Alzheimer's Disease

[Guest guest]

Chris-

>What DOES seem causal, from what I've read so far (and I'll discover

>more as I go along...) is DHA depletion, which is reversable by adding

>DHA to the diet, and which is related to a high rate of DHA oxidation

>in familial AD-mutant genes. (Adding DHA reverses the cognitive

>decline and neurodegeneration while the high rate of oxidation

>persists, so the DHA depletion seems causal.) This has a relation to

>insulin resistance in the brain. Also, it appears that the APP

>protein itself (the protein that generates beta-amyloid when cleaved),

>especially the mutant form found in familial AD, inhibits heme

>oxygenase which generates bilirubin, and antioxidant, which is one of

>the factors in the high rate of oxidation. So interestingly, it

>appears that the intact APP, and not the beta-amyloid being cleaved

>from it, is the culprit.

Figures everyone's charging down the garden path.

Strangely, though, I've read good things about supplementation with pure

EPA (no DHA) for certain problems -- though not for Alzheimers.

>It seems to me that if it was the *increase* that was correlated

>rather than the absolute level of antibody, couldn't this just be a

>guage of immune system health and maybe therefore of general health?

That seems very plausible, but of course because of the crooked way they

designed the study, it would be hard to be sure. However, finding other

studies, particularly general-pop ones, of the same cognitive measures,

might shed some light.

-

[Guest guest]

On 7/28/05, Idol <Idol@...> wrote:

> >It seems to me that if it was the *increase* that was correlated

> >rather than the absolute level of antibody, couldn't this just be a

> >guage of immune system health and maybe therefore of general health?

>

> That seems very plausible, but of course because of the crooked way they

> designed the study, it would be hard to be sure. However, finding other

> studies, particularly general-pop ones, of the same cognitive measures,

> might shed some light.

Well here's the thing. In animal experiments, when beta-amyloid is

bound by something, kind of like a chelation therapy, it's carried out

of the blood, which causes an efflux from the brain and a subsequent

rise in cerebro-spinal fluid and blood plasma. No changes at all were

observed in CSF levels and blood plasma, and current technology

doesn't allow for monitoring brain levels in live humans. So it

*appeared*, at least, that there was no activity.

Second, I found it very annoying that they referenced the average

scores on tests in the literature for one test, and despite finding

that the 1/3 who didn't do better than average did considerably worse

than average, they didn't compare to averages for any of the other

tests. It seems like that's a really obvious point of interest!

Third, they invented their own way of measuring the anti-body levels,

which they called TAPIR. They also tested antibodies with ELISA,

which is the standard, and found ELISA results to have no predictive

value whatsoever for cognitive decline, whereas TAPIR had good

predictive value. So, they posted the TAPIR results in detail and

didin't include any of the ELISA data, and then argued that because

the TAPIR had predictive value, it must be more accurate than ELISA!

But wait a second... if the relationship with cognitive decline is

shown because of the TAPIR data's accuracy, but the accuracy is

affirmed by the fact that it showed a relationship to cognitive

decline... huh? I mean, they may be correct that TAPIR is more

accurate in assessing antibodies with specific binding affinity to

beta-amyloid, but it seems that that warrants more discussion than

they gave it.

Most of the drugs and supplements were evenly distributed except 20%

of the " control " group was taking estrogens and none of the

" experimental " group was taking estrogens.

The authors said that the study was the first experimental

confirmation of the beta-amyloid hypothesis, but the fact that the

authors themselves question whether any beta-amyloid was being carried

out of the brain certainly makes it inconclusive.

Chris

[Guest guest]

On 7/28/05, L. L. <llscott2000@...> wrote:

> Is there a site to list all the acronyms being used?

All the acronyms are in my post, except ELISA and TAPIR. ELISA is

enzyme-linked immunosorbent assay, and TAPIR is tissue amyloid-plaque

something, I forget.

Chris

[Guest guest]

Thanks, I found a great site that was a big help for me understanding this new

vocabulary.

http://www.vitacost.com/science/index.html

Re: Alzheimer's Disease

On 7/28/05, L. L. <llscott2000@...> wrote:

> Is there a site to list all the acronyms being used?

All the acronyms are in my post, except ELISA and TAPIR. ELISA is

enzyme-linked immunosorbent assay, and TAPIR is tissue amyloid-plaque

something, I forget.

Chris

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Alzheimer's Disease Also indexed as: Dementia, Senile Dementia Overview What you need to know Recent scientific studies reveal promising results for preventing and treating this memory-robbing disease. According to this 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 These recommendations are not comprehensive and are not intended to replace the advice of your doctor or pharmacist. Continue reading the full Alzheimer's disease article for more in-depth, fully-referenced information on medicines, vitamins, herbs, and dietary and lifestyle changes that may be helpful. About Alzheimer's disease Alzheimer's disease is a brain disorder that occurs in the later years of life. People with Alzheimers 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. Check list Product ratings for Alzheimer's disease Rating Nutritional Supplements Herbs Ginkgo Acetyl-L-carnitineVitamin B1Vitamin E Huperzine ALemon BalmPeriwinkleSage Coenzyme Q10 (in combination with iron and vitamin B6)DHEADMAE (2-dimethylaminoethanol)Fish oilFolic acidLecithinNADHPhosphatidylserine (bovine brain PS only; soy-derived PS does not appear to be effective)Vitamin B12 Bacopa Reliable and relatively consistent scientific data showing a substantial health benefit. Contradictory, insufficient, or preliminary studies suggesting a health benefit or minimal health benefit. An herb is primarily supported by traditional use, or the herb or supplement has little

scientific support and/or minimal health benefit. Symptoms What are the symptoms? 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. Diet Dietary changes that may be

helpful Whether aluminum in the diet can cause Alzheimer's disease remains controversial.3, 4 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.5 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. 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.6, 7, 8 Whether these associations represent cause and effect is unknown. Lifestyle Lifestyle changes that may be helpful 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.9 Supplements Vitamins that may be helpful Several clinical trials have found that acetyl-L-carnitine

supplementation delays the progression of Alzheimer's disease,10 improves memory,11, 12, 13 and enhances overall performance in some people with Alzheimer's disease.14, 15 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.16 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.17 A typical supplemental amount is 1 gram taken three times per day. 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.18 Other preliminary research shows that higher blood levels of vitamin E correlate with better brain functioning in middle-aged and older adults.19 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.20 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.21 Vitamin B1 is involved in nerve transmission in parts of the brain (called cholinergic neurons) that deteriorate in Alzheimer's disease.22, 23 The activity of vitamin B1-dependent enzymes has been found to be lower in the brains of people with Alzheimer's disease.24 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.25, 26 However, another double-blind trial using the same amount for a year found no effect on mental function.27 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.28 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.29 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.30 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.31 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.32 Soy-derived PS was also ineffective in a double-blind study of elderly people with age-related cognitive decline.33 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.34 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.35, 36, 37, 38 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.39 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.40 However, a subsequent double-blind trial found no significant benefit from DMAE supplementation in people with Alzheimer's disease.41 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.42 Studies in the test tube have shown that zinc can cause biochemical changes associated with Alzheimer's disease.43 For that reason, some scientists have been concerned that zinc supplements might promote the development of this disease. However, in a study of four people with Alzheimer's disease, supplementation with zinc (30 mg per day) actually resulted in improved mental function.44 In a recent review article, one of the leading zinc researchers concluded that zinc does not cause or worsen Alzheimer's disease.45 A small, preliminary trial showed that oral NADH (10 mg per day) improved mental function in people with Alzheimer's disease.46 Further studies are necessary to confirm these early results. Some researchers have found an association between Alzheimer's disease and deficiencies of vitamin B12 and folic acid;47,

48 however, other researchers consider such deficiencies to be of only minor importance.49 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.50 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. Most,51, 52, 53, 54 but not all,55, 56 studies have found that people with Alzheimer's disease have lower blood DHEA 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.57 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.58 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. Are there any side effects or interactions? Refer to the individual supplement for information about any side effects or interactions. Herbs Herbs that may be helpful 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 (GBE) may improve memory and quality of life and slow progression in the early stages of the disease. In addition, four double-blind trials have shown that GBE 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.59, 60, 61, 62 GBE has been found to be nearly as effective against Alzheimer's disease

as donepezil, a prescription drug used to treat the condition.63 One trial reported no effect of GBE supplementation in the treatment of Alzheimer's disease, vascular dementia or age-associated memory impairment.64 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.65 Research studies have used 120 to 240 mg of GBE, standardized to contain 6% terpene lactones and 24% flavone glycosides per day, generally divided into two or three portions. GBE may need to be taken for six to eight weeks before desired actions are noticed. 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.66 Another double-blind trial using injected huperzine A confirmed a positive effect in people

with dementia, including, but not limited to, Alzheimer's disease.67 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.68 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. 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,69 but vincamine itself was shown to be beneficial in a later double-blind trial.70 In a double-blind trial, supplementation with an extract of lemon balm ( officinalis) for 16 weeks significantly improved cognitive function and significantly reduced agitation, compared with a placebo, in people with Alzheimer's disease.71 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. 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.72 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. Animal studies have found the Ayurvedic herb bacopa has constituents that enhance several aspects of mental function and learning ability.73, 74, 75 A controlled study found that a syrup containing an extract of dried bacopa herb

given to children improved several measures of mental performance.76 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.77 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.78 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.79 Are there any side effects or interactions? Refer to the individual herb for information about any side effects or interactions. References at this link: http://www.peacehealth.org/kbase/cam/hn-1007001.htm

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