Scientific studies reveal promising results for preventing and treating this memory-robbing disease. According to research or other evidence, the following self-care steps may be helpful.
Get some extra E
Slow the progression of Alzheimer’s by taking 2,000 IU of vitamin E each day
Go for the ginkgo
Improve memory, enhance quality of life, and slow progression in the early stages of the disease by taking 120 to 240 mg a day of a standardized herbal extract of Ginkgo biloba
Add acetyl-L-carnitine to your routine
Take 1,500 mg a day of this nutritional supplement to improve memory and slow progression of Alzheimer’s disease
About This Condition
Alzheimer’s disease is a brain disorder that occurs in the later years of life. People with Alzheimer's disease develop progressive loss of memory and gradually lose the ability to function and to take care of themselves.
The cause of this disorder is not known, although the problem appears to involve abnormal breakdown of acetylcholine (an important neurotransmitter in the brain). Some studies suggest it may be related to an accumulation of aluminum in the brain.1 Despite this suggestion, aluminum toxicity has been studied in humans, and it is quite distinct from Alzheimer’s disease.2 Therefore, the importance of aluminum in causing Alzheimer’s disease remains an unresolved issue.
Symptoms of Alzheimer’s include a pattern of forgetfulness, short attention span, difficulty in performing routine tasks, language problems, disorientation, poor judgment, problems with thinking, misplacing things, depression, irritability, paranoia, hostility, and lack of initiative.
Healthy Lifestyle Tips
Keeping active outside of one’s work, either physically or mentally, during midlife may help prevent Alzheimer’s disease. People with higher levels of non-occupational activities, such as playing a musical instrument, gardening, physical exercise, or even playing board games, were less likely to develop Alzheimer’s later in life, according to one study.3
The right diet is the key to managing many diseases and to improving general quality of life. For this condition, scientific research has found benefit in the following healthy eating tips.
Eating a diet high in fish has been linked to a decreased Alzheimer’s disease risk.
In population studies, high dietary intake of fat and calories was associated with an increased risk for Alzheimer’s disease, whereas high intake of fish was associated with a decreased risk.4, 5, 6 Whether these associations represent cause and effect is unknown.
Try a low-fat diet
Reduce your risk with a low-fat diet. A diet high in fat and calories has been associated with an increased risk for Alzheimer’s disease.
In population studies, high dietary intake of fat and calories was associated with an increased risk for Alzheimer’s disease, whereas high intake of fish was associated with a decreased risk.7, 8, 9 Whether these associations represent cause and effect is unknown.
Although aluminum’s role in Alzheimer’s development of remains controversial, people wanting to reduce risk can take steps to minimize their dietary exposure to the potentially toxic metal.
Whether aluminum in the diet can cause Alzheimer’s disease remains controversial.10, 11 A preliminary study found Alzheimer’s disease patients are more likely to have consumed foods high in aluminum additives (e.g., some grain product desserts, American cheese, chocolate pudding, chocolate beverages, salt, and some chewing gum), compared to people without the disease.12 Until this issue is resolved, it seems prudent for healthy people to take steps to minimize exposure to this unnecessary and potentially toxic metal by reducing intake of foods cooked in aluminum pots, foods that come into direct contact with aluminum foil, beverages stored in aluminum cans, and foods containing aluminum additives. Aluminum is added to some municipal water supplies to prevent the accumulation of particulates. In such areas, bottled water may be preferable. It appears unlikely, however, that avoidance of aluminum exposure after the diagnosis of Alzheimer’s disease could significantly affect the course of the disease.
Our proprietary “Star-Rating” system was developed to help you easily understand the amount of scientific support behind each supplement in relation to a specific health condition. While there is no way to predict whether a vitamin, mineral, or herb will successfully treat or prevent associated health conditions, our unique ratings tell you how well these supplements are understood by some in the medical community, and whether studies have found them to be effective for other people.
For over a decade, our team has combed through thousands of research articles published in reputable journals. To help you make educated decisions, and to better understand controversial or confusing supplements, our medical experts have digested the science into these three easy-to-follow ratings. We hope this provides you with a helpful resource to make informed decisions towards your health and well-being.
3 StarsReliable and relatively consistent scientific data showing a substantial health benefit.
2 StarsContradictory, insufficient, or preliminary studies suggesting a health benefit or minimal health benefit.
1 StarFor an herb, supported by traditional use but minimal or no scientific evidence. For a supplement, little scientific support.
1 gram taken three times per day
Short-term studies have found that people with Alzheimer’s disease who supplement with acetyl-L-carnitine experience improved memory, enhanced overall performance, and delayed disease progression.
Several clinical trials have found that acetyl-L-carnitine supplementation delays the progression of Alzheimer’s disease,13 improves memory,14, 15, 16 and enhances overall performance in some people with Alzheimer’s disease.17, 18 However, in one double-blind trial, people who received acetyl-L-carnitine (1 gram three times per day) deteriorated at the same rate as those given a placebo.19 Overall, however, most short-term studies have shown clinical benefits, and most long-term studies (one year) have shown a reduction in the rate of deterioration.20 A typical supplemental amount is 1 gram taken three times per day.
120 to 240 mg of a standardized herbal extract daily
Ginkgo biloba extract is an approved treatment for early-stage Alzheimer’s disease in Europe. It is thought to improve memory and quality of life and slow early disease progression.
An extract made from the leaves of the Ginkgo biloba tree is an approved treatment for early-stage Alzheimer’s disease in Europe. While not a cure, Ginkgo biloba extract may improve memory and quality of life and slow progression in the early stages of the disease. In addition, several double-blind trials have shown that ginkgo is helpful for people in early stages of Alzheimer’s disease, as well as for those experiencing another form of dementia known as multi-infarct dementia.21, 22, 23, 24, 25 Ginkgo has been found to be nearly as effective against Alzheimer's disease as donepezil, a prescription drug used to treat the condition.26 One trial reported no effect of ginkgo supplementation in the treatment of Alzheimer’s disease, vascular dementia or age-associated memory impairment.27 However, the results of this trial have been criticized, since analysis of the results does not separate those patients with Alzheimer’s disease or vascular dementia from those with age-associated memory impairment. A comparison of placebo-controlled trials of ginkgo for Alzheimer’s disease concluded that the herb compared favorably with two prescription drugs, donepezil and tacrine, commonly used to treat the condition.28 Research studies have used 120 to 240 mg of ginkgo, standardized to contain 6% terpene lactones and 24% flavone glycosides per day, generally divided into two or three portions. Ginkgo may need to be taken for six to eight weeks before desired actions are noticed. Ginkgo was not effective for preventing Alzheimer's disease in elderly volunteers with normal cognitive function or in those with mild cognitive impairment.29
200 mcg of huperzine A twice per day
Huperzine A, a substance found in the Chinese medicinal herb huperzia (Huperzia serrata), has been shown to improve memory and mental and behavioral function in people with dementia, including Alzheimer’s disease.
Huperzine A is a substance found in huperzia(Huperzia serrata), a Chinese medicinal herb. In a placebo-controlled trial, 58% of people with Alzheimer’s disease had significant improvement in memory and mental and behavioral function after taking 200 mcg of huperzine A twice per day for eight weeks—a statistically significant improvement compared to the 36% who responded to placebo.30 Another double-blind trial using injected huperzine A confirmed a positive effect in people with dementia, including, but not limited to, Alzheimer’s disease.31 Yet another double-blind trial found that huperzine A, given at levels of 100 to 150 mcg two to three times per day for four to six weeks, was more effective at improving minor memory loss associated with age-related cognitive decline than the drug piracetam.32 This study found that huperzine A was not effective in relieving symptoms of Alzheimer’s disease. Clearly, more research is needed before the usefulness of huperzine A for Alzheimer’s disease is confirmed.
60 drops per day of a 1:1 herbal tincture, standardized to contain at least 500 mcg per ml of citral
Supplementing with an herbal extract of lemon balm (Melissa officinalis) has been shown to improve cognitive function and reduce agitation in people with Alzheimer's disease.
In a double-blind trial, supplementation with an extract of lemon balm (Melissa officinalis) for 16 weeks significantly improved cognitive function and significantly reduced agitation, compared with a placebo, in people with Alzheimer's disease.33 The amount of lemon balm used was 60 drops per day of a 1:1 tincture, standardized to contain at least 500 mcg per ml of citral.
Refer to label instructions
Lesser periwinkle contains the alkaloid vincamine, which has shown some benefit to people with Alzheimer’s disease.
Lesser periwinkle contains the alkaloid vincamine. Supplementation with a semi-synthetic derivative of vincamine, known as vinpocentine, showed no benefit for people with Alzheimer’s disease in a preliminary study,34 but vincamine itself was shown to be beneficial in a later double-blind trial.35
60 drops daily of a 1:1 tincture
Sage appears to have an effect on acetylcholine, one of the chemical messengers (neurotransmitters) in the brain and supplementing with sage has resulted in a significant improvement in cognitive function.
In a double-blind study of people with Alzheimer’s disease, supplementing with sage for four months resulted in a significant improvement in cognitive function, compared with a placebo.36 The amount of sage used was 60 drops per day of a 1:1 tincture. Although it is not known for sure how sage improves cognitive function, it appears to have an effect on acetylcholine, one of the chemical messengers (neurotransmitters) in the brain.
3 grams daily
Supplementing with vitamin B1 might slow Alzheimer’s disease progression in people whose vitamin B1–dependent enzymes have low activity.
Vitamin B1 is involved in nerve transmission in parts of the brain (called cholinergic neurons) that deteriorate in Alzheimer’s disease.37, 38 The activity of vitamin B1-dependent enzymes has been found to be lower in the brains of people with Alzheimer’s disease.39 It has therefore been suggested that vitamin B1 supplementation could slow the progression of Alzheimer’s disease. Two double-blind trials have reported small but significant improvements of mental function in people with Alzheimer’s disease who took 3 grams a day of vitamin B1, compared to those who took placebo.40, 41 However, another double-blind trial using the same amount for a year found no effect on mental function.42
2,000 IU daily
Antioxidant supplements such as vitamin E have been associated with lower risk of Alzheimer’s disease and improved brain function in middle-aged and older adults.
In a preliminary study, people who used antioxidant supplements (vitamin C or vitamin E) had a lower risk of Alzheimer’s disease compared with people who did not take antioxidants.43 Other preliminary research shows that higher blood levels of vitamin E correlate with better brain functioning in middle-aged and older adults.44 The possible protective effect of antioxidants may be explained by the observation that oxidative damage appears to play a role in the development of dementia.45 Large amounts of supplemental vitamin E may slow the progression of Alzheimer’s disease. A double-blind trial found that 2,000 IU of vitamin E per day for two years extended the length of time people with moderate Alzheimer’s disease were able to continue caring for themselves (e.g., bathing, dressing, and other necessary daily functions), compared with people taking a placebo.46
4.5 grams per day for 12 weeks
A preliminary trial suggests that taking Panax ginseng may significantly improve a measure of cognitive function in the short term, though long-term use has not been established.
In a preliminary trial, supplementation with 4.5 grams per day of Asian (Panax) ginseng for 12 weeks resulted in a statistically significant 15% improvement in a measure of cognitive function. This improvement waned after the treatment was discontinued.47
Refer to label instructions
Animal studies have found the Ayurvedic herb bacopa has constituents that enhance several aspects of mental function and learning ability.
Animal studies have found the Ayurvedic herb bacopa has constituents that enhance several aspects of mental function and learning ability.48, 49, 50 A controlled study found that a syrup containing an extract of dried bacopa herb given to children improved several measures of mental performance.51 A double-blind trial in adults found that a standardized extract of bacopa (300 mg per day for people weighing under 200 lbs and 450 per day for people over 200 lbs) improved only one out of several measures of memory function after three months.52 Another double-blind trial lasting twelve weeks found 300 mg per day of bacopa improved four out of fifteen measures of learning, memory, and other mental functions in adults.53 A third double-blind study found no effects on mental function in a group of healthy adults given 300 mg of standardized bacopa and tested two hours later. Bacopa has not been tested on people with memory problems.54
Coenzyme Q10, Iron, and Vitamin B6
Refer to label instructions
A combination of coenzyme Q10, iron (sodium ferrous citrate), and vitamin B6 may improve mental status in people with Alzheimer’s disease.
In a preliminary report, two people with a hereditary form of Alzheimer’s disease received daily: coenzyme Q10 (60 mg), iron (150 mg of sodium ferrous citrate), and vitamin B6 (180 mg). Mental status improved in both patients, and one became almost normal after six months.55
Refer to label instructions
People with Alzheimer’s disease may have low DHEA (dehydroepiandrosterone) levels, and supplementation may improve mental performance.
Most,56, 57, 58, 59 but not all,60, 61 studies have found that people with Alzheimer’s disease have lower blood DHEA (dehydroepiandrosterone) levels than do people without the condition. Emerging evidence suggests a possible benefit of DHEA supplementation in people with Alzheimer’s disease. In one double-blind trial, participants who took 50 mg twice daily for six months had significantly better mental performance at the three-month mark than those taking placebo. At six months, statistically significant differences between the two groups were not seen, but results still favored DHEA.62 In another clinical trial, massive amounts of DHEA (1,600 mg per day for four weeks) failed to improve mental function or mood in elderly people with or without Alzheimer’s disease.63 It is likely that the amount of DHEA used in this trial was far in excess of an appropriate amount, illustrating that more is not always better.
Refer to label instructions
DMAE (2-dimethylaminoethanol) may increase levels of a brain neurotransmitter, which may foster positive behavior changes in people with dementia.
DMAE (2-dimethylaminoethanol) may increase levels of the brain neurotransmitter acetylcholine. In one preliminary trial, people with senile dementia were given DMAE supplements of 600 mg three times per day for four weeks. The participants did not show any changes in memory, though some did show positive behavior changes.64 However, a subsequent double-blind trial found no significant benefit from DMAE supplementation in people with Alzheimer’s disease.65
Refer to label instructions
Fish oil may help slow the rate of cognitive decline in people with very mild impairment.
In a double-blind trial, supplementing with the fatty acids present in fish oil (0.6 grams per day of EPA and 1.7 grams per day of DHA) for six months was not beneficial in people with Alzheimer's disease. However, in the subgroup of people with very mild cognitive impairment, supplementation with these fatty acids slowed the rate of cognitive decline compared with a placebo.66
Refer to label instructions
Some researchers feel Alzheimer’s disease may be related to folic acid deficiency.
Some researchers have found an association between Alzheimer’s disease and deficiencies of vitamin B12 and folic acid;67, 68 however, other researchers consider such deficiencies to be of only minor importance.69 In a study of elderly Canadians, those with low blood levels of folate were more likely to have dementia of all types, including Alzheimer’s disease, than those with higher levels of folate.70 Little is known about whether supplementation with either vitamin would significantly help people with this disease. Nonetheless, it makes sense for people with Alzheimer’s disease to be medically tested for vitamin B12 and folate deficiencies and to be treated if they are deficient.
Lecithin (Phosphatidyl Choline)
Refer to label instructions
Weak evidence suggests that moderate amounts of lecithin, a fat used by the body to build membranes that may be obtained through food sources, may slightly improve symptoms.
A double-blind trial of 20 to 25 grams per day of lecithin failed to produce improvements in mental function in people with Alzheimer’s disease.71 However, there were improvements in a subgroup of people who did not fully comply with the program, suggesting that lower amounts of lecithin may possibly be helpful. Lecithin supplementation has also been studied in combination with a cholinesterase inhibitor drug called tacrine, with predominantly negative results.72, 73, 74, 75
10 mg per day
A small, preliminary trial showed that oral NADH improved mental function in people with Alzheimer’s disease.
A small, preliminary trial showed that oral NADH (10 mg per day) improved mental function in people with Alzheimer’s disease.76 Further studies are necessary to confirm these early results.
Refer to label instructions
There is some evidence that cow-derived PS (phosphatidylserine) has been shown to improve mental function and feelings of well-being in people with Alzheimer’s disease, though most research has not found benefit.
Phosphatidylserine (PS), which is related to lecithin, is a naturally occurring compound present in the brain. Although it is not a cure, 100 mg of PS taken three times per day has been shown to improve mental function, such as the ability to remember names and to recall the location of frequently misplaced objects, in people with Alzheimer’s disease.77 However, subsequent studies have not validated these results. In one double-blind trial, only the most seriously impaired participants received benefits from taking PS; people with moderate Alzheimer’s disease did not experience significant improvements in cognitive function.78 In another double-blind trial, people with Alzheimer’s disease who took 300 mg of PS per day for eight weeks had better improvement in overall well-being than those who took placebo, but there were no significant differences in mental function tests.79 In another double-blind trial, 200 mg of PS taken twice daily produced short-term improvements in mental function (after six to eight weeks), but these effects faded toward the end of the six-month study period.80
The PS used in these studies was obtained from bovine brain phospholipids. A plant source of PS is also available. However, the chemical structure of the plant form of PS differs from the bovine form. In a preliminary study, plant-derived PS was no more effective than a placebo at improving the memory of elderly people.81 Soy-derived PS was also ineffective in a double-blind study of elderly people with age-related cognitive decline.82
Refer to label instructions
In case reports, three patients with Alzheimer's disease showed improvements in symptoms such as irritability, agitation, anxiety, and apathy after supplementing with turmeric.
In case reports, three patients with Alzheimer's disease showed improvements in symptoms such as irritability, agitation, anxiety, and apathy after supplementing with turmeric. The amount used was 764 mg per day, providing 100 mg per day of curcumin, a presumed active ingredient.83
Refer to label instructions
Some researchers feel Alzheimer’s disease may be related to vitamin B12 deficiency.
Some researchers have found an association between Alzheimer’s disease and deficiencies of vitamin B12 and folic acid;84, 85 however, other researchers consider such deficiencies to be of only minor importance.86 In a study of elderly Canadians, those with low blood levels of folate were more likely to have dementia of all types, including Alzheimer’s disease, than those with higher levels of folate.87 Little is known about whether supplementation with either vitamin would significantly help people with this disease. Nonetheless, it makes sense for people with Alzheimer’s disease to be medically tested for vitamin B12 and folate deficiencies and to be treated if they are deficient.
Find Drug Interaction Information
1. Priest ND. Satellite symposium on Alzheimer’s disease and
dietary aluminum. Proc Nutr Soc 1993;52:231–40.
2. Munoz DG. Is
exposure to aluminum a risk factor for the development of Alzheimer disease?—No. Arch Neurol
3. Friedland R. American Academy of Neurology's 52nd Annual Meeting in San Diego, CA, April 29-May 6, 2000.
4. Grant WB. Dietary links to Alzheimer's disease. Alzheimer Dis Rev 1997;2:42-55.
5. Smith MA, Petot GJ, Perry G. Diet and oxidative stress: a novel synthesis of epidemiological data on Alzheimer's disease. Alzheimer Dis Rev 1997;2:58-9.
6. Kalmijn S, Lauher LJ, Ott A, et al. Dietary fat intake and the risk of incident dementia in the Rotterdam study. Ann Neurol 1997;42:776-82.
7. Grant WB. Dietary links to Alzheimer's disease. Alzheimer Dis Rev 1997;2:42-55.
8. Smith MA, Petot GJ, Perry G. Diet and oxidative stress: a novel synthesis of epidemiological data on Alzheimer's disease. Alzheimer Dis Rev 1997;2:58-9.
9. Kalmijn S, Lauher LJ, Ott A, et al. Dietary fat intake and the risk of incident dementia in the Rotterdam study. Ann Neurol 1997;42:776-82.
10. Munoz DG. Is exposure to aluminum a risk factor for the development of Alzheimer disease?—No. Arch Neurol 1998;55:737-9.
11. Forbes WF, Hill GB. Is exposure to aluminum a risk factor for the development of Alzheimer disease?—Yes. Arch Neurol 1998;55:740-1.
12. Rogers MA, Simon DG. A preliminary study of dietary aluminium intake and risk of Alzheimer's disease. Age Ageing 1999;28:205-9.
13. Pettegrew JW, Klunk WE, Panchalingam K, et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer's disease. Neurobiol Aging 1995;16:1-4.
14. Salvioli G, Neri M. L-acetylcarnitine treatment of mental decline in the elderly. Drugs Exp Clin Res 1994;20:169-76.
15. Rai G, Wright G, Scott L, et al. Double-blind, placebo controlled study of acetyl-l-carnitine in patients with Alzheimer's dementia. Curr Med Res Opin 1990;11:638-47.
16. Sano M, Bell K, Cote L, et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer's disease. Arch Neurol 1992;49:1137-41.
17. Cucinotta D et al. Multicenter clinical placebo-controlled study with acetyl-L-carnitine (LAC) in the treatment of mildly demented elderly patients. Drug Development Res 1988;14:213-6.
18. Bonavita E. Study of the efficacy and tolerability of L-acetylcarnitine therapy in the senile brain. Int J Clin Pharmacol Ther Toxicol 1986;24:511-6.
19. Thal LJ, Carta A, Clarke WR, et al. A 1-year multi-center placebo-controlled study of aceyl-L-carnitine in patients with Alzheimer's disease. Neurology 1996;47:705-11.
20. Calvani M, Carta A, Caruso G, et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer's disease. Ann NY Acad Sci 1992;663:483-6.
21. Le Bars PL, Katz MM, Berman N, et al. A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group. JAMA 1997;278:1327-32.
22. Hofferberth B. The efficacy of EGb 761 in patients with senile dementia of the Alzheimer type, a double-blind, placebo-controlled study on different levels of investigation. Hum Psychopharmacol 1994;9:215-22.
23. Kanowski S, Herrmann W, Stephan K, et al. Proof of efficacy of the Ginkgo biloba special extract EGb 761 in outpatients suffering from mild to moderate primary degenerative dementia of the Alzheimer type or multi-infarct dementia. Pharmacopsychiatry 1996;29:47-56.
24. Maurer K, Ihl R, Dierks T, Frolich L. Clinical efficacy of Ginkgo biloba special extract EGb 761 in dementia of the Alzheimer's type. J Psychiatr Res 1997;31:645-55.
25. Bachinskaya N, Hoerr R, Ihl R. Alleviating neuropsychiatric symptoms in dementia: the effects of Ginkgo biloba extract EGb 761. Findings from a randomized controlled trial. Neuropsychiatr Dis Treat 2011;7:209-15.
26. Mazza M, Capuano A, Bria P, Mazza S. Ginkgo biloba and donepezil: a comparison in the treatment of Alzheimer's dementia in a randomized placebo-controlled double-blind study. Eur J Neurol 2006;13:981-5.
27. van Dongen M, van Rossum E, Kessels A, et al. The efficacy of ginkgo for elderly people with dementia and age-associated memory impairment: New results of a randomized clinical trial. J Am Geriatr Soc 2000;48:1183-94.
28. Wettstein A. Cholinesterase inhibitors and Ginkgo extracts-are they comparable in the treatment of dementia? Comparison of published placebo-controlled efficacy studies of at least six months' duration. Phytomedicine 2000;6:393-401.
29. DeKosky ST, Williamson JD, Fitzpatrick AL, et al. Ginkgo biloba for prevention of dementia: a randomized controlled trial. JAMA 2008;300:2253-62.
30. Xu SS, Gao ZX, Weng Z, et al. Efficacy of tablet huperzine-A on memory, cognition, and behavior in Alzheimer's disease. Chung Kuo Yao Li Hsueh Pao 1995;16:391-5.
31. Zhang RW, Tang XC, Han YY, et al. Drug evaluation of huperzine A in the treatment of senile memory disorders. Chung Kuo Yao Li Hsueh Pao 1991;12:250-2 [in Chinese].
32. Wang Z, Ren G, Zhao Y, et al. A double-blind study of huperzine A and piracetam in patients with age-associated memory impairment and dementia. In: Kanba S, Richelson E (eds). Herbal Medicines for Nonpsychiatric Diseases. Tokyo: Seiwa Shoten Publishers, 1999, 39-50.
33. Akhondzadeh S, Noroozian M, Mohammadi M, et al. Melissa officinalis extract in the treatment of patients with mild to moderate Alzheimer's disease: a double blind, randomised, placebo controlled trial. J Neurol Neurosurg Psychiatry 2003;74:863-6.
34. Thal LJ, Salmon DP, Lasker B, et al. The safety and lack of efficacy of vinpocetine in Alzheimer's disease. J Am Geriatr Soc 1989;37:515-20.
35. Fischhof PK, Moslinger-Gehmayr R, Herrmann WM, et al. Therapeutic efficacy of vincamine in dementia. Neuropsychobiology 1996;34:29-35.
36. Akhondzadeh S, Noroozian M, Mohammadi M, et al. Salvia officinalis extract in the treatment of patients with mild to moderate Alzheimer's disease: a double blind, randomized and placebo-controlled trial. J Clin Pharm Ther 2003;28:53-9.
37. Eder L, Hirt L, Dunant Y. Possible involvement of thiamine in acetylcholine release. Nature 1976;264:186-8.
38. Eder L, Dunant Y, Loctin F. Thiamine and cholinergic transmission in the electric organ of Torpedo. J Neurochem 1980;35:1278-96.
39. Gibson GE, Sheu KF, Blass JP, et al. Reduced activities of thiamine-dependent enzymes in the brains and peripheral tissues of patients with Alzheimer's disease. Arch Neurol 1988;45:836-40.
40. Meador K, Loring D, Nichols M, et al. Preliminary findings of high-dose thiamine in dementia of Alzheimer's type. J Geriatr Psychiatry Neurol 1993;6:222-9.
41. Blass JP, Gleason P, Brush D, et al. Thiamine and Alzheimer's disease. A pilot study. Arch Neurol 1988;45:833-5.
42. Nolan KA, Black RS, Sheu KF, et al. A trial of thiamine in Alzheimer's disease. Arch Neurol 1991;48:81-3.
43. Morris MC, Beckett LA, Scherr PA, et al. Vitamin E and vitamin C supplement use and risk of incident Alzheimer disease. Alzheimer Dis Assoc Disord 1998;12:121-6.
44. Schmidt R, Hayn M, Reinhart B, et al. Plasma antioxidants and cognitive performance in middle-aged and older adults: results of the Austrian Stroke Prevention Study. J Am Geriatr Soc 1998;46:1407-10.
45. Lethem R, Orrell M. Antioxidants and dementia. Lancet 1997;349:1189-90 [commentary].
46. Sano M, Ernesto C, Thomas RG, et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. N Engl J Med 1997;336:1216-22.
47. Lee ST, Chu K, Sim JY, et al. Panax ginseng enhances cognitive performance in Alzheimer disease. Alzheimer Dis Assoc Disord 2008;22:222-6.
48. Singh HK, Dhawan BN. Neuropsychopharmacological effects of the Ayurvedic nootropic Bacopa monniera Linn. (Brahmi). Indian J Pharmacol 1997;29:S359-S365.
49. Singh HK, Rastogi RP, Srimal RC, Dhawan BN. Effect of bacosides A and B on avoidance responses in rats. Phytother Res 1988;2:70-5.
50. Singh HK, Dhawan BN. Effect of Bacopa monniera Linn. (brahmi) extract on avoidance responses in rat. J Ethnopharmacol 1982;5:205-14.
51. Sharma R, Chaturvedi C, Tewari PV. Efficacy of Bacopa monniera in revitalizing intellectual functions in children. J Res Edu Ind Med 1987:1:12.
52. Roodenrys S, Booth D, Bulzomi S, et al. Chronic effects of Brahmi (Bacopa monnieri) on human memory. Neuropsychopharmacology. 2002;27:279-81.
53. Stough C, Lloyd J, Clarke J, et al. The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects. Psychopharmacology 2001;156:481-4.
54. Nathan PJ, Clarke J, Lloyd J, et al. The acute effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy normal subjects. Hum Psychopharmacol 2001;16:345-51.
55. Imagawa M, Naruse S, Tsuji S, et al. Coenzyme Q10, iron, and vitamin B6 in genetically-confirmed Alzheimer's disease. Lancet 1992;340:671 [letter].
56. Hillen T, Lun A, Reischies FM, et al. DHEA-S plasma levels and incidence of Alzheimer's disease. Biol Psychiatry 2000;47:161-3.
57. Nasman B, Olsson T, Backstrom T, et al. Serum dehydroepiandrosterone sulfate in Alzheimer's disease and in multi-infarct dementia. Biol Psychiatry 1991;30:684-90.
58. Sunderland T, Merril CR, Harrington MG, et al. Reduced plasma dehydroepiandrosterone concentrations in Alzheimer's disease. Lancet 1989;2:570.
59. Yanase T, Fukahori M, Taniguchi S, et al. Serum dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEA-S) in Alzheimer's disease and in cerebrovascular dementia. Endocr J 1996;43:119-23.
60. Birkenhager-Gillesse EG, Derksen J, Lagaay AM. Dehydroepiandrosterone sulphate (DHEAS) in the oldest old, aged 85 and over. Ann N Y Acad Sci 1994;719:543-52.
61. Schneider LS, Hinsey M, Lyness S. Plasma dehydroepiandrosterone sulfate in Alzheimer's disease. Biol Psychiatry 1992;31:205-8.
62. Wolkowitz OM, Kramer JH, Reus VI, et al. Dehydroepiandrosterone (NPI-34133) treatment of Alzheimer's disease: a randomized, double-blind, placebo-controlled, parallel group study. Presented at the annual meeting of the American Psychiatric Association, Washington, DC, May 15-20, 1999.
63. Dukoff R, Molchan S, Putnam K, et al. Dehydroepiandrosterone administration in demented patients and non-demented elderly volunteers. Biol Psychiatry 1999;46:1533-41.
64. Ferris SH, Sathananthan G, Gershon S, et al. Senile dementia. Treatment with Deanol. J Am Geriatr Soc 1977;25:241-4.
65. Fisman M, Mersky H, Helmes E. Double-blind trial of 2-dimethylaminoethanol in Alzheimer's disease. Am J Psychiatry 1981;138:970-2.
66. Freund-Levi Y, Eriksdotter-Jonhagen M, Cederholm T, et al. Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial. Arch Neurol 2006;63:1402-8.
67. Clarke R, Smith D, Jobst KA, et al. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 1998;55:1449-55.
68. Snowdon DA, Tully CL, Smith CD, et al. Serum folate and the severity of atrophy of the neocortex in Alzheimer disease: findings from the Nun study. Am J Clin Nutr 2000;71:993-8.
69. Joosten E, Lesaffre E, Riezler R, et al. Is metabolic evidence for vitamin B-12 and folate deficiency more frequent in elderly patients with Alzheimer's disease? J Gastroenterol 1997;52A:M76-M79.
70. Ebly EM, Schaefer JP, Campbell NR, Hogan DB. Folate status, vascular disease and cognition in elderly Canadians. Age Ageing 1998;27:485-91.
71. Little A, Levy R, Chuaqui-Kidd P, Hand D. A double-blind, placebo controlled trial of high-dose lecithin in Alzheimer's disease. J Neurol Neurosurg Psychiatry 1985;48:736-42.
72. Gauthier S, Bouchard R, Lamontagne A, et al. Tetrahydroaminoacridine-lecithin combination treatment in patients with intermediate-stage Alzheimer's disease. Results of a Canadian double-blind, crossover, multicenter study. N Engl J Med 1990;322:1272-6.
73. Chatellier G, Lacomblez L. Tacrine (tetrahydroaminoacridine; THA) and lecithin in senile dementia of the Alzheimer type: a multicentre trial. Groupe Francais d'Etude de la Tetrahydroaminoacridine. BMJ 1990;300:495-9.
74. Fitten LJ, Perryman KM, Gross PL, et al. Treatment of Alzheimer's disease with short- and long-term oral THA and lecithin: a double-blind study. Am J Psychiatry 1990;147:239-42.
75. Eagger SA, Levy R, Sahakian BJ. Tacrine in Alzheimer's disease. Lancet 1991;338:50-1 [letter; comment].
76. Birkmayer JGD. Coenzyme nicotinamide adenine dinucleotide: New therapeutic approach for improving dementia of the Alzheimer type. Ann Clin Lab Sci 1996;26:1-9.
77. Crook T, Petrie W, Wells C, Massari DC. Effects of phosphatidylserine in Alzheimer's disease. Psychopharmacol Bull 1992;28:61-6.
78. Amaducci L. Phosphatidylserine in the treatment of Alzheimer's disease: results of a multicenter study. Psychopharmacol Bull 1988;24:130-4.
79. Engel RR, Satzger W, Gunther W, et al. Double-blind cross-over study of phosphatidylserine vs. placebo in patients with early dementia of the Alzheimer type. Eur Neuropsychopharmacol 1992;2:149-55.
80. Heiss WD, Kessler J, Mielke R, et al. Long-term effects of phosphatidylserine, pyritinol, and cognitive training in Alzheimer's disease. A neuropsychological, EEG, and PET investigation. Dementia 1994;5:88-98.
81. Gindin J, Novikov M, Kedar D, et al. The effect of plant phosphatidylserine on age-associated memory impairment and mood in the functioning elderly. Rehovot, Israel: Geriatric Institute for Education and Research, and Department of Geriatrics, Kaplan Hospital, 1995.
82. Jorissen BL, Brouns F, Van Boxtel MPJ, et al. The influence of soy-derived phosphatidylserine on cognition in age-associated memory impairment. Nutr Neurosci 2001;4:121-34.
83. Hishikawa N, Takahashi Y, Amakusa Y, et al. Effects of turmeric on Alzheimer's disease with behavioral and psychological symptoms of dementia. Ayu 2012;33:499-504.
84. Clarke R, Smith D, Jobst KA, et al. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 1998;55:1449-55.
85. Snowdon DA, Tully CL, Smith CD, et al. Serum folate and the severity of atrophy of the neocortex in Alzheimer disease: findings from the Nun study. Am J Clin Nutr 2000;71:993-8.
86. Joosten E, Lesaffre E, Riezler R, et al. Is metabolic evidence for vitamin B-12 and folate deficiency more frequent in elderly patients with Alzheimer's disease? J Gastroenterol 1997;52A:M76-M79.
87. Ebly EM, Schaefer JP, Campbell NR, Hogan DB. Folate status, vascular disease and cognition in elderly Canadians. Age Ageing 1998;27:485-91.
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