Natural Supplements to Ward Off Alzheimers

Alzheimer’s disease is a neurodegenerative disease that destroys brain cells, resulting in memory loss and problems with thinking, behavior, lifelong hobbies and social life. It is a progressive and fatal disease without a current cure. It affects both men and women usually 65 years and older, but an early-onset form also exists. Before his death on April 5, 2008, Charlton Heston publicly announced in 2002 he was suffering from symptoms synonymous with Alzheimer’s disease. Alzheimer’s is the seventh leading cause of death in the United States; as many as 5 million Americans are living with the disease, according to the National Alzheimer’s Association (Alz.org)

One of the characteristics of Alzheimer's disease is the deposition of senile plaques containing amyloid-beta (A beta), a protein that promotes inflammation and oxidation. Natural supplementation is becoming a popular preventive method for Alzheimer's disease and other neurodegenerative diseases, by enhancing memory and cognitive functions.

Curcumin, the principal curcuminoid in the Indian curry spice turmeric, for example, has shown antioxidant and anti-inflammatory qualities. A study at the University of California Los Angeles (UCLA) School of Medicine treated macrophages, cells within the tissues that originate from specific white blood cells, from six Alzheimer’s patients and three controls with curcuminoids (as Curcumin C3 Complex, from Sabinsa) in vitro, and measured A beta uptake.¹ After treating the macrophages with curcuminoids, A beta uptake by macrophages of three of the six Alzheimer’s patients was significantly increased (P<.001 to .081).

In 2008, an in vitro model of alpha-synuclein (AS) aggregation, was developed by treatment of purified AS protein with Fenton reaction.² Alpha-synuclein is the primary structural component of Lewy bodies, which are abnormal aggregates of protein (alpha-synuclein) that develop inside nerve cells; an alpha-synuclein fragment, known as the non-A beta component (NAC), is found in amyloid plaques in Alzheimer’s. The addition of curcumin inhibited aggregation in a dose-dependent manner and increased AS solubility. Next, the aggregation-inhibiting effect of curcumin was investigated in a cell culture utilizing catecholaminergic SH-SY5Y cell line. A model system was developed in which the red fluorescent protein (DsRed2) was fused with A53T mutant of AS and its aggregation examined under different concentrations of curcumin. More than a 32 percent decrease in mutant AS aggregation was observed within 48 hours after the curcumin was added.

A Korean study synthesized eight novel derivatives of curcumin and dehydrozingerone, and their binding affinities for A beta aggregates were measured.³ Fluoropropyl-substituted curcumin showed the highest binding affinity (Ki=0.07 nM).

Another study published in the Journal of Neurochemistry used in vivo multiphoton microscopy (MPM) to demonstrate that curcumin crosses the blood-brain barrier and labels senile plaques and cerebrovascular amyloid angiopathy (CAA) in amyloid precursor protein (APP) mice.⁴ Systematic treatment of mice with curcumin cleared and reduced existing plaques after seven days, suggesting a potent disaggregation effect. Curcumin also led to a limited, but significant, reversal of structural changes in dystrophic dendrites, including abnormal curvature and dystrophy size.

At UCLA, under aggregating conditions in vitro, curcumin inhibited aggregation as well as disaggregated fibrillar A beta40.⁵ Curcumin was a better A beta40 aggregation-inhibitor than ibuprofen and naproxen, and it prevented A beta42 oligomer formation and toxicity and decreased dose dependently A beta fibril formation.

Omega-3 essential fatty acids (EFAs) are known to improve cognitive function as well. At Karolinska University Hospital Huddinge, Stockholm, a randomized, double blind, placebo-controlled, clinical trial administered 1.7 g/d of docosahexaenoic acid (DHA) and 0.6 g/d of eicosapentaenoic acid (EPA) or a placebo to 204 patients with Alzheimer’s disease for six months, after which all 204 patients received omega-3 fatty acid supplementation for six more months.⁶ A total of 174 patients completed the trial. At six months, the decline in cognitive function did not differ between the groups; however, in a subgroup (n=32) with very mild cognitive dysfunction, a significant (P<.05) reduction in Mini-Mental State Examination (MMSE) decline rate was observed in the omega-3 EFA-treated group compared with the placebo group. A decline rate was seen between six and 12 months in this placebo subgroup when receiving omega-3 supplementation.

A separate study at UCLA took aged animals (17 to 19 months old) and placed them in one of three groups until they were 22.5 months of age: control (0.09 percent DHA), low DHA (0 percent) or high DHA (0.6 percent) chow.⁷ The DHA-enriched diets significantly reduced the total A beta by more than 70 percent when compared to the low DHA and control chow diets. Dietary DHA also decreased A beta42 levels below those seen with the control chow. The overall plaque burden was significantly reduced by 40.3 percent.

In a study published in The Journal of Neuroscience, researchers reported DHA significantly increases LR11, a neuronal sorting protein that reduces APP trafficking to secretases that generate A beta, in primary rat neurons, aged non-Tg mice and an aged DHA-depleted APPsw Alzheimer’s mouse model.⁸ DHA also increased LR11 in a human neuronal line. In vivo elevation of LR11 was also seen with dietary fish oil in young rats with insulin resistance. Because reduced LR11 is known to increase A beta production and may be a significant genetic cause of late-onset Alzheimer’s disease (LOAD), the results indicated DHA increases LR11 levels and may play an important role in preventing LOAD.

A study at Radboud University Nijmegen, Netherlands, administered regular rodent chow, a Typical Western Diet (TWD) containing 1 percent cholesterol, or a diet with a high (0.5 percent) level of DHA to mice starting at six months of age, for 12 months.⁹ The TWD diet increased plaque burden in the dentate gyrus of the hippocampus, but did not significantly reduce relative cerebral blood volume (rCBV). The DHA-enriched diet increased rCBV, without changing blood flow and decreased the amount of vascular beta-amyloid deposition.

Conversely, a 2007 study gave APP double-transgenic mice, as well as nontransgenic (NT) normal littermates, from two to nine months of age, a high omega-3 supplemented diet or a standard diet with a comprehensive behavioral test battery administered during the final six weeks.¹⁰ The results suggested diets high in omega-3 fatty acids, or use of fish oil supplements (DHA+EPA), will not protect against Alzheimer's disease, at least in high-risk individuals. However, normal individuals conceivably could derive cognitive benefits from high omega-3 intake if it corrects an elevation in the brain level of omega-6 fatty acids as a result. Alternatively, dietary fish may contain nutrients, other than DHA and EPA, which could provide protection against Alzheimer's disease.

Alpha-glyceryl phosphoryl choline (alpha GPC) is a precursor for the synthesis of phosphatidylcholine, which may help stimulate human growth hormone (HGH) release. In a study published in the International Journal of Clinical Pharmacology 12 normal volunteers were studied on three randomized occasions: in a control day without drug administration, after 1,000 mg of intramuscular (IM) alpha GPC (as AlphaSize™, from Chemi Nutra), and after 1,000 mg of IM citicoline, respectively.¹¹ Alpha GPC was associated with a rapid rise in plasma choline, peak levels being usually observed at the first (0.25 h) or second (0.5 h) sampling time after the injection. Thereafter, the concentration of choline declined gradually and returned to near baseline values at the end of the observation period. After the administration of citicoline, plasma choline levels showed a similar time course, but were considerably lower than those observed after alpha GPC. Pharmacokinetic parameters calculated after subtracting the zero time concentration from all post-drug values indicated that exogenously derived choline declined in plasma with a half-life of 0.5 to 6.2 hour, without any significant difference between alpha GPC or citicoline. Choline AUC values after alpha GPC were significantly higher than those observed after citicoline, but the difference was no longer significant when AUC’s were corrected for the different choline content of the two preparations. Researchers concluded that the IM administration of alpha GPC provides an effective means of increasing plasma choline levels.

A Japanese in vivo study examined the neurotoxic effect of A beta and the neuroprotective effect of phosphatidylinositol using transgenic mice.¹² Intrahippocampal CA1 injection of 1.5 mul of 100 nM or 1 microM A beta25-35 increased the number of degenerating neurons in one month, demonstrating an in vivo neurotoxic effect of A beta at lower concentrations after diffusion. Intrahippocampal co-injection or intracerebroventricular administration of 1.5 microl of 500 nM phosphatidylinositol prevented the A beta25-35-induced neuronal degeneration in all the hippocampal regions, while co-injection of another acidic phospholipid, phosphatidylserine (1.5 microl, 500 nM) with A beta25-35 showed no protective effects.

In contrast, studies have shown the positive effects of phosphatidylserine, a phospholipid essential for the normal functioning of neuronal cell membranes, which is mainly found in fish, green leafy vegetables, soybeans and rice.

A double blind Italian study treated 494 elderly patients with moderate to severe cognitive decline with 300 mg/d of bovine cortex-derived phosphatidylserine for six months.¹³ Within the six-month trial period, 69 patients dropped out. Compared to the placebo group, statistically significant improvements in behavioral and cognitive parameters in the phosphatidylserine-treated group were observed. In addition, clinical evaluation and laboratory tests demonstrated that the phosphatidylserine was well tolerated.

Researchers at the University of Munich, Germany, gave 33 patients with mild primary degenerative dementia either 300 mg of bovine-derived phosphatidylserine (from Fidia) or a placebo.¹⁴ Both treatment phases lasted for eight weeks with an eight-week washout phase in between and a four-week washout phase before treatment phase one. The phosphatidylserine treated patients showed significantly more improvement in clinical global improvement ratings than the placebo during treatment phase one. The improvement carried over to the following washout and treatment phases. There were no significant improvements in GBS dementia rating scale, psychometric tests or P300-latency. The patients initially showed higher power values in all frequency bands except alpha, when compared to a younger, healthy control group. Phosphatidylserine reduced the higher power values compared to the placebo, shifting electroencephalographic (EEG) power more toward the normal level.

An open, uncontrolled study published in Clinical Trials Journal involved 27 patients with senile cognitive decline given 300 mg/d of phosphatidylserine for 60 days.¹⁵ A series of neuropsychological tests and the Geriatric Rating Scale were used. During the treatment period, an improvement in cognitive and behavioral functions was observed; the improvement persisted for a month after the end of therapy.

Vinpocetine, a semi-synthetic derivative alkaloid of vincamine, an extract from periwinkle, has been found to increase blood flow and glucose metabolism. A randomized, double blind crossover study at the University of Leeds, Leeds, UK, gave 12 healthy female volunteers pre-treatments with vinpocetine (as BioVinca™, from Cyvex) 10, 20, 40 mg and placebo for two days.¹⁶ On the third day of treatment and one hour following the morning dosage, the subjects completed several psychological tests. There was no significant change in the placebo group on the critical flicker fusion, choice reaction time or subjective ratings of drug effects; however, memory was significantly improved after treatment with 40 mg of vinpocetine when compared to placebo. The results suggest a localized effect of the drug on the serial comparison stage of the reaction process.

Another botanical derived from the root of Angelica gigas Nakai has shown positive effects on memory. A Korean 12-week clinical trial examined the effects of INM 176 (as Cogni-Q, from Maypro) compared with a placebo on the cognitive functions of 92-year-old subjects with cognitive impairment.¹⁷ The subjects scored less than 25 points on the Korean Mini Mental Status Exam (K-MMSE) and showed a high risk of Alzheimer’s from the Neurocognitive Screening Battery. The INM 176 group’s total error score in the Alzheimer’s Disease Assessment Scale-Cognitive (ADAS-cog) decreased significantly (P<0.01), whereas the placebo group showed a slight increase. The mean changes in Instrumental Activities of Daily Living (IADL) and Geriatric Depression Scale (GDS), from baseline scores, favored the INM 176 group more than in the placebo group and outcome changes of ADAS-cog, IADL, KGDS scores during the 12 week clinical trial showed favorable responses in the INM 176 administered group; however, further clinical trials are needed to demonstrate its efficacy. An in vivo study at Seoul National University administered decursin, a major coumarin constituent isolated from Angelica gigas, to mice at 1 and 5 mg/kg body weight with scopolamine-induced amnesia.¹⁸ The decursin significantly ameliorated scopolamine-induced amnesia, measured in the passive avoidance test and the Morris water maze test. Decursin also significantly inhibited acetylcholinesterase (AChE) activity by 34 percent in the hippocampus of the treated mice.

Another study allowed mice free access to drinking water (control group) or water containing different concentrates of an ethanolic extract of Angelica gigas Nakai (EAG).¹⁹ After four weeks, A beta1-42 was injected intracerebroventricular. The mice previously treated with EAG (0.1 percent) significantly blocked the A beta1-42-induced impairment in passive avoidance performance. Next, mice were fed chow mixed with various doses of decursinol for four weeks, before A beta1-42 was injected. The mice pretreated with decursinol (0.001 percent, 0.002 percent and 0.004 percent) significantly attenuated the A beta1-42-induced impairment in passive avoidance performance. Decursinol (0.004 percent) also significantly blunted the A beta1-42-induced decrease in alternation behavior in the Y-maze test without change in general locomotor activity.

Further, a study published in the Journal of Natural Products showed decursinol represented the highest inhibitory activity toward AChE in vitro, out of 11 known isolated coumarins.²⁰

Antioxidants are a weapon beneficial for fighting off oxidation that may cause cell death. A study at the University of Washington, Seattle, gave mouse pups access to drinking water with pomegranate juice, at one of three doses, as well as plain water, sugar water and vitamin C water controls during the last third of pregnancy and throughout the duration of litter suckling.²¹ At postnatal, day seven, the pups underwent unilateral carotid ligation followed by exposure to 8 percent oxygen for 45 minutes. Dietary supplementation with pomegranate juice resulted in markedly decreased brain tissue loss (>60 percent) in all three brain regions assessed, with the highest pomegranate juice dose having the greatest significance (P< or = 0.0001). Pomegranate juice also diminished caspase-3 activation by 84 percent in the hippocampus and 64 percent in the cortex. Ellagic acid, a polyphenolic component in pomegranate juice, was detected in plasma from treated but not control pups.

Coenzyme Q10 (CoQ10) also has powerful antioxidant properties. A Chinese study treated aged transgenic mice over-expressing Alzheimer presenilin 1-L235P (leucine-to-proline mutation at codon 235, 16 to 17 months old) by feeding them CoQ10 for 60 days (1,200 mg/kg(-1)/d (-1)).²² The treatment partially attenuated A beta overproduction and intracellular A beta deposit in the cortex of the transgenic mice compared with the age-matched untreated transgenic mice. An increased oxidative stress and decreased activity of superoxide dismutase (SOD) occurred in the transgenic mice relative to the wild-type mice, and supplementation of CoQ10 partially decreased malondialdehyde level and upregulated the activity of SOD. A Japanese in vitro study found CoQ10 dose-dependently inhibited beta-amyloid fibrils formation from A beta, as well as their extension, and destabilized preformed beta-amyloid fibrils.²³ The anti-amyloidogenic effects of CoQ10 were slightly weaker than nordihydroguaiaretic acid and myricetin.

Green tea is a well-known antioxidant with high levels of polyphenols. A Chinese study injected D-galactose (120 mg/kg) and A beta25-35 into mice for 12 weeks to establish Alzheimer-like mice.²⁴ Green tea polyphenols ameliorated the deleterious effects of D-galactose and A beta25-35 improving the animals’ learning, memory, prolonged latency time and autonomic activities while significantly reducing the error numbers. Similarly, researchers from a Japanese animal model found that long-term administration of green tea catechins provided effective prophylactic benefits against A beta-induced cognitive impairment by increasing antioxidative defenses.²⁵

In a 2007 model, researchers stated that accumulation of iron where neurons degenerate in Alzheimer's disease may play a role in the oxidative stress-induced process of neurodegeneration.²⁶ Iron chelators like VK-28 and its multi-functional derivative, M-30, as well as (-)-epigallocatechin-3-gallate (EGCG), the main polyphenol constituent of green tea, can offer potential benefits for Alzheimer's disease. In the serum deprivation model, M-30 and EGCG decreased apoptosis of cells through multiple protection methods, and promoted morphological changes, resulting in axonal growth-associated protein-43 (GAP-43) implicating neuronal differentiation. Both M-30 and EGCG significantly reduced the levels of cellular holo-APP in cells. EGCG reduced the levels of toxic A beta peptides in CHO cells over-expressing the APP “Swedish” mutation.

Resveratrol is found in the skin of red grapes, blueberries, peanuts and other plants. Researchers from a study at Howard Hughes Medical Institute, Boston, reported in cell-based models for Alzheimer’s and amyotrophic lateral sclerosis (ALS), SIRT1 and resveratrol, a SIRT1-activating molecule, both promote neuronal survival.²⁷ In the inducible p25 transgenic mouse, a model of Alzheimer’s and tauopathies, resveratrol reduced neurodegeneration in the hippocampus; prevented learning impairment; and decreased the acetylation of the known SIRT1 substrates PGC-1alpha and p53. In addition, injection of SIRT1 lentivirus in the hippocampus of p25 transgenic mice conferred significant protection against neurodegeneration.

In another study out of New York, Tg2576 mice, which model Alzheimer’s disease-type A beta-protein neuropathology, received either Cabernet Sauvignon with 6 percent ethanol and 0.2 mg/L of resveratrol, a comparative amount of ethanol or water alone.²⁸ Researchers found the Cabernet Sauvignon significantly attenuated Alzheimer's disease-type deterioration of spatial memory function and A beta neuropathology relative to control Tg2576 mice.

A Chinese study randomly divided 84 Kunming female mice into six groups.²⁹ After 60 days, researchers concluded resveratrol of every dosage could improve the performance records of behavior tests in Alzheimer mice, inhibit the SOD vitality and malondialdehyde (MDA) level both in the serum and in the brain, and could suppress the acetylcholinesterase vitality and the bax expression without a side effects of endometrial hyperplasia.

High blood concentrations of folic acid, a form of the water-soluble vitamin B9, are associated with positive cognitive function. In a 2008 six-month, randomized, double blind, placebo-controlled study, 57 outpatients with probable Alzheimer's disease were treated concurrently with cholinesterase inhibitors (ChI) and either folic acid or a placebo.³⁰ At the end of the six months, there were no significant baseline differences or use of individual ChI between the two arms. A significant difference was seen in the change from baseline in combined IDAL and Social Behaviour scores between arms versus the placebo, but there was no change in MMSE scores. Sixteen of 23 subjects receiving folic acid and seven out of 18 placebo subjects were classified as National Institute of Clinical Excellence (NICE) responders (P=0.05). Researchers concluded that response to ChI in patients with Alzheimer’s may be improved by the use of folic acid.

A study published in The Lancet randomly assigned 818 participants 800 μg/d folic acid or placebo for three years.³¹ Serum folate concentrations increased by 576 percent and plasma total homocysteine concentrations decreased by 26 percent in participants taking folic acid compared with those taking placebo. The three-year change in memory, information processing speed and sensorimotor speed were significantly better in the folic acid group than in the placebo group.

In an Italian study published in the Journal of the American College of Nutrition, 471 consenting subjects participating in the Monzino 80-plus study, a door-to-door population-based survey among very old subjects living in Northern Italy, were assessed for their serum vitamin B12 and folate concentrations.³² Cognitive and functional evaluations included MMSE, IADL and Spontaneous Behavior Interview-basic Activities of Daily Living (SBI-bADL). The MMSE, IADL and SBI-bADL scores were all significantly correlated with folate concentrations, while no significant associations were found with vitamin B12 concentrations. Folate showed a highly significant, curvilinear association with both cognitive and functional scores (P<0.0001). Subjects in low and middle folate tertiles had significantly higher odds ratios for dementia. The findings suggested subclinical folate deficiency may represent a risk factor for the cognitive decline associated with aging that could contribute to Alzheimer’s as well as other dementia development.

Other B vitamins have been studied for their effects on Alzheimer’s disease. A Swedish study used a population-based sample to examine the associations of vitamin B12 and folate with cognitive functioning in clinical (n=44) and preclinical (n=39) Alzheimer’s.³³ The groups were subdivided in terms of low versus normal levels of B12, and low versus normal folate levels. The preclinical Alzheimer’s group performed better than the Alzheimer’s group across most cognitive tests. The effects of low vitamin B12 and folate levels were negligible across all cognitive tests in clinical and preclinical Alzheimer’s indicating the influence of vitamin B deficiency on cognitive functioning is overshadowed by the neurodegenerative processes associated with Alzheimer's disease.

Another trial was conducted at En Chu Kong Hospital, Taipei, Taiwan where 89 male and female patients aged more than 50-years-old with mild to moderate Alzheimer’s, normal folic acid and vitamin B12 concentrations were randomized to receive 500 mg of vitamin B12; plus a multivitamin supplement containing 5 mg of pyridoxine (B6), 1 mg of folic acid, iron and other vitamins; or placebos for 26 weeks.³⁴ At week 26, there were no significant differences in cognition or ADL function scores between the two groups; the mean between-group difference in serum homocysteine concentration versus placebo was -2.²⁵ (P = 0.008) and the mean serum concentrations of vitamin B12 and folic acid were significantly higher, but within normal range, in the multivitamin group compared with placebo. The study showed a multivitamin supplement containing vitamins B6, B12 and folic acid for 26 weeks decreased homocysteine concentrations, but no statistically significant beneficial effects on cognition or ADL function were found between multivitamin and placebo.

Citicoline, a form of the B vitamin choline that supports phospholipid production in the brain, has been used to treat neurodegenerative disorders. In a double blind, placebo-controlled, randomized clinical trial, 30 patients with mild to moderate senile dementia of the Alzheimer type were treated with 1,000 mg/d of citicoline (as Cognizin™, from Kyowa Hakko) (n=13) or placebo (n=17) for 12 weeks.³⁵ Compared to placebo, citicoline improved cognitive performance in Alzheimer's disease patients with apolipoprotein E (APOE); this improvement was more pronounced in patients with mild dementia. Citicoline also increased cerebral blood flow velocities in comparison with the placebo (P<0.05) when transcranial Doppler recordings from both hemispheres were considered together, as well as diastolic velocity in the left middle cerebral artery (P<0.05). Patients treated with citicoline showed an increase in the percentage of brain bioelectrical activity of alpha (occipital electrodes) and theta type (left side electrodes), accompanied by a decrease in relative delta activity particularly marked in the left temporal lobe. Significant differences with respect to placebo (P<0.05) were observed for theta activity in several fronto-parieto-temporal electrodes of the left hemisphere. Treatment with citicoline tended to reduce serum IL-1 beta levels, mainly after four weeks of administration, with no modified blood histamine content. In addition, neither adverse side effects nor alterations in biological and hematological parameters were induced by citicoline.

An Italian study investigated the effects of citicoline (as posatirelin) and ascorbic acid (inactive drug) in elderly patients suffering from late-onset Alzheimer's disease for three months.³⁶ The once daily treatment lasted for three months and was followed by one-month oral treatment with a placebo. At the end of the treatment, Gottfries-Bråne-Steen (GBS) subscale and factor scores assessing intellectual and emotional impairments, orientation and memory, ability to perform activities of daily living, depression-anxiety, attention and motivation were improved in the postatirelin group, showing significant differences with respect to the citicoline and/or ascorbic acid groups.

In a Spanish study, elderly subjects with memory deficits and without dementia were administered 1,000 mg/d or 500 mg/d of citicoline alone (as Cognizin) or 300 mg/d of citicoline plus 90 mg/d of nimpdipine for four weeks.³⁷ Citicoline, in comparison with the placebo, improved memory in free recall tests, but not in recognition tests. There was a significant improvement in word recall (P<0.005), immediate object recall (P<0.05) and delayed object recall after citicoline treatment (P<0.005). In addition, three subgroups of treatment also showed citicoline’s memory-enhancing activity at doses of 300 to 1,000 mg/d.

Ginkgo biloba is a botanical used to enhance memory. In a 24-week, double blind, placebo-controlled study in Italy, patients 50 to 80 years old suffering from mild to moderate dementia were randomized into one of three treatments: 160 mg/d of Ginkgo biloba (as Flavogin®, from Baif International Products); 5 mg/d of donepezil, a cholinesterase inhibitor; or placebo.³⁸ The results confirmed the clinical efficacy of ginkgo biloba E.S. in Alzheimer's disease compared with donepezil clinical efficacy. There was no evidence of relevant differences in the efficacy of Ginkgo biloba EGb 761 and donepezil in the treatment of mild to moderate Alzheimer’s, justifying the use of both substances. Researchers stated the study helped establish the efficacy and tolerability of Ginkgo biloba E.S. in Alzheimer’s with special respect to moderately severe stages.

A double blind, placebo-controlled trial at UCLA took 10 right-handed persons with age-associated memory impairment (AAMI), aged 47 to 75 years old, and randomly assigned them to either 120 mg of Ginkgo biloba EGb 761 twice daily or a placebo for six months.³⁹ The ginkgo group significantly improved immediate verbal recall compared to the placebo group (P=0.03). The placebo and ginkgo groups did not differ significantly in change in cerebral metabolism. All the subjects showed improvement in immediate recall, which significantly correlated with increased glucose metabolism in the right lateral temporal cortex. Researchers stated Ginkgo biloba appeared to improve verbal memory relative to placebo, and the magnitude of cognitive improvement correlated significantly with resting lateral temporal metabolism.

Despite the sad truth that there is no cure for Alzheimer’s, natural supplements can help slow down the degenerative process and improve brain functions, prolonging the process the disease takes as well as play a role in prevention.

Editor's Note: Looking for more information on nutritional ingredients for cognitive health? INSIDER's Free Webinar, "Cognition and Memory: Consumer Attitudes and Ingredients to Remember", will be available on demand May 22, 2008. Click here to learn more.

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