According to the Alzheimer's Association, Alzheimer's disease (AD) is a progressive, neurodegenerative disease characterized by loss of function and death of nerve cells in several areas of the brain, leading to loss of mental functions such as memory and learning. It causes a person to forget recent events or familiar tasks.
How rapidly AD advances varies from person to person.
This brain disease eventually causes confusion, personality and behavior changes and impaired judgment. Communication becomes difficult as the affected person struggles to find words, finish thoughts or follow directions. Eventually, most people with AD are unable to care for themselves.
It can cause one to forget or refuse to eat and this can result in weight loss or even malnutrition.
AD is also known as organic brain syndrome and it is the most common form of dementia.
This disease was first described by German psychiatrist Dr. Alois Alzheimer in 1907 when he performed an autopsy on a 51 year-old woman who died of a stange disease that caused memory and language impairment. He found abnormal clumps called senile or neuritic plaque (a mix of destroyed nerve cells and a protein called beta-amyloid) and neurofibrillary tangles (where tangles of nerve fibers are formed from abnormal nerve cells and a protein called TAU) throughout the cerebral cortex of her brain.
This illness affects the brain's architecture and in some cases, it can turn fatal.
Apolipoprotein E (ApoE) is a gene that helps transport cholesterol and build healthy membranes for the brain's neurons. One who has inherited a certain type of this gene called ApoE4 is 3 times more likely to develop AD. However the presence of this gene may neither be essential nor sufficient for the development of AD.
A study conducted at the Molecular Neurobiology Laboratory in UMIST, Manchester which was reported in the Lancet revealed that the combination of the herpes simplex virus and ApoE4 is a risk factor for AD. Apparently the virus was causing damage to the genes.
Vitamin E and selenium have been shown to stop the damaging effects brought about by viruses.
References : "Herpes simplex virus type 1 in brain and risk of Alzheimer's disease" Itzhaki RF, et al. Lancet (1997) 349:241-244; "Vitamin E and selenium: contrasting and interacting nutritional determinants of host resistance to parasitic and viral infections" Levander OA, et al. Proc Nutr Soc (1995) 54(2):475-87
A drug vaccine named AN-1792 is being tested to determine its safety and effectiveness in preventing AD.
No one is clear about what actually causes this disease.
A study conducted by the British Institute of Psychiatry found that smoking later in life may lead to mental decline. Researchers found that smokers were 4 times more likely to experience a significant intellectual decline than non-smokers. The test that was used to assess intellectual power was similar to those used to screen for dementia and Alzheimer's disease.
Reference : "Smoking, drinking, and incident cognitive impairment: a cohort community based study included in the Gospel Oak Project" J A Cervilla, et al. Journal of Neurology Neurosurgery and Psychiatry (2000) 68:622-626
Mounting studies continue to show that people who exercise their brains will put off the chance of developing AD. In a study published in the New England Journal of Medicine in 2003, researchers from the Albert Einstein College of Medicine in New York carried out their study on 469 people who were above 75. At the start of the study, none were living in nursing homes or had dementia. They found that those who engaged themselves in stimulating mental activities such as reading, playing a musical instrument, playing board games, or even dancing had a lesser chance of developing AD. No link was found between physical activity and a reduced risk of dementia.
Reference : "Leisure Activities and the Risk of Dementia in the Elderly" Joe Verghese, et al. New England Journal of Medicine (2003) 348:2508-2516
Diabetes mellitus is linked to a 65 percent increased risk of developing Alzheimer's disease and affects some aspects of cognitive function differently than others, according to a study. Over the study period, 151 out of the 824 participants developed AD, including 31 who had diabetes.
Reference : Rush University Medical Center (May 2004)
A mice study directed by Mount Sinai School of Medicine suggests that experimental dietary regimens might calm or even reverse symptoms of AD. This study is the first to show that limiting the intake of carbohydrates, may prevent AD by triggering activity in the brain associated with longevity.
A main characteristic of those with AD is elevated levels of beta-amyloid peptides (fiber-like substance) that cause plaque buildup in the brain. SIRT1, a molecule associated with brain longevity, is member of a broad family of proteins known as sirtuins which influences a variety of functions including metabolism and aging.
The mice who were given a low-carbohydrate diet had a higher level of SIRT1 in their brains compared to those fed with high calories (based on saturated fat). In fact, a high caloric intake based on saturated fat was shown to increase levels of beta-amyloid peptides.
Reference : "Calorie restriction may prevent Alzheimer's through promotion of longevity program in the brain" Mount Sinai School of Medicine (14 Jun 2006); "Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer's disease amyloid neuropathology by calorie restriction" Journal Biological Chemistry (2006)
A study suggests that weight loss in older people may be an early sign of AD, in fact the weight loss will occur several years before AD symptoms actually appear. The study was conducted by researchers from the Rush University Medical Center in Chicago, as part of the Religious Orders Study. The Religious Orders Study is a comprehensive, long-term look at aging and AD among Catholic nuns, priests, and brothers nationwide that has been funded by the National Institute on Aging (NIA), a component of the National Institutes of Health, U.S. Department of Health and Human Service.
All the 820 participants were above 65 years old, most were white and of European ancestry and none had dementia when the study began. Their average BMI was 27.4 (in the overweight zone). During the follow-up period, 151 of the participants developed AD. Both baseline BMI and the annual rate of change in BMI were linked to the risk of developing AD. hose who lost one point of BMI per year had a 35 percent greater risk of developing AD than that of people with no change in BMI over the course of the study. Those with no change in BMI had a 20 percent greater risk of developing the disease than those who gained six-tenths of a unit of BMI per year.
The results did not change even after adjusting for factors such as chronic health problems, age, sex and education but raise the possiblity that the disease attacks the brain region that controls weight.
Reference : "Change in body mass index and risk of incident Alzheimer disease" A. S. Buchma, et al. Neurology (2005) 65:892-897
Vitamin B5 - Pantothenic acid People with AD are known to have low levels of a brain chemical (neurotransmitter) called acetylcholine. This chemical is involved in mental functions related to memory and learning.
Vitamin B5 is a component of acetylcholine.
Vitamin B9 - folic acid High blood levels of homocysteine may double the risk of AD. Folic acid, together with vitamin B6 and B12 helps keep homocystene in check.
Vitamin B12 - Cobalamin Researchers at the Karolinska Institute in Stockholm, Sweden found that low levels of vitamin B12 and folic acid increase AD risk in elderly people.
All other B Vitamins Important vitamins crucial for efficient use of oxygen by cells include vitamin B1 and B3. A proper supply of oxygen is critical for proper brain function.
Vitamin A and C Both vitamins are beneficial antioxidants that must be mobilized in the prevention and intervention of AD. Inflammation produces damaging oxidants (also known as free radicals) which must be curb by antioxidants.
Recommended supplement dosage : vitamin A (beta carotene) - 10,000 iu daily; vitamin C - 1000 mg twice a day (prevention), 1000 mg four times a day (intervention)
Vitamin E A study featured on the New England Journal of Medicine found that high doses (2000 iu) of this vitamin helped delay the progression of moderate AD.
Natural forms of vitamin E are d-alpha tocopherol and d-alpha tocopheryl acetate.
Selenium This trace mineral forms part of the antioxidant enzyme glutathione peroxidase. It works well with vitamin E to enhance each other's functions.
Recommended supplement dosage : 200 mcg a day (prevention), 400 mcg (intervention)
Essential fatty acid 60% of the brain consists of fats and DHA (docosahexaenoic acid) is an omega-3 fatty acid that is singled out to be an indispensible component. It provides fluidity to the brain cell membrane and improves communication between brain cells. It controls the flow of substances travelling in and out of the cells, and in Alzheimer's case calcium is of concern because abnormal levels of calcium in the brain cells are known to produce more harmful beta-amyloid protein.
EPA (eicosapentaenoic acid) is a precursor of DHA.
Food sources - flaxseed, salmon, herring, mackerel, halibut and tuna.
Recommended supplement dosage : up to 2 gm (DHA and EPA combined) a day (prevention)
Choline and Lecithin Choline is a component of acetylcholine, i.e. a nutrient which the brain uses to make acetylcholine. Choline is involved in fat metabolism and helps to transport fats from the liver. It is a also a component of cell membranes and of myelin (the white insulating sheath that surrounds the nerve cells).
Most abosorbable form of choline is phosphatidylcholine. Phosphatidylcholine is a substance found in lecithin and it plays a role in proper nerve function.
Recommended supplement dosage : 500 mg a day with a meal (prevention), 500 mg twice a day with meals (intervention)
Magnesium This mineral competes with aluminum for absorption which means it reduces the chance of absorbing aluminum.
Recommended supplement dosage : 270-320 mg a day
Noni A natural tropical fruit found to contain over 150 nutraceuticals which include 20 amino acids, 9 of which are essential because they are not produced in the body, vitamin A, all the B vitamins, vitamin C, vitamin E, beta carotene, ursolic acid, linoleic acid, proxeronine (bromelain), scopoletin, pectin, phytosterols, calcium, magnesium and zinc.
Its traditional uses include immune booster, pain, arthritis, diabetes, headaches, cuts and scrapes, skin problems, cancer, high blood pressure and many more.
The following are other nurtients found in noni that may be beneficial for AD :
:: COX 2 INHIBITOR
The COX 2 enzyme (COX is an abbreviation for cyclooxygenase) creates prostaglandins that cause inflammation especially in the joints. COX 2 is being linked to inflammation of the brain cells. An investigation carried out by Morinda Inc., makers of TAHITIAN NONI™ Juice found that TAHITIAN NONI™ Juice is a selective inhibitor of COX 2. TAHITIAN NONI™ Juice has found favour with many arthritis sufferers.
:: SCOPOLETIN
Scopoletin belongs to a group of compounds called coumarins. It has strong anti-inflammatory influence.
:: PROXERONINE (BROMELAIN)
Noni contains high levels of bromelain which is also known as proxeronine. This substance has potent anti-inflammatory properties.
Noni can be used in conjunction with any medication and natural supplements, in fact, noni may enhance the effects of medications and supplements. It is best taken with clean water on an empty stomach.
References :
"The Pain Fighter : Tahitian Noni Juice - Explore Noni's unique relationship to arthritis, inflammation and the COX 2 Enzyme" Neil Solomon (Direct Source, 2001);
"Tahitian Noni Juice : How Much, How Often, For What" Neil Solomon (Direct Source, 2002)
Ginkgo Best known for it's memory boosting capability, this herb was found useful for patients with AD in some studies.
Consult a physician before combing ginkgo with anti-coagulants, insulin, prochlorperazine (an antipsychotic drug) or trazodone (a modified cyclic antidepressant). People with blood clotting disorders should check with a physician before taking this herb.
Recommended supplement dosage : 40 mg 3 or 4 times a day with or without meals (prevention and intervention)
It may take at 6 to 8 weeks before results can be seen.
SAM-e Stands for S-adenosyl-L-methionine, this compound is formed in the body when the amino acid L-methionine combines with adenosine triphosphate (ATP). This compound can influence the effectiveness of several brain chemicals.
People who suffer from bipolar depression or manic depression or Parkinson's disease should consult a physician before using SAM-e.
SAME-e derived from living organisms is an unstable molecule and sensitive to moisture. Use enteric-coated tablets which protect SAM-e from digestive enzymes. Though rare, mild headaches and diarrhea were experienced by some during SAME-e trials. SAME-e is very safe for most people.
Recommended supplement dosage : start with 200 mg twice a day for the first 2 to 3 days. Increase to 400 mg twice a day and 400 mg 3 times aday after 2 weeks. Pass four weeks, the dosage can be increased (only when needed) to 400 mg 4 times daily.
[Build dose gradually so as to avoid any possible side effects]
Phosphatidylserine It is a phospholipid, a type of fat. A major and essential component in every cell membrane. Besides keeping cell membranes intact, this membrane performs vital functions and improves neurotransmitter action. Benefits include better memory and concentration, supports cognitive functions through improved circulation and enhances both blood and nutrient transportation to the brain and heart.
Recommended supplement dosage : 100 mg a day (prevention), 100 mg 3 times a day (intervention)
Huperzine-A Huperzine-A is an extract from a plant called club moss. It can inhibit the breaking down action of the enzyme acetylcholinesterase on choline so as to enable the level of acetylcholine to increase. It is not a cure for AD, however it could improve cognitive abilities and slow down memory loss. Further research is needed to determine it's safety for prolonged use.
Recommended supplement dosage : 50 mcg twice a day (intervention)
Vinpocetine Derived from vincamine which is found in the leaves of a periwinkle plant. Studies have indicated it's ability to enhance memory and mental function.
Recommended supplement dosage : 10 mg twice a day (intervention)
Acetyl L Carnitine This amino acid can help with brain function.
Recommended supplement dosage : 500 mg a day (intervention)
Green tea
• A study was conducted by researchers from the Tohoku University Graduate School of Medicine in Japan on 1003 Japanese men and women above the age of 70 where they were asked questions that included the frequency of green tea consumption. They were then evaluated using a standard mental status exam. The researchers found that those who drank two or more cups of green tea per day, had a lower the risk of cognitive impairment (or mental decline).
Reference : "Green tea consumption and cognitive function: a cross-sectional study from the Tsurugaya Project" Shinichi Kuriyama, et al. American Journal of Clinical Nutrition (2006) 83(2):355-361
• Scientists from the University of South Florida found that high doses of the antioxidant epigallocatechin-3-gallate (EGCG) found in green tea prevented Alzheimer's-like damage in the brains of mice bred to develop symptoms. One of the possible causes of AD is the harmful accumulation of beta-amyloid, which is just a very small protein fragment of a larger protein in brain cells. After several months of injecting the mice with pure EGCG on a daily basis, the nerve cells of the mice generated 54% less beta-amyloid proteins than not-treated mice. In the case of humans, we would need a daily dose of 1,500 to 1,600 mg of pure EGCG to achieve the similar effect experienced by the mice and this daily dose has been studied in healthy human volunteers and was found to be safe and well tolerated. The drinking of green tea alone would not be sufficient to have the same effect.
Reference : "Green Tea Epigallocatechin-3-Gallate (EGCG) Modulates Amyloid Precursor Protein Cleavage and Reduces Cerebral Amyloidosis in Alzheimer Transgenic Mice" Kavon Rezai-Zadeh, et al. Journal of Neuroscience (2005) 25(38):8807-8814
Zinc This mineral helps prevent lead accumulation in the brain tissue which has been linked to AD.
Recommended supplement dosage : 25 mg a day (prevention)
Aluminum Some studies have shown the link between high levels of aluminum to AD risk. E.g. consumption of aluminum in drinking water with concentrations greater than 0.1 mg/liter. Limit the use of aluminum in utensils, cookwares, foil, food additives (frozen doughs, self-rising flour, cake/pancake mix) and antacids with added aluminum.
Reference : "Relation between Aluminum Concentrations in Drinking Water and Alzheimer's Disease: An 8-year Follow-up Study" Virginie Rondeau, et al. American Journal of Epidemiology (2000) 152(1):59-66
Alzheimer's Tips Revealed A Program That Teaches You How To Provide
Quality Care To Individuals With AD Or Memory
Loss.
"Cardiovascular disease is another factor that increases the risk of Alzheimer's. A connection between the presence of ApoE4, atherosclerosis and increased Alzheimer's risk was made by Professor Hoffman at the Erasmus University Medical School in Rotterdam. The most convincing theory is the blockages in arteries may lead to a poor supply of key nutrients to the brain. Without a good supply of antioxidants, for example, brain cells become more vulnerable to free radical damage.
Another possibility is that both cardiovascular and Alzheimer's disease may result from the same disease process. The diagnostic proof of Alzheimer's is the presence of plaques, or patches of dead cells and other waste material, in the brain. At the core of these plaques has been found a sunstance called beta-amyloid, an abnormal protein that is also found in the plaques of arterial deposits. Beta-amyloid is a toxic invader that results from the body being in 'emergency mode', resulting in flammation as the immune system becomes over-reactive. It's a typical scenario that develops once a person's Total Environmental Load exceeds their capacity to adapt. Indeed research has shown that taking anti-inflammatory drugs offers some protection from Alzheimer's, which is consistent with the hypothesis that the damage that occurs to brain cells is part of an overall inflammatory reaction. It also means that natural anti-inflammatory nutrients may prove to be important in prevention."
"Inflammatory reactions invariably mean increased production of oxidants, hence an increased need for antioxidants such as vitamin A, betacarotene and vitamins C and E, all of which have been shown to be low in people with Alzheimer's"
- Patrick Holford, 100% Health (Judy Piatkus Pub Ltd, 1998)
"In simple terms, in Alzheimer's, brain cells may be inflamed and rendered eventually useless. The more brain cells that a person loses, the more advanced is the memory loss. COX 2 is suspected to be one culprit behind the brain cells' inflammation. At the John Hopkins Hospital and at other academic institutions there is active research going on as to why brain cells start to become inflamed. Regardless of why, if the levels of COX 2 can be controlled and even diminished by using a selective COX 2 inhibitor, there is the possibility of an eventual role in prevention or even that the Alzheimer's may be slowed down. For now, the theories on how COX 2 inhibitors work on cancer and Alzheimer's are still in the early, but promising stages."
- Neil Solomon, The Pain Fighter : Tahitian Noni Juice - Explore Noni's unique relationship to arthritis, inflammation and the COX 2 Enzyme (Direct Source, 2001)
