Cognitive Health

The brain is the master organ, responsible for such glories as emotion, intelligence and personality, as well as more mundane but crucial tasks including management of organ function, hormone regulation and locomotion. Certain nutritional practices can improve the performance of the body’s chief executive officer as it manages the body’s vast range of daily activities, from shaping the governing philosophies of the organism to tending to details at the bottom of the organizational pyramid.

Perhaps the most complex and sophisticated entity on Earth, the human brain could be considered the pinnacle of biological achievement. Indeed, one of life’s greatest miracles is the ability of cognitive tissue to transcend reflexive activities and form thoughts, versus the less sublime capabilities of the humble hair or the lowly leg, both relative dullards in comparison to the gifted brain. In fact, without the governance of the brain, these body parts and all of their compatriots would be rendered a useless collection of flailing limbs and failing systems.

Understandably, furnishing proper nutritional support to such a multifaceted organ involves provision of a comprehensive package of micronutrients and building blocks. These raw materials promote optimal cognitive function by sharpening mental acuity, inhibiting agerelated cognitive decline, and building and maintaining neurons, from the months preceding birth through the Golden Years.

Antioxidants

Antioxidants

contribute to long-term structural and functional integrity of the brain by countering oxidative damage in neural tissues. Antioxidant intake may be of particular importance to older people looking to boost cognitive ability, as the aging brain typically struggles to heal cumulative oxidative damage. Supportive of this premise is a review from Tufts University, Boston; researchers wrote cellular generation of reactive oxygen species (ROS) causes oxidative damage to nucleic acid, carbohydrate, protein and lipid components of the brain, where damaged neuronal cells—which are largely post-mitotic— cannot be replaced readily via mitosis.¹ They added this damage causes morphological and functional modifications resulting in decrements in motor and cognitive performance, and possibly neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Parkinson’s disease (PD). Further, numerous clinical trials confirm the importance of consuming an antioxidant-rich diet to preserve cognitive ability. A study from the University of Perugia in Italy connected depressed peripheral levels of the water-soluble antioxidant vitamin C; lipophilic antioxidants including vitamin A and vitamin E, and carotenoids such as lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alpha-carotene and beta-carotene; and activities of plasma and red blood cell (RBC) antioxidant enzymes such as superoxide dismutase (SOD) with mild cognitive impairment (MCI) and AD in test subjects, as compared to controls.² Further, the researchers noted that since MCI may represent a prodromal stage of AD, and oxidative damage appears to occur as one of the earliest pathophysiological events in AD, an increased intake of antioxidants in patients with MCI could be helpful in lowering the risk of conversion to dementia. And a clinical trial from the University of Washington, Seattle, provides additional reason to increase consumption of antioxidants to ensure optimal cognitive performance over a lifetime; researchers monitored long-term antioxidant status and cognitive function in a seven-year study of 2,082 community-dwelling elderly subjects and found test subjects who supplemented with antioxidants (vitamins A, C or E, plus selenium or zinc) had a 34-percent lower risk of developing cognitive impairment and a 29-percent lower risk of experiencing cognitive decline, compared with non-antioxidant users.³

Vitamin E, in particular, seems to be one of the most neuroprotective antioxidants, with marked efficacy against AD and other neurodegenerative disorders.^4,5 In a cohort of 1,033 elderly people, Italian researchers found participants with plasma vitamin E levels in the bottom tertile had a significantly higher probability of being demented and suffering from cognitive impairment, compared to those in the highest vitamin E tertile.⁶ And a six-year study from Rush University, Chicago, found a slower rate of cognitive decline was associated with intakes of vitamin E, alpha-tocopherols and alphatocopherol equivalents, and gamma-tocopherols.⁷

Other forms of vitamin E that have shown similarly positive results are tocotrienols. Tocomin®, a full-spectrum palm tocotrienol complex from Carotech, may be a particularly neuroprotective form of vitamin E; one mechanism by which the ingredient protects cognitive function is by crossing the blood-brain barrier and protecting neurons from glutamate-induced neurodegeneration, a major contributor to pathological cell death within the nervous system and a factor in development of AD, stroke and other neurodegenerative disorders.^8,9,10 A rat study from Ohio State University Medical Center, Columbus, tested whether oral supplementation of tocotrienols (as Tocomin) during pregnancy is bioavailable to fetal and maternal brains, and whether short-term change in dietary vitamin E levels of pregnant rats influences gene expression profile of developing fetal brains.¹¹ The researchers found supplementation with Tocomin increased tocotrienol levels in maternal and fetal brains by 5- and 20-fold, respectively.

Further, research published in Stroke suggested neuronal cells injected with alpha-tocotrienol (from Carotech), but not alphatocopherol, were protected from a glutamate challenge; and rats supplemented with alpha-tocotrienol experienced enhanced protection against stroke-induced neurodegeneration, as compared to matched controls.¹² The researchers concluded alpha-tocotrienol acts on key molecular checkpoints to protect against glutamate- and strokeinduced neurodegeneration.

In addition to vitamins E and A, one vitamin-like compound implicated in cognitive function is coenzyme Q10 (CoQ10), a highly mobile electron carrier in the mitochondrial respiratory chain and powerful antioxidant.¹³

As CoQ10 levels decline with age,¹⁴ accelerating mitochondrial dysfunction and oxidative damage (both precursors of beta-amyloid deposition), supplementation with the compound could be a preventive measure against AD, PD and other neurodegenerative disorders.¹⁵ Research corroborating this idea was conducted by Portuguese scientists who demonstrated CoQ10 therapy attenuated amyloid betapeptide toxicity in brain mitochondria isolated from elderly rats.¹⁶ The researchers evaluated several mitochondrial parameters including respiratory indexes, transmembrane potential, repolarization lag phase, repolarization and adenosine triphosphate (ATP) levels, as well as mitochondrial production of hydrogen peroxide, and observed that CoQ10 treatment attenuated a significant decrease in oxidative phosphorylation efficiency and ATP content, and a significant increase in hydrogen peroxide production induced by 4 mcM of amyloid betapeptide (Abeta1-40). It was concluded the CoQ10 treatment counteracted brain mitochondrial alterations induced by the neurotoxic peptide, suggesting CoQ10 therapy can help to avoid a drastic energy deficiency that characterizes AD pathophysiology. And research from the University of North Texas, Fort Worth, showed supplementation of aged mice with CoQ10 and alpha-tocopherol improved brain function of aged mice, as measured by cognitive tests.¹⁷ Separate groups of aged mice (24 months) were administered either CoQ10 (123 mg/kg/d), or alpha-tocopherol acetate (200 mg/kg/d), or both, or just the vehicle (soybean oil) as a control, via gavage for a period of 14 weeks. Three weeks following the initiation of these treatments, mice were given a battery of age-sensitive behavioral tests for the assessment of learning and recent memory. In a test that required the mice to rapidly identify and remember the correct arm of a T-maze, and to respond preemptively in order to avoid an electric shock, the intake of alpha-tocopherol plus CoQ10 resulted in more rapid learning compared to the control group.

Fatty Compounds

Certain fatty compounds comprise another major nutritional category known to promote optimal cognitive function. One such class of compounds is polyunsaturated fatty acids (PUFAs), which, much like amino acids, provide raw materials necessary to build lean body mass, and supply building blocks necessary for production of brain tissue and neurotransmitters important in cognitive function. Many scientists believe fish oil is an optimal source of PUFAs, due to its rich content of eicosapentaenoic acid (EPA), which may inhibit stroke by thinning blood and lowering blood pressure, and docosahexaenoic acid (DHA), which is particularly important in the generation and maintenance of neuronal tissues. Since insufficient dietary PUFAs could stunt cognitive development, many experts advise pregnant and lactating women to ensure high dietary intake of these compounds. In fact, according to a meta-analysis from the Harvard School of Public Health, Boston, increasing maternal DHA intake by 100 mg/d during pregnancy and lactation (or providing DHA-enriched formula to neonates) may increase the intelligence quotient (IQ) of offspring by 0.13 points.¹⁸ Further, a study from the University of Kansas, Lawrence, showed infants whose mothers had high serum DHA at birth scored higher on psychophysiological tests and distractibility paradigms and had greater focus during free-play over the first and second years.¹⁹ And a Norwegian study published in Pediatrics showed pregnant women supplemented with 10 mL/d of fish oil from gestational week 18 through delivery, and during the first three months postpartum while breastfeeding, produced offspring with higher scores on the Kaufman Assessment Battery for Children at four years of age than did offspring of mothers given an equivalent dose of corn oil over the same time period.²⁰

Another fatty compound of value to cognitive health is the nutrient choline, a component of brain cell membrane phospholipids and a precursor of acetylcholine (ACh), a neurotransmitter important in memory and concentration. A Children’s Hospital Oakland Research Institute (Calif.) review of 34 studies in rodents linking the availability of choline during gestation and perinatal development to neurological function suggests maternal choline supplementation improves performance on difficult cognitive tests, boosts electrophysiological responsiveness and size of neurons and protects against adverse effects of several neurotoxic agents (including alcohol), in offspring.²¹

Citicoline,

synthesized from choline in the body, is another fatty compound conducive to optimal brainpower.²² Like choline, citicoline is involved in maintaining the structural integrity and functionality of neuronal membranes and is a precursor of ACh. A meta-analysis from the University of Rome conducted to assess the efficacy of citicoline in the treatment of cognitive deficits and other problems associated with chronic cerebral disorders in the elderly, confirmed citicoline has a positive effect on memory, at least in the short to medium term; the researchers noted the evidence for this theory was limited only by the duration of the studies reviewed.²³ Additional positive research on citicoline, conducted by researchers from the Massachusetts Institute of Technology, Cambridge, found three months’ administration of approximately 500 mg/kg/d of citicoline to young rats with induced hippocampal-dependent memory impairments similar to those observed in aging rodents ameliorated the animals’ memory impairment, likely through enhancement of neuronal membrane phosphatide synthesis.²⁴ Further, another rodent study, unpublished and funded by Kyowa Hakko (supplier of Cognizin® citicoline) found mice given a diet of 2-percent citicoline for four weeks exhibited enhanced memory compared to control mice.

Another lipid involved in signal transduction activity and maintenance of neuronal membranes is phosphatidylserine (PS), commonly sourced from soy, egg and bovine brain.25 Like choline and citicoline, PS may support memory and inhibit age-related cognitive impairment. A study from the Yakult Central Institute for Microbiological Research in Tokyo showed oral administration of PS sourced from soybean lecithin (60 mg/kg/d for 60 d) to aged male rats significantly improved performance in the Morris water maze escape test, increased ACh release and restored synaptosomes activities to those seen in young rats.²⁶ And a human clinical study from Tel Aviv University in Israel indicated administration of thrice-daily 100-mg doses of plant-source PS to 18 healthy elderly volunteers meeting Age Associated Memory Impairment inclusion and exclusion criteria for 12 weeks improved test subjects’ cognitive abilities, prompting the researchers to conclude plant-source PS supplementation may be a viable approach to the treatment of age-related cognitive decline, without exposing the patients to possible disease transfer linked to treatment with bovine-source PS.²⁷

Botanicals

Kingdom Plantae provides a vast array of research-backed compounds shown to protect and enhance cognitive ability.

One such compound, huperzine A (HupA), extracted from Chinese club moss (Huperzia serrata), is a sesquiterpene alkaloid with documented neuroprotective effects.²⁸ According to a review from the Shanghai Institutes for Biological Sciences in China, HupA possesses the ability to protect cells against hydrogen peroxide, beta-amyloid protein, glutamate, ischemia and staurosporine-induced cytotoxicity and apoptosis; has been found to reverse or attenuate cognitive deficits in a broad range of animal models; and has significantly attenuated memory deficits in aged human subjects as well as patients with benign senescent forgetfulness, AD and vascular dementia (VD), with minimal peripheral cholinergic side effects.²⁹ A clinical trial from the Chinese Academy of Sciences showed HupA protects cognitive function in animals with impaired cognitive function induced by ischemia.^30,31 Fourteen days of twice-daily oral administration of 0.1 mg/kg HupA to gerbils after the animals were subjected to five minutes of global ischemia significantly reduced memory impairment, reduced neuronal degeneration in the CA1 region, and partially restored hippocampal choline acetyltransferase activity; the researchers concluded the ability of HupA to attenuate memory deficits and neuronal damage after ischemia might be beneficial in cerebrovascular type dementia.

Another herbaceous compound thought to support optimal cognitive function is vinpocetine, an alkaloid derived from the lesser periwinkle Vinca minor L. Vinpocetine has been found to optimize cognitive function by increasing cerebral blood flow^32,33 and glucose metabolism,³⁴ which it may accomplish by altering the rheological properties of blood.³⁵ A study published in the Journal of the Neurological Sciences showed administration of vinpocetine (as BioVinca®, from Cyvex Nutrition) to chronic ischemic stroke patients resulted in increased global cerebral blood flow and beneficial changes in regional cerebral glucose metabolism.³⁶

Neuroprotective berries are concentrated sources of antioxidants known as polyphenols, or more specifically as anthocyanins, which provide some of the most powerful nutritional and therapeutic benefits offered by the botanical world. In a study from the University of Barcelona, Spain, researchers fed rats various vegetable and fruit extracts and found blueberry extracts were particularly effective in reversing age-related deficits in neuronal signaling and behavioral parameters following eight weeks of feeding, likely due to content of anthocyanins.³⁷ Nineteen-month-old rats were fed a 2-percent blueberry or control diet for eight to 10 weeks and tested in the Morris water maze to gauge spatial learning and memory; in addition, the researchers analyzed different brain regions of blueberry-fed and control rats to check for presence of antioxidant compounds; antioxidant berry polyphenols known as anthocyanins were found in the cerebellum, cortex, hippocampus or striatum of rats given blueberries, but not in brains of control animals, likely indicating the blueberry anthocyanins were able to cross the blood brain barrier and localize in various brain regions important for learning and memory. Further, clinical trials from Tufts University, Boston, indicated supplementation of rats with blueberries attenuated age-related declines in spatial memory tasks by restoring hippocampal plasticity,³⁸ and administration of 14.8 g/kg/d of strawberry extract to rats for eight weeks reversed age-related deficits in several neuronal parameters by enhancing release of dopamine from striatal slices, benefiting synaptosomes, and improving performance on the accelerating rotating rod test, and Morris water maze tests.³⁹ And Russian and Spanish research on bilberries has shown rats supplemented with bilberry extract (2 g/kg of diet) and vitamin E (140 mg/kg of diet) showed improvement in cognitive deficits, and 0.2 mg kg/d bilberry and blueberry extracts improved cognitive performance on step-down inhibitory avoidance and open field tests.^40,41

Spirulina

also appears to protect and enhance cognitive function. Research from Umea University in Sweden has shown spirulinaenriched diets enhance striatal dopamine recovery and induce rapid, transient microglia activation after injury of the nigrostriatal dopamine system in rats.⁴² Further, a study from the National Institute on Drug Abuse, Baltimore, showed a spirulina-rich diet may reduce neurodegenerative changes in aged animals by demonstrating rats fed spirulina were protected from cerebral ischemia, as evidenced by significant reduction in the volume of infarction in the cerebral cortex and an increase in post-stroke locomotor activity.⁴³

Another botanical boon to cognitive function is extract of French maritime pine bark. In vitro research conducted by scientists from Loma Linda University, Calif., has shown treatment of a rat pheochromocytoma (PC12) cell line with pine bark extract (as Pycnogenol®, from Natural Health Science) suppressed neuronal apoptosis and generation of ROS and DNA fragmentation, and eventually protected against beta-amyloid-induced apoptosis, one of the pathological features of AD.⁴⁴ Further, a study from the University of Florida, Gainesville, showed Pycnogenol inhibited death of neurons exposed to ethanol,⁴⁵ which could mean the compound protects cognitive function in individuals who consume alcohol.

Tea

is one more herbaceous ingredient with neuroprotective effects. A review from the Eve Topf and USA National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research in Haifa, Israel, noted tea flavonoids (catechins) have been reported to possess potent antioxidant and anti-inflammatory activities useful in countering age-associated cognitive decline and neuronal loss in neurodegenerative conditions including AD, PD and Huntington’s diseases; and inhibit neuronal death in a wide array of cellular and animal models of neurological disorders.⁴⁶ Further, the authors of the review wrote tea is an iron chelator, a boon to patients with neurological diseases, since one chemical pathology observed in these disorders is the accumulation of iron at sites where the neurons die. Numerous clinical trials substantiate the beneficial effects of tea on the brain. One study from Shimane University in Izumo, Japan, showed 26 weeks of oral administration of green tea catechins (as Polyphenon® E, from Mitsui Norin) mixed with water improved the spatial cognition learning ability of young rats.⁴⁷ Relative to controls, animals administered PE had improved reference and working memory-related learning ability in the partially baited eight-arm radial maze, as well as lower plasma concentrations of lipid peroxides and lower hippocampal ROS concentrations; the researchers suggested the improvements in spatial cognitive learning ability may have been due to the antioxidative activity of green tea catechins. Further, research from Tohoku University in Sendai, Japan, found inverse associations between black, green and oolong tea consumption and cognitive impairment in 1,003 elderly Japanese subjects.⁴⁸

Soy

has been shown to promote cognitive wellness, particularly among postmenopausal women. A study confirming this premise was conducted by English researchers; 33 postmenopausal women (aged 50-65 years) not receiving conventional hormone replacement therapy (HRT) were randomly allocated in a double blind, parallel fashion to receive a soy supplement (60 mg/d total isoflavone equivalents) or placebo for 12 weeks.⁴⁹ At baseline and at the end of the intervention period, the women were subjected a battery of cognitive tests; those who received the soy supplement showed significantly greater improvements in recall of pictures and in a sustained attention task as well as greater improvements in learning rule reversals and completing a planning task. Further, a six-month, double blind, randomized, placebo-controlled trial from the University of California, San Diego, in healthy women who were postmenopausal at least two years and not using HRT, showed administration of a 110 mg/d soy isoflavone supplement (as Healthy Woman, from McNeil-PPC Inc.) improved test subjects’ scores on cognitive tests designed to measure verbal memory.⁵⁰

Resveratrol

, a polyphenolic phytoalexin found abundantly in grape skins, is another botanical compound shown to confer benefits to the brain. An Indian study indicated administration of resveratrol to rats in a model of sporadic AD dementia preserved the animals’ learning and memory capabilities, as assessed by passive avoidance paradigms, elevated plus maze and the closed field activity, and lowered the animals’ oxidative stress as shown by reduced malondialdehyde (MDA) and glutathione levels, compared to rats given a control treatment.⁵¹ And resveratrol may also protect against the ravages of ischemia in the brain; researchers from National Chia- Yi University gave 60 adult male rats general anesthesia and randomized them to receive an ischemia treatment (bilateral ligation of carotid artery), ischemia combined with resveratrol administration (20 mg/kg) or a sham treatment.⁵² In rats not administered resveratrol, hydroxyl radical levels were elevated and severe neuronal loss occurred in the brain. In contrast, brains of animals given resveratrol had significantly increased concentrations of nitric oxide (NO) and decreased population of hydroxyl radicals.

Intake of curcumin, a polyphenolic diketone derived from turmeric root, may also promote optimal cognitive function. Like tea, curcumin may function as a chelator of metals, which can induce beta-amyloid aggregation and toxicity in the brain, and are concentrated in the brains of patients with AD and other neurodegenerative conditions. In fact, curcumin was shown to bind with copper, zinc and iron ions in an in vitro study from the Chinese University of Hong Kong, Shatin, conducted to test this premise.⁵³ Further, the ability of curcumin to inhibit beta-amyloid accumulation was shown in a trial from the University of Los Angeles.⁵⁴ When administered to aged Tg2576 mice with advanced amyloid accumulation, curcumin targeted plaques and reduced amyloid levels and plaque burden, directly binding small betaamyloid species to block aggregation and fibril formation in vitro and in vivo. And another clinical trial conducted at the University of Los Angeles demonstrated supplementation with curcumin attenuated the effects of traumatic brain injury on cognition and synaptic plasticity in a rat model.⁵⁵

Ginseng

, a Chinese adaptogenic herb, produces a root with cognitive-enhancing effects, according to several clinical trials. One such trial, a double blind, placebo-controlled, crossover study conducted at Northumbria University, Newcastle-upon-Tyne, England, showed administration of Panax ginseng to healthy young adults subjected to a 10-minute test battery at baseline, and then six times in immediate succession after receiving ginseng extract or placebo. Blood glucose was measured prior to each day’s treatment, and before, during and after the post-dose completions of the battery. Administration of ginseng produced significant reductions in blood glucose levels at all three post-treatment measurements; the researchers concluded ginseng can improve performance and subjective feelings of mental fatigue during sustained mental activity, possibly due to acute gluco-regulatory properties of the extract.⁵⁶ And an in vitro study from the University of Alberta, Edmonton, showed ginsenosides enhanced neurite outgrowth in the absence of a nerve growth factor.⁵⁷

Ashwagandha

(Withania somnifera), traditionally used by Ayurvedic practitioners in India, is another adaptogenic herb thought to benefit the brain through beneficial actions on dendrites and axons damaged by neurodegeneration.⁵⁸ An in vitro study from Toyama Medical and Pharmaceutical University in Japan showed administration of methanol extract of ashwagandha root (5 mcg/mL) significantly and dose-dependently increased the percentage of cells with neurites in human neuroblastoma SK-N-SH cells; mRNA levels of dendritic markers were markedly increased by treatment with the extract, whereas those of the axonal marker Tau were not.⁵⁹ The researchers concluded ashwagandha promotes the formation of dendrites, which may compensate for and repair damaged neuronal circuits in the dementia brain. Additional studies from the same institution found oral administration of withanoside extracted from ashwagandha significantly improved memory deficits in betaamyloid- injected mice (to induce dendritic and axonal atrophy) and prevented loss of axons, dendrites, and synapses in the cerebral cortex and hippocampus.^60,61

Another brain-friendly Ayurvedic herb is Bacopa monniera (BM). An Indian study in showed administration of BM extract to mice with cognitive impairment induced by phenytoin improved the animals’ scores on a passive avoidance test.⁶² Further, a clinical trial held at the School of Biophysical Science and Electrical Engineering, Victoria, Australia, tested the effects of chronic administration of a BM extract (as Keenmind®, from Keenmind Pty Ltd.) on cognitive function in healthy human subjects in a double-blind placebo-controlled independent-group design, and found BM significantly improved speed of visual information processing, learning rate, memory consolidation and state anxiety compared to placebo, with maximal effects evident after 12 weeks.⁶³ The researchers concluded BM may improve higher order cognitive processes that are critically dependent on the input of information from our environment such as learning and memory. And a study from the Central Drug Research Institute, in Lucknow, India, tested the antidementic potential of BM and Ginkgo biloba in mice with scopolamine-induced deficits on the animals’ performance on the passive avoidance test; BM- and ginkgo-treated mice showed significant increases in TLT and NTR after scopolamine treatment, indicating BM and ginkgo attenuated scopolamine’s dementic effect.⁶⁴ Further, both extracts showed additional anti-dementic capability by dose-dependently inhibiting acetylcholinesterase (AChE) activity in vitro.

Other studies on ginkgo have shown similarly positive results, including normalization of stress- and corticosterone-induced impairment of recall in rats, suppression of beta-amyloid production by lowering free cholesterol levels, and enhancement of spatial learning and memory in aged and yohimbine-treated rats. In one such study, from Medical University of Bialystok, in Bialystok, Poland, preventive doses of 100 mg/kg ginkgo (as EGb 761, from Willmar Schwabe Group) prior to a two-hour episode of restraint stress or corticosterone injection, abolished cognitive deficits as measured by decreased re-entry latencies in a passive avoidance test.⁶⁵ Further, another study by the same researchers showed 100 mg/kg doses of EGB 761 improved spatial and nonspatial memory in the Morris water maze and object recognition tests in chronically stressed or corticosterone-treated rats.⁶⁶ Ginkgo’s potential to suppress beta-amyloid production by lowering free cholesterol levels was shown in a study conducted by Georgetown University Medical Center (Washington); researchers showed EGb 761 treatment lowered circulating free cholesterol in rats, resulting in lowered production of beta-amyloid precursor protein and amyloid beta-peptide in the animals’ brains; they further demonstrated that exposure of PC12 cells to EGb 761 decreased processing and abolished cholesterol-induced overproduction of the beta-amyloid precursor protein, and treatment of human NT2 cells with EGb 761 decreased free cholesterol influx and increased free cholesterol efflux.⁶⁷ And ginkgo’s positive effects on spatial learning and memory have been demonstrated by two studies from China.^68,69

In the first study, spatial learning and memory, as well as magnitude of hippocampal long-term potentiation of aged rats fed an EGb 761-supplemented diet (60 mg/kg) for 30 days were significantly better than those of control aged rats. In the second study, acute oral pre-treatment with doses of 50, 100, or 200 mg/kg of extract of ginkgo prevented a reduction in choice accuracy induced by 4 mg/kg yohimbine (administered intraperitoneally) in male Wistar rats performing the delayed alternation task; the researchers concluded the prefrontal cognition-enhancing effects of ginkgo are related to its actions on alpha-2- adrenoceptors.

The Ginkgo Evaluation of Memory (GEM) study is a randomized, double blind, placebo-controlled trial of ginkgo (as EGb761; 120 mg twice daily) in prevention of dementia (especially AD) in older people (aged 75+), currently being conducted by the University of Pittsburgh.⁷⁰ The 3,000- subject study anticipates 8.5 years of participant follow-up; the primary outcome is incidence of all-cause dementia; secondary outcomes include rate of cognitive and functional decline, the incidence of cardiovascular and cerebrovascular events, and mortality.

Increasing numbers of consumers who are growing older or just looking to gain a competitive edge will likely turn to suppliers and manufacturers to provide high-quality, research-backed ingredients marketed for cognitive health.

References start on next page.

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