |
Oxygen, Hyperbaric
 | Senile patients, including those with Alzheimer's type, have shown measurable improvement after hyperbaric oxygen treatments. Some doctors claim that patients seem to respond better when chelation and hyperbaric oxygen are used together compared to either one alone. The use of hyperbaric oxygen for this condition is still experimental and needs further study. |
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Vitamins |
Vitamin Niacinamide
 | An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer's disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.
Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer's disease. This is also known as niacinamide and nicotinic acid amide. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer's.
"Nicotinamide has a very robust effect on neurons," said Kim Green, UCI scientist and lead author of the study. "Nicotinamide prevents loss of cognition in mice with Alzheimer's disease, and the beauty of it is we already are moving forward with a clinical trial."
Scientists found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer's tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer's lesion.
Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer's patients.
"Microtubules are like highways inside cells. What we're doing with nicotinamide is making a wider, more stable highway," Green said. "In Alzheimer's disease, this highway breaks down. We are preventing that from happening."
The study appeared online Nov. 5, 2008 in the Journal of Neuroscience. |
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