~Age-Associated Mental Impairment, Including "Senile Dementia"
Reprinted with permission of Life Extension®.
Many people experience a progressive decline in overall cognitive function as they age. Often this begins with a loss in their ability to store and retrieve from short-term memory and to learn new information that progressively worsens over the years.
This protocol has been designed specifically for those experiencing age-associated mental impairment due either to aging itself or an age-related disease.
Age-associated neurological impairment can take a variety of forms including memory loss, senility, and dementia. Dementia, a general term for diseases involving nerve cell deterioration, is defined as a loss in at least two areas of complex behavior -- areas including language, memory, visual and spatial abilities, and judgment-so as to interfere with a person's daily living. Dementia, the most serious form of age-associated mental impairment, is often a slow, gradual process that may take months or even years to become noticeable. Symptoms vary depending on which areas of the brain are affected.
A helpful guideline is that many people with serious mental impairment do not recognize or will not admit that they have a problem, while it is obvious to those around them. The recommendations given in this protocol can help age-associated mental impairment of any form or cause, but significant impairment arising from diseases such as stroke should be treated with the help of medical professionals.
Taking steps to improve overall health is highly recommended to prevent or minimize age-associated mental impairment. For example, exercising regularly, not smoking, and monitoring blood cholesterol level can reduce the risk of stroke and heart disease and keep arteries open, supplying the brain with oxygen and nutrients. Regular exercise improves some mental abilities by an average of 20 to 30%. Abstaining from alcohol or drug use, or minimizing it, can also help preserve mental function. Since people tend to eat less food as they age, the use of low-fat, nutrient-rich foods is recommended. Such a diet will help prevent nutrient deficiencies, which can impair mental function through physical illness.
The most commonly used memory-enhancing nutrients are choline, lecithin, and phosphatidylcholine, which are precursors to the chemical neurotransmitter acetylcholine that carries messages between brain cells. Because acetylcholine helps brain cells communicate with each other it plays an important role in learning and memory. Acetylcholine deficiency can predispose a person to a wide range of neurological diseases, including Alzheimer's disease and stroke.
One study found that phosphatidylcholine administered with vitamin B12 improved the memory of rats in which brain damage had caused memory impairment (Masuda et al. 1998).
A recent study reported by Buchman et al. (2001) examined the effects of choline chloride when given to patients receiving total parenteral nutrition (TPN). Significant improvements were found in the delayed visual recall of the Weschler Memory Scale-Revised, and borderline improvements were found in the List B subset of the California Verbal Learning Test (rote verbal learning ability) and the Trails A test (visual scanning, psychomotor speed and set shifting). The authors concluded that both verbal and visual memory may be impaired in patients who require long-term TPN and both may be improved with choline supplementation (Buchman et al. 2001).
Choline, lecithin, and phosphatidylcholine (in Cogitex, for example) are best taken early in the day to maximize improvement in brain productivity throughout the day. Suggested dosage ranges are 1,000 to 3,000 mg a day of choline or 10,000 mg a day of lecithin, and/or 100 to 600 mg a day of phosphatidylcholine.
NADH (nicotinamide adenine dinucleotide) is a coenzyme that acts as an electron carrier in the body. A recent study concluded that nicotinamide enhances brain choline concentrations by mobilizing choline from choline-containing phospholipids (Koppen 1996; Erb et al. 1998).
The recommended dose of NADH is 5 to 10 mg a day.
Extracts from Ginkgo biloba, the "maidenhair tree," have been shown to thin the blood and improve blood flow to the brain, protect against free radicals, and improve memory. Ginkgo biloba is approved in Germany for the treatment of dementia. There are over 1,200 published studies in the scientific literature on ginkgo biloba extract (Yoshikawa et al. 1999; DeFeudis et al. 2000; Diamond et al. 2000).
Treatment with ginkgo biloba extract can also partially prevent certain harmful, age-related structural changes as well as free radical damage to the mitochondria (where energy is produced in a cell) in the brains of old rats (Sastre et al. 1998).
In one study, patients with memory disturbances were supplemented with ginkgo biloba. Following ginkgo treatment, 15% of patients reported the total absence of memory disturbance symptoms, and 62% reported that the remaining symptoms were mild to moderate (Enrique Gomez 1997).
The recommended dose of ginkgo biloba extract is 120 mg per day.
Essential Fatty Acids
Essential fatty acids (EFAs) serve as the basic building block of nerve cells and are used as fuel for brain metabolism. They are used to make prostaglandins that regulate inflammation in the brain. About 75% of myelin (the sheath that covers nerve cells) is composed of fats.
Docosahexaenoic acid (DHA) is a long chain omega-3 fatty acid that is present in high concentrations in the central nervous system. Fish oil contains both EPA (eicosapentaeonic acid) and DHA.
DHA supplementation was found to significantly decrease the number of reference memory errors and working memory errors in aged male rats and in young rats fed a fish oil-deficient diet through three generations. The authors of the study proposed that the mechanism was due to the ability of DHA to reduce the levels of lipid peroxide in the hippocampus.(Gamoh et al. 1999, 2001).
Brain Cell Energy Boosters
The brain requires a lot of energy to perform its myriad of functions. An effective memory enhancement technique involves boosting the energy output of brain cells. With aging there is a decline in the ability of neurons to take up glucose (the primary fuel for the brain) and to produce energy. This decline in energy production not only causes memory and cognitive deficits but also results in the accumulation of cellular debris, which eventually kills brain cells. When enough brain cells have died from accumulated cellular debris, senility is usually diagnosed.
About 95% of cellular energy production occurs in the mitochondria. Many diseases of aging are increasingly being referred to as "mitochondrial disorders." Acetyl-L-Carnitine is the biologically active amino acid involved in the transport of fatty acids into the cell's mitochondria for the purpose of producing energy. Acetyl-L-carnitine is sold as an expensive drug in Europe to treat heart and neurological disease.
Acetyl-L-carnitine can increase muscle mass and convert body fat into energy. It has been shown to protect brain cells against aging related degeneration and to improve mood, memory, and cognition. Many people use acetyl-L-carnitine to maintain immune competence and reduce the formation of the aging pigment lipofuscin. The most important effect of acetyl-L-carnitine, however, is to maintain the function of the cell's energy powerhouse, the mitochondria.
A recent article by Aureli (2000) examined the anti-aging effects of acetyl-L-carnitine on Fischer rats. The study showed that long-term feeding with acetyl-L-carnitine was able to reduce the age-dependent increase of both sphingomyelin and cholesterol cerebral levels with no effect on the other measured phospholipids (Aureli 2000).
Another study by Seidman (2000) examined the effects of acetyl-L-carnitine on age-associated hearing loss in Fischer rats. Acetyl-L-carnitine and alpha-lipoic acid were found to reduce age-associated deterioration in auditory sensitivity and improve cochlear function. The effect appeared to be related to their ability to protect and repair age-induced cochlear mitochondrial DNA damage, thereby up-regulating mitochondrial function and improving energy-producing capabilities (Seidman 2000).
A Stanford University study of patients with Alzheimer's disease found that acetyl-L-carnitine slowed the progression of the disease in younger subjects (Brooks et al. 1998).
The recommended dose of Acetyl-L-carnitine is 1,000 to 2,000 mg a day.
When coenzyme Q10 is orally administered, it is incorporated into the mitochondria of cells throughout the body where it facilitates and regulates the oxidation of fats and sugars into energy. Heart cells have a high energy demand, and initial clinical studies investigated the effect of Coenzyme Q10 on cardiac mitochondrial function. Therapeutic efficacy was shown in double-blind studies when coQ10 was used in the treatment of congestive heart disease, coronary artery disease, and valvular disorders. Scientists are now looking at the effects of coQ10 on the brain-another organ whose cells also require a high level of energy metabolism.
The following are highlights from a study by Mathews et al. (1998):
When Coenzyme Q10 was administered to middle-aged and old rats, the level of coQ10 increased by 10 to 40% in the cerebral cortex region of the brain. This increase was sufficient to restore levels of coQ10 to those seen in young animals.
After only two months of coQ10 supplementation, mitochondrial energy expenditure in the brain increased by 29% compared to the group not getting coQ10. The human equivalent dose of coQ10 to achieve these results was 100-200 mg a day.
When a neurotoxin was administered, coQ10 helped protect against damage to the striatal region of the brain where dopamine is produced.
When coQ10 was administered to rats genetically bred to develop ALS (Lou Gehrig's disease), a significant increase in survival time was observed.
The conclusion by the scientists was "coQ10 can exert neuroprotective effects that might be useful in the treatment of neurodegenerative diseases."
This study showed that short-term supplementation with moderate amounts of coQ10 produced profound anti-aging effects in the brain. Previous studies have shown that coQ10 may protect the brain via several mechanisms including reduction in free radical generation and protection against glutamate-inducted excitotoxicity. This study documented that orally supplemented coQ10 specifically enhanced metabolic energy levels of brain cells. While this effect in the brain has been previously postulated, the new study provides hard-core evidence.
Based on the types of brain cell injury that coQ10 protected against, the scientists suggested that it may be useful in the prevention or treatment of Huntington's disease and Lou Gehrig's disease (amyotrophic lateral sclerosis). It was noted that while vitamin E delays the onset of Lou Gehrig's disease in mice, it does not increase survival time. coQ10 was suggested as a more effective treatment strategy for neurodegenerative disease than vitamin E because survival time was increased in mice treated with coQ10.
coQ10 might be effective in the prevention and treatment of Parkinson's disease. A study showed that the brain cells of Parkinson's patients have a specific impairment that causes the disruption of healthy mitochondrial function. It is known that "mitochondrial disorder" causes cells in the substantia nigra region of the brain to malfunction and die, thus creating a shortage of dopamine (Shults et al. 1997).
An interesting finding was that coQ10 levels in Parkinson's patients were 35% lower than age-matched controls. This deficit of coQ10 caused a significant reduction in the activity of enzyme complexes that are critical to the mitochondrial function of the brain cells affected by Parkinson's disease.
The ramifications of this study are significant. Parkinson's disease is becoming more prevalent as the human life span is increased. This new study confirms previous studies that Parkinson's disease may be related to coQ10 deficiency. The conclusion of the scientists was:
"The causes of Parkinson's disease are unknown. Evidence suggests that mitochondrial dysfunction and oxygen free radicals may be involved in its pathogenesis. The dual function of coQ10 as a constituent of the mitochondrial electron transport chain and a potent antioxidant suggest that it has the potential to slow the progression of Parkinson's disease" (see Parkinson's protocol for more information).
coQ10 levels decrease with aging. Depletion is caused by reduced synthesis of coQ10 in the body along with increased oxidation of coQ10 in the mitochondria. A coQ10 deficit results in the inactivation of enzymes needed for mitochondrial energy production, whereas supplementation with coQ10 preserves mitochondrial function.
Aged humans have only 50% of the coQ10 compared to young adults, thus making coQ10 one of the most important nutrients for people to supplement. coQ10 is the most important supplement on this list to take on a daily basis. Thousands of published studies show that ginkgo, acetyl-L-carnitine, and coQ10 play a critical role in brain cell energy metabolism, not only in healthy people, but also in those suffering from neurological diseases.
The recommended dose of coQ10 is 100 to 300 mg a day.
Phosphatidylserine plays an important role in maintaining the integrity of brain cell membranes. The breakdown of brain cell membranes prevents glucose and other nutrients from entering the cell. By protecting the integrity of brain cell membranes, phosphatidylserine facilitates the efficient transport of energy-producing nutrients into cells, enhancing brain cell energy metabolism.
Abnormalities in the composition of phosphatidylserine have been found in patients with Alzheimer's disease (Corrigan et al. 1998).
The recommended dose of phosphatidylserine (PS) is 100 to 300 mg a day.
Hormones are required to facilitate brain cell energy, maintain proper levels of acetylcholine, and protect brain cell membrane function. These hormones help restore youthful synchronization of nerve impulses within the brain. Hormone supplementation is often required to achieve the requisite levels.
Pregnenolone and DHEA improve brain cell activity and enhance memory. (Pregnenolone is converted into DHEA in the body.) DHEA is the most plentiful steroid hormone in the human body, but its exact function is unknown. What is known is that its concentration plummets with age: its daily production drops from 30 mg at age 20 to less than 6 mg at age 80. DHEA is naturally synthesized in abundance in young people from pregnenolone in the brain and the adrenal glands. It is known to affect the excitability of neurons in the hippocampus, the part of the brain responsible for memory.
Current findings suggest that DHEA enhances memory by facilitating the induction of neural plasticity, the condition that permits the neurons (nerve cells of the brain) to change in order to record new memories. Studies have shown that DHEA not only improves memory deficits, but also relieves depression in older people and increases perceived physical and psychological well being. DHEA has been shown to help preserve youthful neurological function. Together, pregnenolone and DHEA help to maintain the brain cells' ability to store and retrieve information in short-term memory.
A recent study found that DHEA and 7-oxo-DHEA-acetate, which is formed from DHEA, completely reversed the memory deficit induced by an injection of scopolamine in young mice. Only 7-oxo-DHEA-acetate was effective, however, in similar tests on older mice (Shi et al. 2000).
Pregnenolone initiates the memory storage process by stimulating the activity of an important molecule known as adenylate cyclase, which is needed to activate and regulate enzymes crucial to cellular energy production. Pregnenolone then regulates the sequential flow of calcium ions through the cell membrane. The pattern of calcium ion exchange may determine how memories are encoded by neurons. Pregnenolone also modulates chemical reactions, calcium-protein binding, gene activation, protein turnover, and enzymatic reactions involved in the storage and retrieval of memory.
An article by Darnaudery et al. (2000) reported that pregnenolone sulfate increased acetylcholine release and enhanced spatial memory performance. Studies on rats showed that injections of pregnenolone into the brain caused a dose-dependant increase of acetylcholine output. The lower dose caused a short-term elevation (20 minutes) and the higher dose caused a long-term elevation (80 minutes). This study confirmed previous work suggesting that a modest increase in acetylcholine facilitates memory processes (Darnaudery et al. 2000).
The suggested supplementation range for pregnenolone is 50 to 150 mg a day in three equal doses. The recommended dosage for DHEA is 25 to 50 mg a day. Women usually need less DHEA than men. Refer to the DHEA Replacement Therapy protocol before using pregnenolone or DHEA.
Melatonin, a naturally occurring hormone produced in the brain's pineal gland, also enhances cognitive function. It is one of the body's most potent natural antioxidants, making it ideal to prevent age-related dementias such as Alzheimer's disease that are thought to be caused, or at least exacerbated, by a lifetime of free-radical damage, especially since melatonin easily enters the brain from the bloodstream. Melatonin is also the primary regulator of brain cell synchronization, the body's internal clock, and is being researched as a possible treatment for various psychological conditions.
Abnormally low levels of melatonin have been discovered in patients suffering from some kinds of depression.
The suggested level of melatonin supplementation for enhancing neurological function in those over age 35 is 300 micrograms to 3 milligrams a night, one half hour before going to bed (melatonin has a sedative effect). Those over age 50 can take up to 6 milligrams before bedtime.
An article by Kampen et al. (1994) evaluated 71 postmenopausal women, 28 of whom were taking estrogen hormone replacement therapy, relative to memory function. There was significantly better verbal memory function (paragraph recall) in those women taking estrogen than those who were not.
A recent article by Farr et al. (2000) described an experiment of mice whose ovaries were surgically removed. The administration of both 17 beta-estradiol and estrone improved retention in a test of foot-shock avoidance on a T-maze. Further, a low dose of 17 beta-estradiol reduced by at least tenfold the dose of either arecoline (a cholinergic agonist) or L-glutamate (a glutamatergic agonist) needed to improve retention. Farr et al. (2000) concluded that these findings support the concept that estrogen improves memory by potentiating the activity of the cholinergic and glutamatergic systems.
An article by Cherrier et al. (2001) described a randomized, double-blind, placebo-controlled study of 25 healthy volunteers aged 50 to 80 years. Participants received weekly intramuscular injections of either 100 mg testosterone enanthate or placebo (saline) for 6 weeks. Circulating total testosterone was raised an average of 130% from baseline at week 3 and 116% at week 6 in the treatment group. Estradiol increased an average of 77% at week 3 and 73% at week 6 in the treatment group. The treatment group had significant improvements in cognition for spatial memory (recall of a walking route), spatial ability (block construction), and verbal memory (recall of a short story) compared with baseline and the placebo group. The results suggest that short-term testosterone administration enhances cognitive function in healthy older men (Cherrier et al. 2001).
Vitamins can protect and enhance cognitive function. B vitamins in particular play an integral role in the functioning of the nervous system and help the brain synthesize chemicals that affect moods. A balanced complex of the B vitamins is also essential for energy and for balancing hormone levels.
One recent study determined not only that low folate (a B vitamin) levels are associated with cognitive deficits, but also that patients treated with folic acid for 60 days showed a significant improvement in both memory and attention efficiency (Fioravanti et al. 1997).
In a 6-year study to determine the relationship between nutritional status and cognitive performance in 137 elderly people, several significant associations were observed between cognition and vitamin status. Higher present and past intake of vitamins A, C, E, and B complex were significantly related to better performance on abstraction and visuospatial tests (La Rue et al. 1997).
In addition to a direct effect, vitamins indirectly impact mental function by altering the levels of harmful or beneficial substances in the body. For instance, elevated homocysteine (an amino acid) levels have been linked to heart disease and poorer cognitive function. In one study, vitamin B6 and folate, taken at higher than recommended dosages, reduced blood levels of homocysteine.
Another study showed that less-than-optimal levels of vitamin B6, B12, and folic acid lead to a deficiency of S-adenosylmethionine (SAMe). SAMe deficiency can cause depression, dementia, or demyelinating myelopathy (a degeneration of the nerves) (Abou-Saleh et al. 1986).
The typical American diet does not always provide these essential vitamins, at least in high doses. Because vitamin C and the B complex are water soluble and excreted from the body daily, they must be replenished daily. Older people are at greater risk for vitamin deficiency because they tend to eat less of a variety of foods, although their requirements for certain vitamins such as B6 are actually higher. Older people may also have problems with efficient nutrient absorption from food. Even healthy older people often exhibit deficiencies in vitamin B6, vitamin B12, and folate, as well as zinc.
An article by Deijen et al. (1992) described a study of 76 elderly males given vitamin B6 versus placebo in relation to memory function. Deijen et al. (1992) concluded that vitamin B6 improves the storage and retrieval of information in the elderly patient.
An article by Carmel (1996) reviewed vitamin B12 deficiency in the elderly population relative to memory impairment and neuropathy. The authors conclude that both memory problems and neuropathy have been treated successfully with vitamin B12 injections or supplementation.
Lindenbaum et al. (1988) reviewed subclinical vitamin B12 deficiency and the resulting neurological symptoms. The author states that many common difficulties, such as memory loss, muscle weakness and parasthesias might well be a product of vitamin B12 deficiency without accompanying macrocytosis or other clinical indicators.
Methylcobalamin is a coenzyme form of vitamin B that has been identified to protect against neurological disease associated with aging. The sublingual form of methylcobalamin is better absorbed since it does not become bound to food. Because most sources of B12 are from protein (meat products), vegetarian diets may be lacking in this vitamin.
Free radicals are atoms or groups of atoms that can cause damage to cells by a process known as oxidation, which impairs the immune system and leads to infections and degenerative diseases. Free radicals occur as a result of air pollutants, smoke, radiation, environmental toxins, and processed foods, and are also released in the human body through sun exposure and stress. Antioxidants neutralize free radicals and help prevent such free-radical damage as normal brain aging. Their destructive activity has been implicated in many disease processes, including stroke and heart disease.
A study by Perrig et al. (1997) compared groups of older people over time and at a given moment with regard to antioxidant intake and memory performance. The study found that free recall, recognition, and vocabulary were significantly related to vitamin C and beta carotene levels. The levels of these antioxidants were found to be significant predictors of cognitive function even after adjusting for possible confounding variables such as differences in education, age, and gender.
Life Extension Mix is a multi-nutrient formula that contains the ideal potencies of antioxidants, vitamins C and E, and beta carotene. It provides an easy and cost-effective way to supplement the optimal combination of vitamins, minerals, amino acids, and antioxidants.
Vinpocetine was introduced into clinical practice 22 years ago in Hungary for the treatment of cerebrovascular disorders and symptoms related to senility. Since then, it has been used increasingly throughout the world in the treatment of cognitive deficits related to normal aging. Vinpocetine is a pharmaceutical extraction from the periwinkle plant.
CEREBRAL BLOOD FLOW
It is well established that normal aging results in a reduction of blood flow to the brain and a decrease in the metabolic activity of brain cells. Vinpocetine functions via several important mechanisms to correct known multiple causes of brain aging. The biological actions of vinpocetine initially showed that it enhances circulation and oxygen utilization in the brain, increases tolerance of the brain toward diminished blood flow, and inhibits abnormal platelet aggregation that can interfere with circulation or cause a stroke.
Vinpocetine enhances cyclic GMP levels in the vascular smooth muscle, leading to reduced resistance of cerebral vessels and increased cerebral blood flow.
The effect of vinpocetine on memory functions was studied in 50 patients with disturbances of cerebral circulation. Improvement of cerebral circulation was observed after i.v. and oral administration of vinpocetine. Blood flow was most markedly increased in the gray matter of the brain. Improvement of memorizing capacity evaluated by psychological tests was recorded after 1 month of vinpocetine treatment. Longer-term use was associated with alleviation or complete disappearance of symptoms of neurological deficit. No side effects attributable to the drug were observed. The doctors stated that vinpocetine is indicated in the treatment of ischemic disorders of the cerebral circulation, particularly in chronic vascular insufficiency (Hadjiev 1976).
More recent studies demonstrate that vinpocetine offers significant and direct protection against neurological damage caused by aging. The molecular evidence indicates that the neuroprotective action of vinpocetine is related to the ability to maintain brain cell electrical conductivity and to protect against damage caused by excessive intracellular release of calcium and sodium (Bonoczk et al. 2000; Solntseva et al. 2001).
In a study to ascertain how vinpocetine boosts cognition, scientists measured the electrical firing effects in the neurons of anesthetized rats. The administration of vinpocetine produced a significant increase in the firing rate of neurons. The scientists noted that the dose of vinpocetine used to increase electrical firing corresponded to the dose range that produced memory-enhancing effects. These results provided direct electrophysiological evidence that vinpocetine increases the activity of ascending noradrenergic pathways and that this effect can be related to the cognitive-enhancing characteristics of the compound (Gaal et al.1990).
Vinpocetine has been shown to protect against oxidative damage from beta-amyloid, which may make it clinically useful for Alzheimer's disease (Pereira et al. 2000).
Recent studies have suggested that the antioxidant effect of vinpocetine might contribute to the protective role exerted by the drug in reducing neuronal damage (Santos et al. 2000).
In one double-blind clinical trial, vinpocetine was shown to effect significant improvement in elderly patients with chronic cerebral dysfunction. Forty-two patients received 10 mg of vinpocetine 3 times a day for 30 days, then 5 mg 3 times a day for 60 days. Placebo tablets were given to another 42 patients for the 90-day trial period. Patients on vinpocetine scored consistently better in all evaluations of the effectiveness of treatment, including measurements on the Clinical Global Impression (CGI) scale, the Sandoz Clinical Assessment-Geriatric (SCAG) scale, and the Mini-Mental Status Questionnaire (MMSQ). There were no serious side effects related to the treatment drug (Balestreri et al. 1987).
In another double-blind study, 22 elderly patients with central nervous system degenerative disorders were treated with vinpocetine or placebo. Patients received 10 mg of vinpocetine 3 times a day for 30 days, then 5 mg 3 times a day for 60 days. Another 18 elderly patients were given matching placebo tablets for the 90-day trial. Vinpocetine-treated patients scored consistently better in all evaluations of the effectiveness of treatment, including measurements on the CGI and SCAG scales, and the MMSQ. According to CGI assessments, severity of illness decreased in 73% of the patients in the vinpocetine group at day 30 and in 77% of patients at day 90. Improvement was seen in 77% and 87% of the patients at days 30 and 90, respectively. Patients also showed statistically significant improvement for all SCAG items except one at days 30 and 90. The physician rated the improvement in 59% of the vinpocetine-treated patients as "good" to "excellent." There were no serious side effects associated with the treatment drug (Manconi 1986).
Vinpocetine safety and efficacy were demonstrated in a study of infants who suffered severe brain damage caused by birth trauma. Vinpocetine caused a significant reduction or disappearance of seizures. The vinpocetine group also showed a decrease of the phenomena of intracranial hypertension and normalization of psychomotor development (Dutov et al. 1991).
The damaging effects of glutamate-induced excitotoxicity has been well established. A vitamin B12 metabolite called methylcobalamin has been shown to specifically protect against this type of neuronal injury. Vinpocetine has been documented to partially protect against excitotoxicity induced by a wide range of glutamate-related neurotoxins.
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