Additional Nutrients Your Brain Needs by Age 55-60

Additional Nutrients Your Brain Needs By Age 55-60

- Dr. James Meschino, DC, MS, ROHP

Table Of Content

Introduction How The Brain Deteriorates As We Age CDP-Choline Phosphatidylserine Acetyl-L-Carnitine Bacopa Monnieri Huperzine A Don’t Take Brain Support Supplements With Other Alzheimer’s disease Or Brain Support Medications Without Your Doctor’s Consent Take Brain Support Supplements Before The Age-related Changes Get To You Other Brain Support Supplements Are Dangerous And Should Be Avoided Introduction

Another aspect of aging that must be addressed is the decline in brain function that is programmed into our aging clock. One of the saddest situations that we often see in life, is a person who has taken good care of themselves over their lifetime, who have worked to remain in good physical shape well into their sixties, seventies or eighties, only to develop senile dementia, Alzheimer’s disease or some form of significant memory loss and decline in mental capacities. Having our minds deteriorate while remaining in good physical health is one of the outcomes that we fear most, as we grow older, because most of us have seen or experienced the devastating emotional trauma felt by both the afflicted individual and their inner circle of family and friends. Approximately 6-8% of all persons aged 65 and older have Alzheimer’s disease, with the prevalence of the disease doubling every 5 years, such that as many as 47% of persons 85 years of age and older have Alzheimer’s disease.

It is indeed, a disease that creates one of life’s most difficult and heart-wrenching situations. If there were a method to prevent this from happening to us, or our loved ones, I know it would be of great interest to many people.. Researchers in the ant-aging world have made some significant progress in this area in recent years. Their revolutionary discoveries have demonstrated that certain natural agents, when taken as nutritional supplements, can slow or reverse many of the age-related changes in the brain that make us susceptible to memory loss and decline in our mental capacities. As such, the use of an all-in-one supplement, containing brain and memory enhancing natural agents, is another ant-aging supplement I suggest you consider taking each day, beginning between ages 50 and 60. How The Brain Deteriorates As We Age

There are two essential components of the aging process that result in a decline in mental acuity and memory loss that commonly occur as we age. The first component involves the cumulative damage to our brain cells caused by free radicals over our lifetime. As I mentioned previously, the brain consumes at least 10% of the body’s oxygen at any given moment, which it requires to support its high demand for energy production. As a consequence, the high utilization of oxygen by brain cells gives rise to oxygen free radicals, which have been shown to damage brain cells and possibly encourage the formation of the amyloid protein that promotes the development and progression of Alzheimer’s disease. Thus, the older we get, the greater is our brain’s cumulative lifetime exposure to free radicals, and the more extensive becomes the damage to our brain cells. Free radical damage is known to disrupt the normal functioning of brain cells, such that as we get older some brain cells become completely destroyed by the many years of free radical attack, or their function becomes significantly impaired. As noted in Step 2, studies show that you can protect your brain from free radical damage to a significant degree by ingesting a high potency multi-vitamin that is enriched with certain levels of antioxidant supplements (e.g. vitamin E, beta-carotene, vitamin C etc.) throughout your lifetime. Supplementation with melatonin may also be important in this regard after the age of 40-50. Lifetime antioxidant supplementation is emerging as a key foundation step in preventing age-related memory loss and a decline in mental acuity as we age. Without a doubt, it is the first consideration that must be addressed in regards to slowing the age-related decline in brain function and preserving the number of functional brain cells as we age.

The second component of brain aging that leads to a reduction in mental acuity, and greatly contributes to memory loss and Alzheimer’s-type dementia, is the age-related decrease in the synthesis of certain brain chemicals known as neurotransmitters. For instance, after a certain age it appears that our body’s our genetically programmed to make less of the enzyme responsible for making the brain chemical that is responsible for memory. This brain chemical, which provides us with memory and recall ability, is known as acetylcholine. Throughout our lifetime the enzyme choline acetyltransferase attaches choline (a B-vitamin-like substance) to acetyl coenzyme A to make acetylcholine, which enables us to retrieve things from the brain’s memory bank, and maintain our ability to learn and process information on a cognitive levels. After the age of 60 there is often a significant drop off in acetylcholine synthesis, due to reduced activity of the choline acetyltransferase enzyme. If the decline is severe enough, this results in progressive memory loss and other manifestations of cognitive decline commonly seen in aging. The good news is that several natural supplements can help boost the brain’s synthesis of acetylcholine and other important brain chemicals back to more functional levels, or slow the breakdown of these important neurotransmitters, by inhibiting certain brain enzymes that destroy acetylcholine and other neurotransmitter agents. The net result of supplementation with these brain-specific natural supplements is that the brain levels of acetylcholine and other important neurotransmitters, required for optimal mental acuity, can be returned to more youthful levels. Thus, I recommend that between ages 50-60, you begin to introduce a brain support nutritional supplement into the your anti-aging regiment, as a vital means to counter the body’s internal program that otherwise encourages cognitive decline, memory loss and dementia as we age. Let’s look at how these brain support nutrients have been shown to help combat age-related memory loss, cognitive decline and other aspects of failing mental acuity. CDP-Choline

CDP-Choline (cytidine 5-diphosphocholine or citidinediphosphocholine or citicholine) is a recently discovered nutrient that has been shown to be very effective in the management of senile dementia, Alzheimer’s disease and Parkinson’s disease. It has been known for many years that choline (a B- vitamin-like substance) is an essential component of the outer skin (cell membrane) of brain cells and is a building block of the brain chemical required for memory known as acetylcholine. The brain makes acetylcholine by attaching choline to acetyl coenzyme A, a process that requires the enzyme choline acetyltransferase. A very rich source of choline is found in a product called lecithin, which has received a great deal of attention over the years in the health food and wellness industry. Most lecithin supplements only contain 10-20% choline, but higher yield lecithin products are now available that contain up to 90% choline content, and these are much superior, if you are a lecithin user. However, the use of lecithin as a supplement to increase brain levels of acetylcholine and reverse mental decline in patients with senile dementia and Alzheimer’s disease has been disappointing in the trials performed to date. This is where CDP-Choline comes in. Unlike lecithin, choline delivered to the brain in the form of CDP-Choline has been shown to increase brain levels of acetylcholine and thereby improve many signs and symptoms of cognitive decline.

CDP-Choline is an essential building block in the synthesis of certain structural components called phospholipids that make up the outer skin (cell membranes) of brain cells. These phospholipids in the nerve cell membrane are responsible, in part, for the conduction of electrical impulses that move across the brain, enabling us to think and function as we do as cognitive beings. After oral administration, CDP-Choline has been shown to cross the blood-brain barrier and reach the central nervous system, where it is incorporated into the phospholipid fraction of the brain cell membrane and other components of the cell. CDP-Choline supplementation has been shown to activate the synthesis of structural phospholipids in the brain, increase brain cell metabolism and increases the synthesis of various neurotransmitters required for mental acuity. Human trials reveal that CDP- Choline has been effective in cases of senile cognitive impairment (e.g., Alzheimer’s disease), slowing the progression of the disease, and in the management of Parkinson’s disease. Further, CDP-Choline also has been shown experimentally to increase noradrenaline and dopamine levels in the central nervous system, which are two vital brain chemicals required for many cognitive and unconscious brain functions. CDP-Choline also has been shown to accelerate the resorption of cerebral swelling (edema) in various experimental models. In studies carried out on the treatment of patients with head trauma, CDP-Choline accelerated the recovery from post-traumatic coma and the recuperation of walking ability. Its use achieved a better final functional result and reduced the hospital stay of these patients, in addition to improving the cognitive and memory disturbances which are normally observed after head trauma of lesser severity and which constitute the disorder known as post-concussion syndrome. Of particular note is the fact that CDP-Choline is well tolerated by patients and no serious side effects have occurred in any of the groups of patients treated with high doses of CDP-Choline, in the range of 1,000 mg per day. Toxicology studies also indicate that it is a safe intervention and highlight the fact that CDP-choline produces no adverse effects on the brain function.

The proven ability of CDP-choline to enter the brain and increase synthesis of acetylcholine and other important brain chemicals, as well as its ability to preserve the structural integrity of the brain cell membrane (outer skin of brain cells), suggests that CDP-choline can help forestall important age-related changes that contribute to the decline in memory and cognitive capabilities that commonly accompany advancing age.It is the most reliable form of choline supplementation available to support our brain synthesis of the memory chemical acetylcholine. Phosphatidylserine

Phosphatidylserine is the major phospholipid in the brain and plays a role in determining the integrity and fluidity of nerve cell membranes (the outer skin of brain cells). The brain can manufacture phosphatidylserine, but requires folic acid, vitamin B12 and S-adenosylmethionine as cofactors (methyl donors) for its synthesis. Low levels of phosphatidylserine in the brain are associated with impaired cognitive function and depression in the elderly. In Italy, Scandinavia and other parts of Europe phosphatidylserine supplementation is widely used to help restore declining mental function and depression in the elderly. As noted, the body makes its own phosphatidylserine, but as we age there appears to be a requirement for phosphatidylserine supplementation to prevent or treat mental decline and memory loss, at proven therapeutic dosages.

The serine portion of phosphatidylserine can also be converted in the brain into choline and thereby significantly improve acetylcholine synthesis, aiding memory and reversing some age-related brain changes in recall ability and cognitive function. As stated previously, acetylcholine is the neurotransmitter (brain chemical) required for memory. Thus, phosphatidylserine supplementation can help maintain memory and cognitive function via its participation as a vital phospholipid component of the nerve cell membrane and as a bioactive agent that can increase brain levels of the memory chemical acetylcholine.

Numerous studies involving elderly patients (65-93 yrs) with moderate to severe senility, as well as depressed elderly patients, have demonstrated significant improvement in memory, behaviour, mood states, and cognitive function with phosphatidylserine supplementation of 100 mg, three times daily. A number of double-blind studies, involving more than 1,000 patients suggest that phosphatidylserine supplementation improves behaviour and mental function in patients with moderate to severe mental decline, including Alzheimer’s disease patients. This is largely attributable to the role that phosphatidylserine plays within the nerve cell membrane, aiding the conduction of nerve impulses and improving the movement of nutrients in and out of nerve cells. The serine fraction of Phosphatidylserine can also be converted into choline within the brain and is used as building block from which brain cells can synthesize acetylcholine, the neurotransmitter required for memory function.

Most of the studies cited above, used bovine (cow-brain)-derived phosphatidylserine, a product that is no longer available (due to the possible risk of “mad cow” disease, or more correctly Creutzfeld- Jacob disease). Most of the phosphatidylserine available in the marketplace today is derived from soy, but there have been only a limited number of studies using this source of phosphatidylserine in studies evaluating cognitive function. Soy-derived Phosphatidylserine is a relatively new product. Soy and bovine-derived phosphatidylserine are not chemically identical; however, preliminary animal studies show that soy-derived Phosphatidylserine does have effects on brain function similar to that of bovine-derived, and it is undoubtedly a safer substance. Phosphatidylserine supplementation is extremely safe (soy-derived) and no significant side effects or adverse reactions have been noted with its use other than mild gastrointestinal distress on rare occasions. As a means to support brain levels of acetylcholine and to preserve the integrity of the brain cell membrane as we age, I recommend that an all-in-one brain support supplement include an adequate amount of soy- derived phosphatidylserine. Acetyl-L-Carnitine

Acetyl-L-Carnitine (ALC) is normally produced by the body with high concentrations found in the brain, muscles, liver, kidney, and testes. The carnitine portion of ALC participates in the burning of fat, which releases the energy required (ATP energy) for cells to stay alive and perform their various specialized functions. The acetyl portion of ALC provides the brain with one of the building blocks to make the memory chemical known as acetylcholine.

Studies show that as we age our bodies make less ACL, which may deprive the brain and other tissues of optimal concentrations of this important nutrient.

Several double-blind clinical trials have shown improvement in Alzheimer’s disease patients and other patients age-related cognitive impairment problems, when AL C was administered at daily dosages ranging from 1,000-2,000 mg per day. ACL supplementation provides three important effects on brain cells to enable them to produce more optimal levels of the memory chemical, acetylcholine. ACL facilitates enhanced energy production by brain cells for the production of acetylcholine. The acetyl portion of ACL provides the brain with an essential raw material for acetylcholine synthesis, and ACL promotes the synthesis of cardiolipin, which is a fatty material (phospholipid) required by the brain cells for optimal energy production.

It is thought that the decline in ACL synthesis by the body after age 50 is a major contributing factor to age-related cognitive impairment and possibly Alzheimer’s disease. Both animal and human studies demonstrate that ACL supplementation increases brain concentration of this vital nutrient and improves brain function and memory in individuals with early to moderate memory loss and cognitive impairment. ACL has been shown to be a very non-toxic, and extremely safe supplement for human use. Rare side effects from its use include skin rash, nausea, vomiting agitation. By age 60 I believe all individuals should take a moderate dose of ACL, as part of a brain support supplement, in order to maintain optimal brain levels of this vital nutrient and help forestall age-related decline in cognitive performance. Bacopa Monnieri

The leaf of Bacopa, or water hyssop, has been used in the Indian medical system of Ayurveda since the 6th century A.D. to help improve mental performance. Its active ingredients (bacosides A and B) have been shown to enhance nerve transmission and are potent antioxidants, which may help to protect brain cells and other lipid-rich tissues in the body from free radical damage (including LDL- cholesterol). Under experimental conditions 100 mcgs of Bacopa monnieri extract was equivalent to 247 micrograms of EDTA and 58 micrograms of Vitamin E in regards to its antioxidant potency. Bacopa is presently being used and studied as a natural substance to strengthen memory and general cognition and to help control epilepsy.

The primary active constituents in Bacopa include Bacosides A and B. The alcohol fraction of Bacopa extract has been shown to provide its strong antioxidant properties. Studies demonstrate that Bacopa supplementation can increase learning ability in laboratory animals. Human studies have also provided evidence that Bacopa may improve intellectual activity in children as well as improve memory and mental performance in adults. As such, it may be of value in the preservation of cognitive function and memory as we age and in the treatment of dementia and other severe cognitive dysfunction states (e.g., Alzheimer’s disease). In the study by C Stough et al, healthy volunteers were given Bacopa monnieri supplementation (300 mg per day) or a placebo, with follow- up neuropsychological testing performed at weeks 5 and 12. Compared to the placebo group, the subjects given the Bacopa significantly improved speed of visual information processing, learning rate, memory consolidation and demonstrated a reduced state of anxiety. The researchers concluded that these findings suggest that Bacopa monnieri may improve higher order cognitive processes that are critically dependent on the input of information from our environment such as learning and memory. Ayurvedic practitioners have routinely recommended Bacopa supplementaion for impaired memory or cognitive dysfunction for many centuries with reported good results. There are no well-known side effects from the use of Bacopa monnieri at recommended doses. It has demonstrated a long and safe history of use in Ayurvedic medicine. I strongly recommend its inclusion in an all-in-one brain support supplement to be taken daily by individuals, beginning at ages 50-60.

Huperzine A

Huperzine A is an extract from a club moss (from the Lycopodiaceae family) that has been used for centuries in Chinese folk medicine for a variety of conditions. In modern times Huperzine A research has focused on its ability to raise brain levels of the memory chemical acetylcholine, hence its potential role in the treatment and prevention of Alzheimer’s Disease, dementia and other cases of memory and learning impairment.

Huperzine A or HupA is a specific alkaloid compound that is found in very low concentrations in the moss where it occurs naturally at only a 1% concentration. Thus, when used therapeutically, Huperzine A is given as a concentrated extract. Commercially available extracts contain up to 95% HupA concentration. HupA was first synthesized in 1990, which has helped to increase its availability in the marketplace.

Huperzine A has been shown to be effective in treating Alzhiemer’s disease and dementia. In a double-blind trial with Alzheimer’s disease patients, the group given 200 mcg of Huperzine A, twice per day for eight weeks demonstrated significant improvement in memory, cognitive and behavioural functions. Huperzine A has been used successfully in a clinical setting with approximately 100,000 Alzheimer’s and dementia patients in China. At Beijing’s Institute of Mental Health, Huperzine A was tested against fodine (a drug for Alzheimer’s disease) in 101 patients with benign senescent forgetfulness (age-related memory impairment). After four weeks of supplementation, 70% of the group receiving Huperzine A showed significant improvement in their memory as measured by memory quotient (MQ). An additional 111 Alzheimer’s patients were also included in the study. Overall, the group receiving HupA demonstrated a 10% improvement in the memory quotient over the four- week test period, and significant improvement in other measures of cognitive function. Side effects occurred in only 3% of these patients, with the most frequent side effects involving dizziness and gastrointestinal symptoms. In a study done at Zhejiang Medical University in Shanghai, 103 patients with Alzheimer’s disease were given 200 mcg of HupA per day or a placebo. After eight weeks, 58% of those receiving HupA showed marked improvement in mental function, compared to 36% in the placebo group. In another double-blind study, the administration of Huperzine A at 100-150 mcg two to three times per day, was shown to be more effective than the drug piracetam in a trial involving patients with age-related cognitive decline. Animal research shows that Huperzine A has a greater ability to preserve acetylcholine levels than may be available through the use of some prescription drugs that act as acetylcholinesterase inhibitors. The enzyme acetylcholinesterase is the enzyme that breaks down acetylcholine in the brain.

Animal studies show that Huperzine A supplementation provides animals with memory-enhancement and a broad range of improved cognitive behaviors. There is some suggestion that Huperzine A supplementation in otherwise normal individuals can enhance memory and recall ability as well as learning capacity. In a small controlled trial of adolescent middle school students, the administration of 100 mcg of Huperzine A two times per day, was shown to be effective in improving memory and learning performance over a four week period. Although no side effects were reported, the researchers caution that this was a high dose of Huperzine A for subjects with no apparent signs of acetylcholine deficiency and the long term safety of such a practice needs to be established before young, healthy individuals should ingest doses in this range in an attempt to boost their learning capacity. HupA is rapidly absorbed by the brain where it acts as a potent, reversible, and selective inhibitor of the enzyme acetylcholinesterase, which breaks down the memory chemical acetylcholine. By inhibiting this enzyme, brain concentrations of acetylcholine are increased, thereby facilitating improvements in memory and learning capacity. A hallmark feature of Alzheimer’s disease is reduced concentrations of acetylcholine in specific areas of the brain involved with memory and other cognitive functions. Huperzine A supplementation appears to help increase acetylcholine levels in Alzheimer’s patients in cases where the condition has not yet advanced to the point where brain cells are permanently damaged.

Studies show that Huperzine A provides a longer acting effect than the drugs tacrine and doneprizil, which are used in Alzheimer’s disease, and it also appears to produce fewer side effects. This is due to the fact that only very small doses of Huperzine A are required due to its high specificity for the acetylcholinesterase enzyme. As such, HupA is under intensive investigation as a viable intervention in the prevention and treatment of Alzheimer’s disease, dementia, and other conditions involving learning and memory impairment. Further, it has recently been reported that HupA also reduces neuronal death (death of nerve cells) caused by glutamate (glutamate toxicity results in seizures associated with exposure to nerve gas), suggesting that HupA may act to protect brain cells from various types of degenerative damage and chemical insults. The dual bio-activities (preserving acetylcholine and protecting nerve cells) make HupA an attractive agent to include as a supplement to help preserve brain function as we age and counter the age-related decline in cognitive function programmed into the body’s aging clock. Side effects associated with Huperzine A supplementation are rare at recommended doses, but may include dizziness and gastrointestinal symptoms.

Don’t Take Brain Support Supplements With Other Alzheimer’s disease Or Brain Support Medications Without Your Doctor’s Consent

Individuals with Alzheimer’s disease, dementia, depression or other mental or psychological ailments, who are on medication for these problems, must check with their attending physician before supplementing your diet with the herbal and accessory nutrients mentioned above. Combining prescription medications with these supplements may boost the effectiveness of certain drugs to a point where it can cause toxicity leading to severe and life threatening side effects. For instance, Donepezil and Tacrine used to treat Alzheimer’s disease patients should not be combined with the herbal and accessory nutrients I have described in this section on brain nutrients. Like Huperzine A, these drugs inhibit the breakdown of acetylcholine and therefore, the addition of Huperzine A, CDP- choline, phosphatidlyserine, and/or ginkgo biloba may boost concentrations of acetylcholine to toxic levels, increasing the likelihood of developing cholinergic syndrome as a serious side effect. The drugs Donepezil and Tacrine, on their own can produce signs of acetylcholine toxicity in that they are are noted for the side effects of vomiting, excess saliva and tear production, and increased sweating, which indicate their tendency to over stimulate the cholinergic system. (aceetylcholine neurotransmitter system). Thus, the addition of Huperzine A, CDP-Choline, phosphatidylserine and/or ginkgo biloba, in these cases is not advisable. Take Brain Support Supplements Before The Age-related Changes Get To You

From a standpoint of prevention, it is advisable in my opinion, to take an all-in-one brain support supplement beginning between ages 50 and 60, as means to combat the body’s programming for age-related decline in memory ability and cognitive function. This brain support supplement should be used in conjunction with a life long practice of supplementation with a high potency multi-vitamin and mineral, and an essential fatty acid supplement, both of which also contain nutrients that play a vital role in preserving the functional integrity of our brain cells.

An example of an all-in-one brain support supplement that I recommend for prevention and anti- aging purposes includes the following ingredients and dosages on a per capsule basis:

1. CDP-Choline - 50 mg 2. Phosphatidylserine – 50 mg 3. Huperzine A - 25 mcg 4. Bacopa Monnieri – 50 mg (standardized to 20% bacosides content) 5. Acetyl-L-Carnitine – 150 mg

I recommend taking two capsules per day for brain support beginning between ages 50-60 years of age. Other Brain Support Supplements Are Dangerous And Should Be Avoided

There are three other brain support supplements that may offer benefit to preserving or restoring memory and other aspects of cognitive function, however, the side effects associated with these supplements make them a risky intervention. I therefore, do not recommend them as daily anti-aging supplements to support brain function, on a preventive basis. These supplements include ginkgo biloba, vinpocetine and dimethylaminoethanol (Deanol).

Ginkgo biloba extract has been shown to increase blood flow to the brain and improve cases of memory loss, Alzheimer’s disease and age-related cognitive decline. Unfortunately, some of the active ingredients in ginkgo biloba extract produce a powerful anti-coagulant effect, which has caused internal bleeding in several reported cases and in some instances, the bleeding, has occurred in the brain.

Vinpocetine is an isolated substance from a plant called the lesser periwinkle. Like ginkgo biloba, vinpocetine also increases blood flow to the brain and has shown good success in patients with Alzheimer’s disease, ischemic stroke, dementia and chronic cerebral insufficiency (reduced blood flow to the brain causing disturbances in memory and cognitive function). Vinpocetine is also a very powerful anti-coagulant, which may increase risk of internal bleeding. As such, ginkgo biloba and vinpocetine should not be taken by individuals who regularly use other anti-coagualant drugs, including aspirin, coumadin, warfarin, Plavix etc. Even their concurrent use with garlic extract supplements or devil’s claw may increase the risk of internal bleeding as these herbal agents contain anti-coagulant substances, which have caused internal bleeding on their own in rare instances. Supplementation with ginkgo biloba and/or vinpocetine requires that you routinely have your bleeding time (prothrombin time or INR) assessed by your physician to ensure that you are not putting yourself at risk for a significant bleeding disorder. They should not be supplements that you take without the proper monitoring. Their indiscriminant use is not advised.

Dimethylaminoethanol (DMAE or Deanol) is another natural product that has been shown to possibly increase brain levels of choline. However, in clinical trials it has been associated with a number of frequent side effects including drowsiness, confusion, lucid dreams, depression, dull headache, increased tension of the jaw and other muscles, and insomnia. I therefore, don’t recommend its daily use as an anti-aging and preventive supplement. I do however, recommend that brain support combination formula outlined above which contains, CDP-choline, phosphatidylserine, bacopa monniera and huperzine A, as a supplement to be used for anti-aging and preventive purpose for individuals beginning at ages 50-60.

REFERENCES

Choline Agnoli A, et al. New strategies in the management of Parkinson’s disease: A biological approach using a phospholipid precursor (CDP- Choline) Neuropsycholbiology 1982;8(6):289-96 Canty DJ, et al. Lecithin and chloine in human health and disease. Nutr Reviews 1994;52:327-339 Citicoline, Alzheimer’s disease, and cognitive performance. Life Extension 2000:6(9):69,2(Alt Health Watch data base) Encyclopedia of Nutritional Supplements. Prima Publishing 1996;Murray M:137-141 Foiravanti M, Yanagi M. Cytidinediphosphocholine (CDP-Choline) for cognitive and behavioral disturbances associated with chronic cerebral disorders in the elderly. Cochrane Syst Revi 2002;(2):000269 In: The Cochrane Library, 1,2002. Oxford: Update Software Present Knowledge in Nutrition (5th edition). The Nutrition Foundation, Inc 1984;Choline:383-399 Secades JJ, et al. CDP-Choline: pharmacological and clinical review. Methods Find Exp Clin Pharmacol 1995;17(Suppl B):1-54 Zeisel SH, et al. Choline,an essential nutrient for humans. FASEB J 1991;5:20093-2098 Phosphatidylserine Cenacchi T, Bertoldin T, Farina C, et al. Cognitive decline in the elderly: A double-blind, placebo-controlled multicenter study on efficacy of phosphatidylserine administration. Aging 1993;5:123-33 Crook T, Petrie W, Wells C, Massari DC. Effects of phosphatidylserine in Alzheimer’s disease. Psychopharmacol Bull 1992;28:61-6 Crook TH, Tinklenberg J, Yesavage J, Petrie W, Nunzi MG, Massari DC. Effect of phosphatidylserine in age-associated memory impairment. Neurology 1991;41:644-9 Engel RR, Satzger W, Gunther W, Kathmann N, Bove D, Gerke S, et al. Double-blind cross-over study of phosphatidylserine vs. placebo in subjects with early cognitive deterioration of the Alzheimer type. Eur. Neuropsychopharmacol, 1992;2:149-55 Funfgeld EW, Baggen M, Nedwidek P, Richstein B, Mistlberger G. Double-blind study with phosphatidylserine (PS) in parkinsonian patients with senile dementia of Alzheimer’s type (SKAT). Prog Clin Biol Res 1989;317:1235-46 Healthnotes Online. Healthnotes Inc, 2000 Maggioni M, Picotti GB, Bondiolotti GP, Panerai A, Cenacchi T, Nobil P, et al. Effects of phosphatidylserine therapy in geriatric patients with depressive disorders. Acta Psychiatr Scand 1990;81:265-70 Murray M. Encyclopedia of Nutritional Supplements. Rocklin, CA: Prima Publishing 1996; 356-358 Natural Products Encyclopedia. www.consumerlab.com Phosphatidylserine Nunzi MG, Milan F, Guidolin D, et al. Effects of phosphatidylserine administration on age-related structural changes in the rat hippocampus and septal complex. Pharmacopsychiat 1989;22:125-8 Valzelli L, Kozak W, Zanotti A, Toffano G. Activity of phosphatidylserine on memory retrieval and on exploration in mice. Meth Find Extl Clin Pharmacol 1987;9:657-60 Vannucchi MG, Casamenti F, Pepeu G. Decrease of acetylcholine release from cortical slices in aged rats: Investigations into its reversal by phosphatidylserine. J Neurochem 1990;55:819-25 Acetyl-L-Carnitine Calvani M, Carta A, Caruso G, Bendetti N, Iannuccelli M. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Ann NY Acad Sci 1993;663:483-6 Cipolli C, Chiari G. Effects of L-acetylcarnitine on mental deterioration in the aged: initial results. Clin Ther 1990;132:479-510 Garzya G, Corallo D, Fiore A, Lecciso G, Tetrelli G, Zotti C. Evaluation of the effects of the L-acetylcarnitine on senile patients suffering from depression. Drugs Exp Clin Res 1990;16(2):101-6 Pettegrew JW, Klunk WE, Panchalingam K, Kanfer JN, McClure RJ. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Agin 1995;16:1-4 Sano M, Bell K, Cote L, Dooneief G, Lawton A, Legler L, et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol 1995;49:1137-41 Savioli G, Neri M. L-acetylcarnitine treatment of mental decline in the elderly. Drugs Exp Clin Res 1994;20:169-76 Spagnoli A, Lucca U, Menasce G, Bandera L, Cizza G, Forloni G, et al. Long-term acetyl-L-carnitine treatment in Alzheimer’s disease. Neurology 1991;41:1726-32 Tempesta E, Casella L, Pirrongelli C, Janiri L, Calvani M, Ancona L. L-acetylcarnitine in depressed elderly subjects. A cross-over study vs. placebo. Drugs Exp Clin Res 1987;8:417-23 Vecchi GP, Chiari G, Cipolli C, et al. Acetyl-L-carnitine treatment of mental impairment in the elderly: evidence from a multicenter study. Arch Gerontol Geriatr 1991;2(Suppl):159S-68S Bacopa Monnieri (Bacopa) Dar A, Channa S. Calcium antagonistic activity of Bacopa monniera on vascular intestinal smooth muscles of rabbit and ginea-pig. J Ethnopharmacol 1999;66(2):167-74 Dietary Supplement Information Bureau. www.content.intramedicine.com: Bacopa monnieri Kidd PM. A review of nutrients and botanicals in the integrative management of cognitive dysfunction. Altern Med Rev 1999 Jun;4(3):144-61 Mukherjee GD et al. Clinical trial on brahmi. I. J Exp Med Sci 1966;10(1):5-11 Stough C, Lloyd J, Clarke J, Downey LA, Hutchison CW, Rodgers T, et la. The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects. Psychopharmacology (Berl) 2001 Aug;156(4):481-4 Tripathi YB, et al. Bacopa monniera linn. As an antioxidant: Mechanism of action. Indian J Exp Biol 1996 Jun;34(6):523-6 Vohora D, Pal SN, Pillai KK. Protection from phenbytoin-induced cognitive deficit by Bacopa monniera, a reputed Indian nootropic plant. J Ethnopharmacol 2000 Aug;71(3):383-90 Huperzine A Ashani Y, Peggins JO, Doctor BP. Mechanism of inhibition of cholinesterases by huperzine A. Biochem Biophys Res Commun, 1992:184:719- 26 Bai DL, et al. Huperzine A, a potential therapeutic agent for treatment of Alzheimer’s disease. Curr Med Chem, 2000 Mar;7(3):355-74 Cheng DH, Ren H, Tang XC. Huperzine A, a novel promising acetylcholinesterase inhibitor. Neuroreport 1996;8:97-101 Cheng DH, Tang XC. Comparative studies of huperzine A, E2020, and tacrine on behavior and cholinesterase activites. Pharmacol Biochem Behav 1998;60:377-86 Dworkin N. Restoring memory. Psychology Today 2000 Jul/Aug;32(4):p28 McCaleb R. Huperzia looks promising for improving memory. HerbalGram, 10/31/1995;35:p14 Pirisi, Angela. Plant wisdom: Memory moss. Yoga Journal, 08/31/1999;147:p95 Sun QQ, Xu SS, Pan JL, et al. Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students. Acta Pharmacol Sin 1999;20:601-3 Tang XC. Huperzine A (shuangyiping): A promising drug for Alzheimer’s disease. Chung Kuo Yao Li Hsueh Pao, 1996 Nov;17(6):481-4 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 Choten Publishers 1999:39-50 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 Ginkgo Biloba, Vinpocetine and Dimethylaminoethanol Bereczki D, Fekete I. A systematic review of vinpocetine therapy in acute ischaemic stroke. Eur J Clin Pharmacol 1999;55:349–352 Braquet P, et al. Ethnopharmacology and the development of natural PAF antagonists as therapeutic agents. J Ethnopharmacol 1991 April;32(1-3):135-9 Braquet P. Anti-anaphylactic properties of BN 52021: A potent platelet activating factor antagonist. Advances in Experimental Medicine and Biology 1987;215:215-33 Casey DE. Mood alterations during deanol therapy. Psychopharmacology 1979;62:187-91 Dietary Supplement Information Bureau. www.intramedicine.com/DMAE Fisman M, Mersky H, Helmes E. Double-blind trial of 2-dimethylaminoethanol in Alzheimer’s disease. Am J Psychiatry, Jul1981;138(7):970-2 Fisman M, Mersky H, Helmes E. Double-blind trial of 2-dimethylaminoethanol in Alzheimer’s disease. Am J Psychiatry, 1981;138:970-2 Kiss B, Karpati E. Mechanism of action of vinpocetine [in Hungarian; English abstract]. Acta Pharm Hung 1996;66:213–214 Kleijnen J et al. Ginkgo biloba. Lancet 1992;340(8828):1136-9 Miyazaki M. The effect of a cerebral vasodilator, vinpocetine, on cerebral vascular resistance evaluated by the Doppler ultrasonic technique in patients with cerebrovascular diseases. Angiology. 1995;46:53–58 Natural Product Encyclopedia. www.consumerlab.com:Ginkgo Biloba Osawa M, Maruyama S. Effects of TCV-3B (Vinpocetine) on blood viscosity in ischemic cerebrovascular disease. Ther Hung 1985;33:7-12 Rosenblatt M, Mindel J. Spontaneous hyphema associated with ingestion of ginkgo biloba extract. N Engl J Med 1997 April 10;336(15):p1108 Rowin J, Lewis SL. Spontaneous bilateral subdural hematomas associated with chronic Ginkgo biloba ingestion. Neurology 1996 June;46(6):1775-6 Sergio W. Use of DMAE (2-dimethylaminoethanol) in the induction of lucid dreams. Med Hypotheses, 1988;26:255-7 Walker, Morton. Meical journalist report of innovative biologics: Forestalling the effects of aging with Dimethylaminoethanol. Townsend Letters for Doctors & Patients; 11/01/1990;8:752-6 White HL et al. Extracts of ginkgo biloba leaves inhibit monoamine oxidase. Life Sci 1996;58(16):1315-21

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