~Alzheimer's Disease, Part 5 - Alternative Treatments

Alternative Treatments
  • Acetylcholine Support
  • Anti-Inflammatory Supplements
  • Homocysteine
  • Nervous System Support
  • Natural Hormone Replacement
  • Herbal Treatments
Acetylcholine Support
  • Phosphatidylcholine
  • Pantothenic Acid
  • Antioxidants
  • Vitamin E
  • Ginkgo Biloba
  • Vitamin C
  • Acetyl-L-Carnitine
  • Coenzyme Q10
  • N-Acetyl-Cysteine
  • Flavonoids
Phosphatidylcholine (Lecithin). Lecithin (phosphatidylcholine) has a long history of use with Alzheimer's disease. Phosphatidylcholine is a source of choline, the major component of acetylcholine, which is needed for cell membrane integrity and to facilitate the movement of fats in and out of cells.

When given to animals, lecithin causes increased acetylcholine levels. Clinical trials, however, failed to show actual improvement. Alzheimer's disease and other dementias do show increased choline levels, which may indicate inadequate metabolism. Therefore, simply supplementing the lecithin would not necessarily help the metabolic defect in the cellular use of phosphatidylcholine (Peters et al. 1979; Thal et al. 1983; Little et al. 1985; Blusztajn et al. 1987; Fitten et al. 1990).

A review article analyzed 12 clinical trials using lecithin to treat Alzheimer's disease (265 patients), Parkinsonian dementia (21 patients), and subjective memory problems (90 patients). No trial reported any clear clinical benefit of lecithin for Alzheimer's disease or Parkinsonian dementia. A dramatic result in favor of lecithin was obtained, however, in a trial of subjects with subjective memory problems (Higgins et al. 2000).

Pantothenic Acid. The body uses choline and pantothenic acid (vitamin B5) to form acetylcholine. Pantothenic acid is also needed to produce, transport, and release energy from fats.

Antioxidants. Oxidative stress is very important in the development of Alzheimer's disease. Antioxidant supplements help block this process. "Beta-amyloid is aggregated and produces more free radicals in the presence of free radicals; beta-amyloid toxicity is eliminated by free radical scavengers" (Grundman 2000).

Vitamin E. Researchers have shown that cultured cells are prevented from beta-amyloid toxicity with the addition of vitamin E (Grundman 2000). Researchers at the University of Kentucky published a ground-breaking article showing that vitamin E prevented the increase of polyamine metabolism in response to free-radical mediated oxidative stress caused by the addition of beta-amyloid to the rat neurons (Yatin et al. 1999).

Research conducted in Germany showed that both natural and synthetic vitamin E were more effective than estrogen (17-beta estradiol) in protecting neurons against oxidative death caused by beta-amyloid, hydrogen peroxide, and the excitatory amino acid glutamate (Behl 2000).

Research conducted at the University of California, San Diego, School of Medicine studied the protective effects of vitamin E in apolipoprotein E-deficient mice. Those treated with vitamin E displayed a significantly improved behavioral performance in the Morris water maze. Also, the untreated mice displayed increased levels of lipid peroxidation and glutathione, whereas the vitamin E-treated mice showed near normal levels of both lipid peroxidation and glutathione (Veinbergs et al. 2000).

A study of 44 patients with Alzheimer's disease and 37 matched controls showed that vitamin E levels in the cerebrospinal fluid (CSF) and serum were significantly lower in Alzheimer's patients (Jimenez-Jimenez et al. 1997).

In the Alzheimer's Disease Cooperative Study, 2000 mg of vitamin E were given to Alzheimer's disease patients. This slowed the functional deterioration leading to nursing home placement (Grundman 2000).

An article by Sano et al. (1997) described a double-blind, placebo-controlled, randomized, multicenter trial of patients with Alzheimer's disease of moderate severity. A total of 341 patients received the selective monoamine oxidase inhibitor selegiline (10 mg a day), alpha-tocopherol (vitamin E, 2000 IU a day), both selegiline and alpha-tocopherol, or placebo for two years. The baseline score on the Mini-Mental State Examination was higher in the placebo group than in the other three groups. Both vitamin E and selegeline delayed the progression of the disease with vitamin E acting slightly better than selegeline (median time 670 vs. 655 days, respectively).

A review of the published research on vitamin E for Alzheimer's disease stated that, although there is insufficient evidence of efficacy of vitamin E, there is sufficient evidence of possible benefit to justify further studies (Tabet et al. 2000). Researchers are suggesting that the combination of vitamin E and donepezil should be adopted as a current standard of Alzheimer's disease therapy (Doody 1999b).

Ginkgo Biloba. Ginkgo biloba is the world's oldest living tree. It has been traditionally used for improving memory and Alzheimer's disease. It is a powerful antioxidant and also functions as a mild vasodilator (improves circulation), anti-inflammatory (via antioxidant effects), membrane protector, antiplatelet agent, and neurotransmitter modulator (Perry et al. 1999; Diamond et al. 2000).

Ginkgo was shown to protect neurons against toxicity induced by beta-amyloid fragments, with a maximal and complete protection at the highest concentration tested. Ginkgo also completely blocked beta-amyloid-induced events, such as reactive oxygen species accumulation (Bastianetto et al. 2000; Yao et al. 2001).

A study of the effects of bilobalide, the main constituent of the nonflavone fraction of ginkgo biloba, provided the first direct evidence that bilobalide can protect neurons against oxidative stress. Bilobalide may block the apoptosis in the early stage and then attenuate the elevation of c-Myc, p53, and Bax genes and activation of caspase-3 in cells (Zhou et al. 2000).

An article by Yao et al. (1999) showed that pretreatment of nerve cells with isolated ginkgolides, the antioxidant component of ginkgo biloba leaves, or vitamin E, prevented the beta-amyloid-induced increase of reactive oxygen species (ROS). Ginkgolides, but not vitamin E, inhibited the beta-amyloid-induced HNE (4-hydroxy-2-nonenal) modification of mitochondrial proteins.

A 52-week, double-blind, placebo-controlled, fixed dose, parallel-group, multicenter study of ginkgo biloba at a dose of 120 mg (40 mg three times a day) was conducted and published in 2000. The placebo group showed a statistically significant worsening in all domains of assessment, while the group receiving ginkgo biloba was considered slightly improved in the areas of cognitive assessment, daily living, and social behavior. No differences in safety between ginkgo biloba and placebo were observed (Le Bars et al. 2000).

A similar 52-week, randomized double-blind, placebo-controlled, parallel-group, multicenter study of ginkgo biloba by the same research team was published in 1997. The group treated with ginkgo biloba had an ADAS-Cog score 1.4 points better than the placebo group (p = 0.04) and a Geriatric Evaluation by Relative's Rating Instrument (GERRI) score 0.14 points better than the placebo group (Le Bars et al. 1997).

In an analysis of various studies and as measured by the ADAS-Cog, the four anticholinesterases and ginkgo were equally effective in mild to moderate Alzheimer's disease. Tacrine had a high dropout rate due to side effects. Most studies showed benefit from ginkgo, but one did not (van Dongen et al. 2000).

Extracts of ginkgo contain different amounts of the various active substances and are also of variable quality. A high-quality, pharmaceutical-grade ginkgo supplement is recommended because some commercial companies do not contain the same kind of extract that was used in the clinical studies (Kidd 1999).

Vitamin C. An article by Riviere et al. (1998) described a study of Alzheimer's disease patients in the region of Toulouse, France. Vitamin E and C levels in plasma were measured and consumption of raw and cooked fruit and vegetables was evaluated in order to determine the mean vitamin C intakes. Mini-Nutritional Assessment (MNA) and plasma albumin were used to measure nutritional status. The hospitalized Alzheimer's subjects had lower MNA scores and albumin levels and normal vitamin C intakes, but their plasma vitamin C was lower than that of community-living subjects. In the home-living Alzheimer subjects, vitamin C plasma levels decreased in proportion to the severity of the cognitive impairment despite similar vitamin C intakes.

A prospective study of 633 persons 65 years and older examined the relation between the use of vitamins E and C and the incidence of Alzheimer's disease. After an average follow-up period of 4.3 years, 91 of the participants with vitamin information were evaluable. None of the 27 vitamin E supplement users and none of the 23 vitamin C supplement users had Alzheimer's disease. There was no relation between Alzheimer's disease and use of low-potency multivitamins (Morris et al. 1998).

A study of 10 patients with Alzheimer's disease showed that one month supplementation of 400 IU vitamin E and 1000 mg vitamin C significantly increased the concentration of both vitamins in the plasma and cerebral spinal fluid. In contrast, supplementation with vitamin E alone increased its CSF and plasma concentrations but was unable to decrease lipoprotein oxidizability (Kontush et al. 2001).

Acetyl-L-Carnitine. There are multiple modes of action for acetyl-L-carnitine, including antioxidant effects, molecular chaperone effects, and others. This agent possibly helps correct the acetylcholine deficit and has been tried in rodents (Butterworth 2000). Double-blind studies have been done and have shown some benefit (Pettegrew et al. 2000). Acetyl-L-carnitine was shown to protect neurons from the detrimental effects of beta-amyloid in the cortex of rats (Virmani et al. 2001).

In humans, a one-year controlled trial in early Alzheimer's disease measured ADAS-Cog and the Clinical Dementia Rating Scale in 229 patients. Acetyl-L-carnitine use slowed the clinical deterioration. This study concluded by recommending more research using both acetyl-L-carnitine plus a cholinesterase inhibitor (such as donepezil, tacrine, rivastigmine, or metrifonate) (Thal et al. 2000).

A study by Jimenez-Jimenez et al. (1999) compared serum levels of beta-carotene, alpha-carotene, and vitamin A of 38 Alzheimer's disease patients and 42 controls. They found that the serum levels of beta-carotene and vitamin A were significantly lower in the Alzheimer's disease patient group.

Coenzyme Q10 (CoQ10). CoQ10 is used in the mitochondrial production of energy in the electron transport chain. A role for mitochondrial dysfunction in neurodegenerative disease is gaining support. Studies have implicated mitochondrial defects in Alzheimer's disease and use of CoQ10 has been suggested for this reason. However, the appropriate clinical studies using CoQ10 have not yet been done (Beal 1999).

N-Acetyl-Cysteine. N-acetyl-cysteine (NAC) is a precursor of glutathione, a powerful scavenger of free radicals. Glutathione deficiency has been associated with a number of neurodegenerative diseases, including Lou Gehrig's and Parkinson's diseases. A study showed that NAC significantly increased the glutathione levels and reduced oxidative stress in rodents treated with a known free-radical producer (Pocernich et al. 2000).

NAC has been shown to protect mitochondrial respiration and neuronal microtubule structure from the toxic effects of HNE (4-hydroxy-2-nonenal), a reactive aldehyde product of lipid peroxidation (Neely et al. 2000).

Flavonoids. A study showed that flavonoids have a protective effect on neurons exposed to oxidized lipids in the form of low-density lipoprotein (Schroeter et al. 2000).

Anti-Inflammatory Supplements
  • Curcumin
  • Essential Fatty Acids
  • DHA
  • EPA
  • GLA
Curcumin. Curcumin, the active ingredient in the herb turmeric, is being investigated for use in Alzheimer's disease due to its potent anti-inflammatory action (Joe 1997; Grilli 1999).

Essential Fatty Acids. Essential fatty acids are found in oils including flax, borage, and fish oils. Fish oils contain EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), both of which are omega-3 oils. Essential fatty acids are important for healthy skin and hair. They also have significant anti-inflammatory action.

It has been proposed that a dietary deficiency of essential fatty acids could be a risk factor for Alzheimer's disease (Newman 1992; Newman 2000; Youdim et al. 2000). Several small studies have explored the use of essential fatty acids in the treatment of Alzheimer's disease and found it to be beneficial (Corrigan et al. 1991; Yehuda et al. 1996).

DHA. The neuron is composed of about 30% DHA (docosahexaenoic acid), which is an important fatty acid in the neuronal membrane. Most of our DHA comes from fish consumption but also may be taken as a supplement. Low DHA has been found to be a risk factor for development of Alzheimer's disease. The decreased levels of DHA in later life could be related to decreased synthesis secondary to lower levels of delta 6-desaturase activity (Horrocks et al. 1999; Kyle et al. 1999). This means that while the alpha-linoleic acid in flax oil may have converted to DHA in youth, when people age beyond 50 years, a delta 6-desaturase enzyme deficit develops, meaning that one has to eat lots of cold water fish or take a supplement that contains DHA in order to obtain optimal quantities of DHA.

EPA. A Japanese study found that administration of EPA (900 mg a day) in patients with Alzheimer's disease improved MMSE significantly with maximal effects at three months, while the effects lasted six months. However, the score of MMSE decreased after six months (Otsuka 2000).

GLA. Researchers have proposed that fish oils and GLA (gamma-linolenic acid) may help prevent Alzheimer's disease by its anti-inflammatory effect of suppressing interleukin-1 production by monocytes (McCarty 1999).

  • Vitamin B12
  • Folate
  • SAMe
Vitamin B12. Research has shown that low cobalamin (vitamin B12) levels are related to dementias in general. A common cause of cobalamin deficiency in elderly people is protein-bound cobalamin malabsorption due to atrophic gastritis with hypo- or achlorhydria (low stomach acid). Often, however, the serum B12 levels are normal. The measurement of the metabolites homocysteine, methylmalonic acid, or both is recommended as a more accurate assessment of cobalamin status (Bopp-Kistler et al. 1999; McCaddon et al. 2001a).

Lower levels of vitamin B12 (below 200 pg/mL) in the blood are associated with dementia symptoms. Because of this, and the absence of toxicity with use of vitamin B12, the argument has been voiced to raise recommended minimum serum levels of vitamin B12 and also liberally administer vitamin B12 to the elderly. "Vitamin B12 could play a role in the behavioral changes in Alzheimer's disease" (Eastley et al. 2000). Another study was conducted with outpatients at a geriatric memory clinic. Seventy-three consecutive outpatients with probable Alzheimer's disease showed that low vitamin B12 status was related to an increase in behavioral and psychological symptoms of dementia: irritability and disturbed behavior (Meins et al. 2000).

A population-based longitudinal study of 370 non-demented persons, aged 75 years and older, conducted in Sweden found that subjects with low levels of B12 or folate had twice the risk of developing Alzheimer's disease over the 3-year period of the study (Wang et al. 2001).

Folate. Folate or folic acid derives its name from foliage (green plants). Folacin was first isolated from spinach and other leafy green vegetables in 1941. Folic acid is needed for DNA synthesis and is also needed to make S-adenosyl methionine (SAMe). A study of 126 patients, including 30 with Alzheimer's disease, found that the levels of folate in the cerebral spinal fluid (CSF) were significantly lower in late-onset Alzheimer's disease patients (Serot et al. 2001).

A study by Renvall et al. (1989) found low levels of folate (along with deficiencies of thiamin and vitamin B12) in elderly individuals with senile dementia of the Alzheimer's type (22 subjects) as compared to the cognitively normal control group (41 subjects).

SAMe. SAMe is perhaps the safest and most effective antidepressant in the world. SAMe is a precursor for glutathione, coenzyme A, cysteine, and taurine.

One study measured the postmortem levels of SAMe in the brains of 11 patients with Alzheimer's disease. Decreased levels of S-adenosylmethionine (-67 to -85%) and its demethylated product S-adenosylhomocysteine (-56 to -79%) were found in all brain areas examined as compared with matched controls (n = 14) (Morrison et al. 1996).

A review article of SAMe concluded that intravenous or oral administration of SAMe represents a possible treatment for Alzheimer's dementia, subacute combined degeneration of the spinal cord (SACD), and HIV-related neuropathies, as well as in patients with metabolic disorders such as folate reductase deficiency (Bottiglieri et al. 1994).

Nervous System Support
  • Phosphatidylserine
  • Inositol
  • Vitamin K
  • Idebenone
Phosphatidylserine. Phosphatidylserine is a major building block for nerve cells. Phosphatidylserine has been studied for use with Alzheimer's disease and age-related mental decline (Delwaide et al. 1986; Crook et al. 1992; Engel et al. 1992). In a study by Heiss et al. (1994), a 6-month study of 70 patients with Alzheimer's disease divided into four groups indicated that phosphatidylserine treatment has an effect on different measures of brain function. The improvements, however, were best documented after 8 and 16 weeks and faded toward the end of the treatment period (Heiss et al. 1994).

Inositol. Inositol is required for the formation of cell membranes. It helps in transporting fats and affects nerve transmission. A double-blind controlled crossover trial examined use of inositol, at a dose of 6 grams a day for one month, in 11 patients with Alzheimer's disease. Language and orientation improved significantly more on inositol than on placebo (glucose) (Barak et al. 1996).

Vitamin K. An article by Allison (2001) proposes that vitamin K deficiency may contribute to the pathogenesis of Alzheimer's disease. The authors offer the following as evidence:
  • A relative deficiency of vitamin K is common in aging men and women.
  • The concentration of vitamin K is lower in the circulating blood of ApoE e4 carriers than in that of persons with other ApoE genotypes. The ApoE e4 genotype is associated with Alzheimer's disease.
  • Vitamin K has important functions in the brain, including the regulation of sulfotransferase activity and the activity of a growth factor/tyrosine kinase receptor (Gas 6/Axl).
  • Vitamin K may also reduce neuronal damage associated with cardiovascular disease.
Some have proposed that vitamin K supplementation may have a beneficial effect in preventing or treating the disease (Allison 2001).

Idebenone. Idebenone is a synthetic analogue of coenzyme Q10 (CoQ10), a cell membrane antioxidant and essential component of the mitochondrial electron transport chain which produces ATP (the energy molecule of the body). The following mechanisms have been proposed for the use of idebenone in Alzheimer's disease:
  • Idebenone has been shown to stimulate nerve growth factor (Nitta et al. 1993; Nitta et al. 1994; Yamada et al. 1997).
  • Treatment with idebenone and alpha-tocopherol prevented learning and memory deficits caused by beta-amyloid in rats (Yamada et al. 1999).
Three hundred patients with Alzheimer's disease were randomized to receive either placebo or idebenone, 30 mg 3 times a day, or 90 mg three times a day for 6 months. Statistically significant improvement was noted in the total score of the Alzheimer's Disease Assessment Scale (ADAS-total) and in one cognitive parameter (ADAS-cog) in the idebenone 90 mg 3 times a day group, as compared to placebo. (Bergamasco et al. 1994; Anon. 2001).

An article by Weyer et al. (1997) described the results of a double-blind, placebo-controlled multi-center study using idebenone in patients suffering from mild to moderate dementia of the Alzheimer type. A total of 300 patients were randomized to either placebo or idebenone 30 mg or 90 mg 3 times a day and treated for 6 months. After month 6, the idebenone 90 mg group showed statistically significant improvement in both the Total and Cognitive Alzheimer's Disease Assessment Scales (Weyer et al. 1997).

Natural Hormone Replacement
  • Melatonin
  • Music Therapy
  • Tryptophan
  • Adrenal Stress
  • DHEA
  • Inhibition of AGE Formation
  • Vitamins B1 and B6
  • Carnosine
Estrogen replacement therapy (ERT) was discussed previously as conventional treatment for the prevention of Alzheimer's disease. From a broader perspective, estrogen replacement is but one hormone in a complex system that includes three forms of estrogen (estrone, estradiol, and estriol), progesterone, testosterone, their precursors (DHEA and pregnenolone); and other hormones (melatonin and cortisol). A comprehensive hormone panel is highly recommended to determine which hormones are deficient or in excess and to help guide appropriate supplementation.

Melatonin. Melatonin is a hormone that is released in mammals during the dark phase of the circadian cycle. Its production declines with age in animals and humans. The main use of melatonin is for insomnia and to establish normal sleeping patterns after long air flights. The doses used in the research studies were higher than the 1 to 10 mg most persons use. Higher doses may cause sleepiness, although no other serious side effects have been found with melatonin.

Melatonin is an antioxidant that has been shown to be highly effective in reducing oxidative damage to the central nervous system. Melatonin also stimulates several antioxidant enzymes, including glutathione peroxidase and glutathione reductase (Reiter et al. 1999).

Several studies have investigated the mechanism of melatonin in Alzheimer's disease:
  • Melatonin was shown to significantly inhibit the release of free radicals in neuroblastoma cells (Lahiri et al. 1999).
  • Treatment of cells with high doses of melatonin have been found to decrease the secretion of soluble beta-amyloid (Lahiri 1999).
  • Melatonin prevented damage by beta-amyloid to neuroblastoma cells (Pappolla et al. 1999).
In a retrospective study, 14 Alzheimer's disease patients received 9 mg of melatonin daily for 22 to 35 months. A significant improvement of sleep quality was found (Brusco et al. 1999).

One study measured the melatonin levels in the cerebrospinal fluid (CSF) of 85 patients with Alzheimer's disease and in 82 age-matched controls. In Alzheimer's disease patients the CSF melatonin levels were only one-fifth of those in control subjects (Liu et al. 1999).

Brusco et al. examined the efficacy of melatonin in treatment of sleep and cognitive disorders of Alzheimer's disease. Fourteen patients (8 females, 6 males, mean age 72 years) received 9 mg melatonin capsules daily at bedtime for 22-35 months. Overall quality of sleep was assessed from sleep logs filled in by the patients or their caretakers. At the time of assessment, a significant improvement of sleep quality was found in all cases examined. Clinically, the patients exhibited lack of progression of the cognitive and behavioral signs of the disease during the time they received melatonin (Brusco et al. 2000).

Music Therapy. A novel study assessed the effects of music therapy on the concentrations of melatonin, norepinephrine, epinephrine, serotonin, and prolactin in the blood of 20 male patients with Alzheimer's disease at the Miami Veterans Administration Medical Center, Miami, Florida. Patients listened to 30-40 minute morning sessions of music therapy 5 times a week for 4 weeks. Melatonin concentration in serum increased significantly after music therapy and was found to increase further at 6 weeks follow-up. Norepinephrine and epinephrine levels increased significantly after 4 weeks of music therapy, but returned to pretherapy levels at 6 weeks follow-up. The authors concluded that increased levels of melatonin following music therapy might have contributed to patients' relaxed and calm mood (Kumar et al. 1999).

Tryptophan. Tryptophan is the precursor of serotonin and melatonin. It has been proposed that a dietary lack of tryptophan may make deficiencies of serotonin and melatonin common (Maurizi 1990; Widner et al. 2000). In a double-blind, crossover study of 16 patients with dementia of the Alzheimer type and 16 cognitively intact controls, subjects received either a tryptophan-free amino acid drink to induce acute tryptophan depletion, or a placebo drink containing a balanced mixture of amino acids. On each occasion, ratings of depressed mood were made at baseline and at 4 and 7 hours later, and the Modified Mini-Mental State was administered at baseline and 4 hours later. Patients with dementia of the Alz-heimer type had a significantly lower mean score on the Modified Mini-Mental State after acute tryptophan depletion than after receiving placebo, while the comparison group showed no difference (Porter et al. 2000).

Adrenal Stress. The relationship between age-related memory loss and stress is central to the protocol used by Dharma Singh Khalsa. Excessive stress from a modern life causes the adrenal glands to secrete excessive amounts of cortisol, eventually leading to adrenal fatigue (Khalsa 1997).

DHEA. Alzheimer's disease patients with higher dehydroepiandrosterone (DHEA) levels did better on memory tests than those with lower DHEA levels (Carlson et al. 1999; Murialdo et al. 2000). Other data suggest that DHEA has a role in antioxidant status, Natural Killer (NK) cell immune function, and other immune functions. This study showed low DHEA was a risk factor for the development of Alzheimer's disease but did not show that replacing DHEA was of benefit. These studies still need to be done (Hillen et al. 2000).

A study of adrenal secretion in 23 healthy elderly subjects, 23 elderly demented patients and 10 healthy young subjects found a significant increase in cortisol levels during evening and nighttime in both groups of the aged subjects. In elderly subjects, particularly if demented, the mean serum dehydroepiandrosterone sulfate (DHEAs) levels throughout the 24-hour cycle were significantly lower than in young controls (Magri et al. 2000).

A cross-sectional study, called the Berlin Aging Study, found lower levels of DHEAs in cases that developed dementia of the Alzheimer type within 3 years as compared to matched controls (Hillen et al. 2000).

Inhibition of AGE Formation. Central to the process of forming advanced glycation end products (AGEs) is the presence of sugar (glucose) which is central to the diagnosis of both diabetes and insulin insensitivity (referred to as Syndrome X). Appropriate lab tests would include the glucose tolerance test and insulin levels. Appropriate treatment is covered in the section on diabetes.

Vitamins B1 and B6. Derivatives of vitamins B1 and B6 (thiamine pyrophosphate and pyridoxamine) have been shown to decrease AGE formation (Booth et al. 1996; Booth et al. 1997).

Carnosine. Carnosine is a multifunctional dipeptide made from a combination of the amino acids beta-alanine and L-histidine. Meat is the main dietary source of carnosine. High doses of carnosine are necessary for therapeutic effect because the body naturally degrades carnosine with the enzyme carnosinase.

Copper and zinc are released during normal synaptic activity. However, in the presence of a mildly acidic environment which is a characteristic of Alzheimer's disease, they reduce to their ionic forms and become toxic to the nervous system. Research has shown that carnosine can buffer copper and zinc toxicity in the brain (Horning et al. 2000; Trombley et al. 2000).

Carnosine has also been shown, in vitro, to inhibit nonenzymic glycosylation and cross-linking of proteins induced by reactive aldehydes, including aldose and ketose sugars, certain triose glycolytic intermediates, and malondialdehyde (MDA, a lipid peroxidation product). Carnosine also inhibits formation of MDA-induced protein-associated advanced glycosylation end products (AGEs) and formation of DNA-protein cross-links induced by acetaldehyde and formaldehyde (Munch et al. 1997; Hipkiss 1998; Hipkiss et al. 1998; Preston et al. 1998).

Herbal Treatments
  • Huperzine A
  • KUT
Huperzine A. Huperzine A is an alkaloid isolated from the Chinese herb Huperzia serrata. In experiments using rats, Huperzine A improved the decrease in acetylcholine activity in cortex and hippocampus (Cheng 1996; Tang 1996; Bai et al. 2000; Wang et al. 2000). A double-blind, multicenter study of Huperzine A was conducted in China. Fifty patients were given 0.2 mg Huperzine and 53 patients were given placebo for 8 weeks. About 58% (29/50) of patients treated with Huperzine showed improvements in their memory and cognitive and behavioral functions. The efficacy of Huperzine was better than placebo. No severe side effects were found (Xu et al. 1995).

KUT. KUT is a Japanese herbal formula named "Kami-Umtan-To" that consists of 13 different herbs. KUT has been used since 1626 for neuropsychiatric problems. KUT has been shown to increase choline acetyltransferase levels and nerve growth factor in cultured rat brain cells.

In a 12-month open clinical trial using KUT and estrogen, vitamin E, and NSAIDs, the rate of cognitive decline per year was measured using the Mini-Mental Status Exam (MMSE). Twenty patients with Alzheimer's disease (MMSE score: 18.6 5.8) received extracts from original KUT herbs, seven Alzheimer's disease patients (MMSE score: 21.3 2.8) were placed on the combination therapy, and 32 patients served as controls (MMSE score: 20.8 5.6). The rate of cognitive decline per year was significantly slower in the KUT group (1.4 points) and the combination group (0.4 points) as compared to the 32 control patients who received no medicine (4.1 points). The efficacy of KUT alone was most noticeable after 3 months of use (Arai et al. 2000).

Continued . . .

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