Nootropic

From Wikipedia, the free encyclopedia

Nootropics (/noʊ.əˈtrɒpɨks/ noh-ə-TROP-iks), also referred to as smart drugs, memory enhancers, neuro enhancers, cognitive enhancers, and intelligence enhancers, are drugs, supplements, nutraceuticals, and functional foods that purportedly improve mental functions such as cognition, memory, intelligence, motivation, attention, and concentration.[1][2] The word nootropic was coined in 1972 by the Romanian Dr. Corneliu E. Giurgea,[3][4] derived from the Greek words νους nous, or "mind," and τρέπειν trepein meaning "to bend/turn". Nootropics are thought to work by altering the availability of the brain's supply of neurochemicals (neurotransmitters, enzymes, and hormones), by improving the brain's oxygen supply, or by stimulating nerve growth.

Nootropics vs. cognitive enhancers

Cognitive enhancers are drugs, supplements, nutraceuticals, and functional foods that enhance attentional control and memory.[5][6] Nootropics are cognitive enhancers that are neuroprotective or extremely nontoxic. Nootropics (such as Modafinil) are by definition cognitive enhancers, but a cognitive enhancer is not necessarily a nootropic.

Giurgea's nootropic criteria:

  1. Enhances learning and memory.
  2. Enhances learned behaviors under conditions which are known to disrupt them (e.g. hypoxia (oxygen deficiency)).
  3. Protects the brain from physical or chemical injury.
  4. Enhances the tonic cortical/subcortical control mechanisms
  5. Exhibits few side effects and extremely low toxicity, while lacking the pharmacology of typical psychotropic drugs (motor stimulation, sedation, etc.).

Since Giurgea's original criteria were first published, there has been little agreement as to what truly constitutes a nootropic compound. The most well defined criteria to date was established by Skondia in 1979. Skondia uses a metabolic approach, taking into account the pharmacological mode of action.

Skondia's nootropic criteria:

I. No direct vasoactivity

A. No vasodilation
B. No vasoconstriction

II. EEG activity: No change in basic rhythm

A. Quantitative EEG: Increased power spectrum (beta 2 and alpha)
B. Qualitative EEG: Decreased delta waves and cerebral suffering

III. Must pass blood-brain barrier

A. Under normal conditions
B. Under pathological conditions

IV. Must show metabolic activity in:

A. Animal brain metabolism
1. Molecular
2. Physiopathological
B. Human brain metabolism (clinical evaluation)
1. A-V differences
a. Increased extraction quotients of O2
b. Increased extraction quotients of glucose
c. Reduced lactate pyruvate ratio
2. Regional cerebral metabolic rates (rCMR)
a. Increased ICMR of O2
b. Increased rCMR of glucose
3. Regional cerebral blood flow: Normalization

V. Minimal side effects

VI. Clinical trials must be conducted with several rating scales designed to objectify metabolic cerebral improvement.

Availability and prevalence

At present, there are several drugs on the market that improve memory, concentration, and planning, and reduce impulsive behavior. Many more are in different stages of development.[7] The most commonly used class of drug is stimulants.[8]

These drugs are used primarily to treat people with cognitive or motor function difficulties attributable to such disorders as Alzheimer's disease, Parkinson's disease, Huntington's disease and ADHD. However, more widespread use is being recommended by some researchers.[9] These drugs have a variety of human enhancement applications as well, and are marketed heavily on the Internet. Nevertheless, intense marketing may not correlate with efficacy; while scientific studies support some of the claimed benefits, it is worth noting that not all of the claims from certain nootropics suppliers have been formally tested.

Academic doping

Main article: Academic doping

In academia a Nootropic called modafinil has been used to increase productivity, although its long-term effects have not been assessed in healthy individuals.[7] Stimulants such as methylphenidate, a cognitive enhancer (which is not considered as a Nootropic according to the criteria above), are being used on college campuses, and by an increasingly younger group.[7] One survey found that 7% of students had used stimulants for a cognitive edge, and on some campuses use in the past year is as high as 25%.[8][10] The use of prescription stimulants is especially prevalent among students attending academically competitive colleges and students who are members of a fraternity/sorority.[10]

Hazards

The main concern with pharmaceutical drugs is adverse effects, and these concerns apply to cognitive-enhancing drugs as well. Cognitive enhancers are often taken for the long-term when little data is available.[7]

Dr. Corneliu E. Giurgea originally coined the word nootropics for brain-enhancing drugs with very few side-effects. Racetams are sometimes cited as an example of a nootropic with few side-effects and a wide therapeutic window.[11] In the United States, unapproved drugs or dietary supplements do not have to have safety or efficacy approval before being sold.[12]

Drugs

Racetams

The word nootropic was coined upon discovery of the effects of piracetam, developed in the 1960s.[13] Although piracetam is the most commonly taken nootropic,[13] there are many relatives in the family that have different potencies and side-effects. Studies of the racetams have revealed that these structurally similar compounds often act via different mechanisms. These other common racetams include pramiracetam, oxiracetam, and aniracetam. Their mechanisms of action are not fully understood, however, piracetam and aniracetam are known to act as positive allosteric modulators of AMPA receptors. They also appear to modulate acetylcholinergic systems.[14] Although aniracetam and nebracetam show affinity for muscarinic receptors, only nefiracetam shows it at the nanomolar range. Racetams have been called "pharmacologically safe" drugs.[11]

Vitamins and supplements

  • B Vitamins—may influence cognitive function through an effect on methylation and homocysteine levels, as excess homocysteine has been associated with cognitive impairment and the B vitamins work to reduce homocysteine.[15] However, although epidemiological evidence shows an association, two studies did not find B vitamin supplementation improves cognitive function, and another that found an association was criticized.[16] In 2008 a systematic review of trials found "little evidence of a beneficial impact" from supplements on cognitive function later in life.[17] A randomized, placebo-controlled trial in 168 70 year olds with mild cognitive impairment showed that a mix of B vitamins slowed the rate of brain atrophy; the slowing was related to a decrease in homocysteine levels.[18]
  • Choline— Higher concurrent choline intake was related to better cognitive performance.[19] It improves long-term memory in animal models.[20]
  • Omega-3—linked to the maintenance of brain function. Omega-3's provide docosahexaenoic acid, Important in the function and growth of nervous tissue. It is especially important during brain development.[21] A study preformed in Norway[22] demonstrated a potential link between Omega-3 consumption during pregnancy and child intelligence test scores.[23] A cross-sectional population-based study of 1,613 subjects found an association between PUFA intake and decreased risk for impairment of cognitive function & cognitive speed.[24] Another study showed that boys with lower levels of Omega-3 had more behavior issues, such as ADHD.[25]
  • Isoflavones—may be related to cognitive function.[26] A double-blind, placebo-controlled study showed improvement in spatial working memory after administration of an isoflavone combination containing daidzein, genistein & glycitein.[27] In a randomized, double-blind, placebo-controlled study of older, non-demented men & women, soy isoflavone supplementation improved performance on 6 of 11 cognitive tests, including visual-spatial memory and construction, verbal fluency and speeded dexterity; unexpectedly, the placebo group performed better on 2 tests of executive function.[28]
  • Vitamin D—has positive effects on cardiovascular health and may have positive effects on cognitive function separately; the active form of Vitamin D seems to be involved in brain development and in adult brain function. In particular, metabolic pathways for Vitamin D in the hippocampus and cerebellum have been found. Epidemiological data show that higher Vitamin D levels (>20 ng/mL or 50nmol/L) are associated with better cognitive function, but do not seem to be associated with better memory performance.[29] Vitamin D has also been shown to be necessary in the production of Dopamine [30]
  • Vitamin C— has been shown to help reduce brain injury and also reduce the amount of Cortisol in the body. High levels of Cortisol have been linked to Alzheimer's Disease.[31]
  • Vitamin E—protects neurons from injury caused by Free Radicals.[32]
  • A 2007 survey of online databases for herbs used in traditional herbal medicine to treat cognitive decline – without any proof of safety or efficacy – found over 150 plant species, such as Ginkgo biloba.[33]

Stimulants

Stimulants are often seen as smart drugs, but may be more accurately termed productivity enhancers. Some stimulants can enhance cognition and memory in some people, but cause psychosis in others.[citation needed] These typically improve concentration and a few areas of cognitive performance, but only while the drug is still in the blood. Some scientists recommend widespread use of stimulants such as methylphenidate and amphetamines by the general population to increase brain power.[8][43]

Concentration and memory enhancement

The nootropics in this section are purported or shown to enhance concentration or the recollection and formation of memories.

Cholinergics

Cholinergics are substances that affect the neurotransmitter acetylcholine or the components of the nervous system that use acetylcholine. Acetylcholine is a facilitator of memory formation. Increasing the availability of this neurotransmitter in the brain may improve these functions. Cholinergic nootropics include acetylcholine precursors and cofactors, and acetylcholinesterase inhibitors:

GABA blockers

The GABAA α5 receptor site has recently displayed memory improvements when inverse agonized.

  • α5IA—α5 inverse agonist. A number of α5IA analogues exist that, like α5IA, selectively and partially agonize some GABA receptor subtypes while inverse agonizing others, which may provide a nootropic effect without the associated anxiogenic effects of general GABA inverse agonism.
  • Suritozole—α5 partial inverse agonist
  • Pantogam has a direct effect on the GABA-B receptor-channel complex.[51]

Glutamate activators

The AMPA transmitter and the AMPA receptors are currently being researched, and there are signs that significant memory improvement and possible alertness enhancement may occur when agonized. The drug class for AMPA system modulation is called Ampakines. Although there are many Ampakines currently in-research, those mentioned here are significantly notable, and/or show reasonable signs of coming to market.

Some racetams have shown this activity, such as aniracetam

  • CX-717—pending FDA approval for memory-impairing illnesses
  • IDRA-21—believed to improve memory by significantly enhancing long-term potentiation but used only in animals; incredibly potent
  • LY-503,430—under development for Parkinson's but showing increase in BDNF, specifically in areas of memory and higher cognitive skills

cAMP

Cyclic adenosine monophosphate is a secondary messenger that, if increased, has shown memory improvements. One common method is by decreasing the activity of phosphodiesterase-4, an enzyme that breaks down cAMP. Typical effects include wakefulness and memory enhancement.

  • Propentofylline—nonselective phosphodiesterase inhibitor with some neuroenhancement
  • Rolipram—PDE4 inhibitor, shows alertness enhancement, long term memory improvement and neuroprotection
  • Mesembrine—PDE4-inhibitor with possible serotonergic activity

Other

α2A receptors are concentrated heavily in the prefrontal cortex and the locus coeruleus, with the potential to improve attention abilities via modulating post-synaptic α2A receptors in the prefrontal cortex.[52]

  • Guanfacine is an α2A receptor agonist, FDA approved for and frequently used to treat ADHD symptoms.[53][54] Studies have shown guanfacine to strengthen working memory, reduce distractibility, improve response inhibition, increase regional cerebral blood flow, reduce locomotor hyperactivity, and improve attentional control in animal models, as well as enhance memory function in humans.[55] Another study found no effect on healthy male adult's executive functions and working memory, and small decrements on 2 tasks relating to the sedative effect of guanfacine.[56]

PRL-8-53 is a potent hypermnesic drug that significantly increases long term memory with a currently unknown mechanism of action involving cholinergic and dopaminergic activation.[57][58]

Serotonergics

Serotonin is a neurotransmitter with various effects on mood and possible effects on neurogenesis. Serotonergics are substances that affect the neurotransmitter serotonin or the components of the nervous system that use serotonin. Serotonergic nootropics include serotonin precursors and cofactors, and serotonin reuptake inhibitors:

  • Precursors
    • 5-HTP—precursor (intermediate between tryptophan and serotonin)
    • Tryptophan—essential amino acid precursor
  • Cofactors
  • Reuptake inhibitors
    • SSRIs—class of antidepressants that increase active serotonin levels by inhibiting reuptake, also shown to promote Neurogenesis in the hippocampus
    • Sceletium tortuosum—active constituent mesembrine shown to act as an SSRI[61] and PDE4 inhibitor. (Half-life unknown)
    • Hypericum perforatum—inhibits reuptake of serotonin (as well as Norepinephrine, Dopamine, GABA and Glutamate) via activation of TRPC6
  • MAO-A inhibitors
  • Reuptake enhancers
  • 5-HT2A receptor agonists
    • 2C-x—it has been reported that some these compounds causes nootropic, stimulant, or anti-anxiety effects at low doses. 2C-D, 2C-I, and 2C-C are examples. However, at hallucinogenic doses, these chemical compounds may be unpredictable.

Anti-depression, adaptogenic (anti-stress), and mood stabilization

Stress (specifically elevated levels of circulating corticosteroids) has been associated with the cognitive deficits seen in human aging.[70] Many studies show that stress and fatigue negatively impact cognitive functioning in young adults.[71][72] Some level of stress in the learning environment may aid the ability to focus and retain information. However, stress levels, especially high, sustained or traumatic stressors, hinder declarative memory, spatial reasoning, learning, attention and working memory. Fatigue is also a stressor that impedes attention, processing, retrieval, working memory and short term memory.[71] The effects of stress on cognitive performance seem to be controlled by the sympatho-adrenal system and the hypothalamic-hypophysial-adrenal axis.[72]

Depression and depressed mood negatively affect cognitive performance and memory.[73] Depression was found to increase false memory, especially with negative words or subjects.[73]

It is reasoned that counteracting and preventing depression and stress management may be an effective nootropic strategy.[71][72] Proper nutrition, adequate sleep, and mechanisms for coping with stress, such as meditation, have been shown to improve learning and cognitive functioning both in the short and long term.[71][72]

The term adaptogen applies to most herbal anti-stress claims.[citation needed]

The substances below may not have been mentioned earlier on the page:

  • Beta blockers—evidence from controlled trials spanning 25 years supports the claim that beta-blockers are effective for reducing anxiety, likely through peripheral blockade of beta-receptors; most data comes from studies of generalized anxiety and acute stress.[74]
  • Theanine—relaxation; found in green tea; increases nicotinic acetylcholine and reduces nicotinic dopamine
  • Lemon Balm—displays adaptogen properties; in rats it has been shown to possess GABA transaminase inhibitor activity[75] and in homogenates of human cerebral cortical cell membranes possesses activity at acetylcholine receptors.[76] In a randomized, double-blind, placebo-controlled study of 18 healthy volunteers, 600 mg of 'Melissa officinalis' extract attenuated volunteers' response to a laboratory-induced stress test 1 hour after administration; 300 mg significantly improved speed of mathematical processing 1 hour after administration.[77]
  • Passion Flower—possible MAOI and neurotransmitter reuptake activity [citation needed]
  • Rhodiola Rosea—adaptogen; possible MAOI activity[78]
  • St John's Wort—herbal supplement approved (in Europe) to treat mild depression. Method of action is unproven but exhibits effects similar to both MAOIs and SSRIs. [citation needed] There is evidence that it may decrease the effectiveness of methylphenidate treatment.[79]
  • Ginseng (including Siberian ginseng)—adaptogenic effects shown[citation needed]
  • Sutherlandia frutescens—possible anti-inflammatory, reducing pain from those illnesses [citation needed]
  • Kava—anxiolytic herb[citation needed]
  • Grape seed extract—has shown some efficacy in reducing bodily stress[citation needed]
  • Adafenoxate—possible anxiolytic effect[citation needed]
  • Phenibut GABA receptor agonist excerting anxiolytic effects
  • Picamilon GABA prodrug which excerts anxiolytic effects by releasing GABA and niacin in the CNS.
  • Valerian—possible anxiolytic effect through agonism at GABA-A receptors[citation needed]
  • Butea frondosa—possible anxiolytic effect[80]
  • Gotu Kola—adaptogen and anxiolytic [citation needed]
  • Foti—adaptogen; possible MAOI activity [citation needed]
  • Panax ginseng—Multiple randomized, placebo-controlled studies in healthy volunteers have been performed, results include increases in accuracy of memory, speed in performing attention tasks and improvement in performing difficult mental arithmetic tasks, as well as reduction in fatigue and improvement in mood.[81]
  • Many Chinese herbs such as Polygala tenuifolia, Acorus gramineus and Huperzia serrata.[82]
  • Bacopa monnieri[83]
  • Tulsi (Ocimum sanctum, sweet holy basil)[84]

Blood flow and metabolic function

Brain function is dependent on many basic processes such as the usage of ATP, removal of waste, and intake of new materials. Improving blood flow or altering these processes can benefit brain function. The list below contains only vasodilators that have shown at least probable mental enhancement.

  • Mildronate may improve the ability of learning and memory, as the drug changes the expression of hippocampal proteins related to synaptic plasticity
  • Blessed Thistle—increases blood circulation, improving memory [citation needed]
  • Coenzyme q-10—antioxidant; increases oxygen usage by mitochondria
  • Creatine—protects ATP during transport
  • Lipoic acid—improves oxygen usage and antioxidant recycling, possibly improving memory
  • Pyritinol—Drug similar to B vitamin Pyridoxine
  • Picamilon—GABA activity and blood flow improver
  • Ginkgo biloba—vasodilator. Acts as an NRI.[85] A double-blind, placebo-controlled trial in young healthy females showed an improvement in short-term memory performance 1 hour after administration of a 600 mg dose.[86] An analysis of 29 placebo-controlled RCTs showed that "there is consistent evidence that chronic administration improves selective attention, some executive processes and long-term memory for verbal and non-verbal material."[87] A double-blind, placebo-controlled study in 20 young healthy volunteers showed a dose-dependent improvement in speed-of-attention following administration of 240 mg and 360 mg of Ginkgo extract, effects were measured 2.5h after administration and persisted at least until 6h; various other time- and dose-specific changes (some positive, some negative) in other areas were observed.[88]
  • Vinpocetine— is reported to have cerebral blood-flow enhancing[89] and neuroprotective effects,[90] and is used as a drug in Eastern Europe for the treatment of cerebrovascular disorders and age-related memory impairment.[91] Also shown to inhibit voltage-sensitive Na+ channels—however, through a similar mechanism to reserpine, Vinpocetine may temporarily deplete the monoamines serotonin, dopamine and norepinephrine by inhibiting VMAT, thus preventing them from reaching the synapse.[92] Vinpocetine may therefore induce or exacerbate depressive symptoms as an adverse effect. However, this effect tends to be reversible upon cessation of Vinpocetine administration, with full remission typically occurring within 3–4 weeks. Vinpocetine has been identified as a potent anti-inflammatory agent that might have a potential role in the treatment of Parkinson's disease and Alzheimer's disease.[93][94]
  • Vincamine—increases blood circulation (vasodilator) and metabolism in the brain; related to vinpocetine; used in sustained release.
  • Nicergoline—an ergot derivative used to treat senile dementia and other disorders with vascular origins; it has been found to increase mental agility and enhance clarity and perception; it decreases vascular resistance and increases arterial blood flow in the brain, improving the utilization of oxygen and glucose by brain cells; it has been used for more than three decades for the treatment of cognitive, affective, and behavioral disorders of older people.[95]

Experimental histamine antagonists

The H3-receptor decreases neurotransmitter release: histamine, acetylcholine, norepinephrine, serotonin. Thus, H3-receptor-antagonists increases cognition, vigilance, and wakefulness.

  • Ciproxifan—produces wakefulness and attentiveness in animal studies, and produced cognitive enhancing effects without prominent stimulant effects at relatively low levels of receptor occupancy, and pronounced wakefulness at higher doses.[96]
  • A-349,821—It has nootropic effects in animal studies.[97]
  • ABT-239 – strong H3 receptor inverse agonist that is more active than ciproxifan, but its investigation into human use was dropped after it was discovered to cause QT prolongation in subjects
  • Betahistine
  • Modafinil

Nerve growth stimulation and brain cell protection

Nerves are necessary to the foundation of brain communication and their degeneracy, underperformance, or lacking can have disastrous results on brain functions. Antioxidants may prevent oxidative stress and cell death, therefore exerting a neuroprotective effect.

  • Idebenone—antioxidant [citation needed]
  • Melatonin—antioxidant [citation needed]
  • Glutathione—chief antioxidant [citation needed]
  • Sesamol—antioxidant [98]
  • Acetylcarnitine (Acetyl-L-Carnitine Arginate or Hydrochloride) [citation needed]
  • Inositol—implicated in memory function, deficit linked to some psychiatric illnesses—has been shown particularly efficacious in OCD patients
  • Anticonvulsants—inhibit seizure related brain malfunction if a person has seizures [citation needed]
  • Phosphatidylserine—possible membrane stabilizer [citation needed]
  • Lion's Mane Mushroom—Stimulated myelination in an in vitro experiment[99] and stimulated nerve growth factor in an in vitro experiment with human astrocytoma cells.[100] Also improved cognitive ability, in a double-blind, parallel-group, placebo-controlled trial.[101]
  • SAM-e (S-Adenosyl methionine)—crucial for cellular regeneration (fuels DNA methylation[102]), also involved with the biosynthesis of dopamine & serotonin[103]
  • Acetylcysteine (L-cysteine)—precursor to antioxidant glutathione[104]
  • Uncaria tomentosa (Cat's Claw)—in an in vitro experiment with rats, it inhibited formation of brain beta amyloid deposits,[105] which have been connected to Alzheimer's disease.[citation needed]
  • (Dopamine enhancers)—dopamine is an antioxidant that can enhance dendrite extension[citation needed]
  • (Cannabidiol and Δ9-tetrahydrocannabinol)—Cannabidiol (nonpsychoactive) and Δ9-tetrahydrocannabinol (psychotropic) antioxidant.[106]

Direct hormones

These are hormones that have activity not necessarily attributable to another specific chemical interaction, but have shown effectiveness. Only specific nootropic effects are stated.

  • Vasopressin—memory hormone that improves both memory encoding and recall. Desmopressin (1-desamino-8-D-arginine vasopressin, DDAVP) was given to 17 children with attention & learning disorders daily for 10 days in a placebo-controlled, randomized, double-blind study; memory & learning were improved compared with placebo; the same study failed to find similar benefits after administration of a single dose.[107]
  • Pregnenolone—increases neurogenesis
  • Orexin or Hypocretin—significant wakefulness promoter

Secondary enhancers

These are substances that by themselves may not improve brain function, but may have benefits for those who lack them (in the case of hormones) or may alter the balance of neurotransmitters.

Unknown enhancement

Other agents purported to have nootropic effects but do not (yet) have attributable mechanisms or clinically significant effects (but may upon refinement of administration) are listed below.

Nootropics with proven or purported benefits:

  • Polygala tenuifolia (Yuan Zhi)— A randomized, double-blind, placebo-controlled, parallel-group study of the extract of dried roots of Polygala tenuifolia in healthy adults produced memory-enhancing effects.[108] A similar trial with elderly humans also found significant cognitive improvement.[109]
  • Bacopa monniera (Brahmi) — Shown to possess adaptogenic properties and enhance memory and concentration.[110] Folk use in Ayurvedic medicine purports "enhancement of curiosity"; Brahmi rasayana has been shown to improve learning and memory in mice[111]
  • Clitoria ternatea (Shankhpushpi) — In traditional Ayurvedic medicine, it has been used for centuries as a memory enhancer, nootropic, antistress, anxiolytic, antidepressant, anticonvulsant, tranquilizing and sedative agent.
  • Fipexide—drug for Dementia
  • Piperic acid—allegedly a mild serotonergic, nootropic, antistress, anxiolytic, and allegedly has mild to moderate memory enhancing effects.
  • Gerovital H3—famous alleged anti-aging mixture, most effects disproven but some mind enhancement shown
  • Sulbutiamine—fat soluble vitamin B1 derivative—caused mice to perform better on operant conditioning tests[112] and object recognition tests[113]
  • Royal Jelly—Increases brain cell growth and diversity, only demonstrated in-vitro, improbable in-vivo (it has been reported to stimulate the growth of glial cells[114] and neural stem cells in the brain.[115])
  • Curcumin—significant in-vitro activity, but in-vivo activity limited by low bioavailability unless accompanied by ingestion of piperine

Other nootropics

Other substances sometimes classified as nootropics include jujube, mexidol, hydergine,[11] noopept, selank, semax and bifemelane.

See also

References

  1. ↑ "Dorlands Medical Dictionary". Archived from the original on 2008-01-30. 
  2. ↑ Lanni C, Lenzken SC, Pascale A, et al. (March 2008). "Cognition enhancers between treating and doping the mind". Pharmacol. Res. 57 (3): 196–213. doi:10.1016/j.phrs.2008.02.004. PMID 18353672. 
  3. ↑ Gazzaniga, Michael S. (2006). The Ethical Brain: The Science of Our Moral Dilemmas (P.S.). New York, N.Y: Harper Perennial. p. 184. ISBN 0-06-088473-8. 
  4. ↑ Giurgea C (1972). "[Pharmacology of integrative activity of the brain. Attempt at nootropic concept in psychopharmacology] ("Vers une pharmacologie de l'active integrative du cerveau: Tentative du concept nootrope en psychopharmacologie")". Actual Pharmacol (Paris) (in French) 25: 115–56. PMID 4541214. 
  5. ↑ "Dorlands Medical Dictionary". Archived from the original on 2008-01-30. 
  6. ↑ Lanni C, Lenzken SC, Pascale A, et al. (March 2008). "Cognition enhancers between treating and doping the mind". Pharmacol. Res. 57 (3): 196–213. doi:10.1016/j.phrs.2008.02.004. PMID 18353672. 
  7. ↑ 7.0 7.1 7.2 7.3 Sahakian B; Morein-Zamir S (December 2007). "Professor's little helper". Nature 450 (7173): 1157–9. Bibcode:2007Natur.450.1157S. doi:10.1038/4501157a. PMID 18097378. 
  8. ↑ 8.0 8.1 8.2 ""Towards responsible use of cognitive-enhancing drugs by the healthy" in Nature: International Weekly Journal of Science". Retrieved December 2008. 
  9. ↑ "Smart Drugs and Should We Take Them?". Dolan DNA Learning Center. Retrieved 2012-11-04. 
  10. ↑ 10.0 10.1 McCabe, Sean Esteban; Knight, John R.; Teter, Christian J.; Wechsler, Henry (1 January 2005). "Non-medical use of prescription stimulants among US college students: prevalence and correlates from a national survey". Addiction 100 (1): 96–106. doi:10.1111/j.1360-0443.2005.00944.x. PMID 15598197. Retrieved 15 August 2013. 
  11. ↑ 11.0 11.1 11.2 Malik R, Sangwan A, Saihgal R, Jindal DP, Piplani P (2007). "Towards better brain management: nootropics". Curr. Med. Chem. 14 (2): 123–31. doi:10.2174/092986707779313408. PMID 17266573. 
  12. ↑ Goldman P (2001). "Herbal medicines today and the roots of modern pharmacology". Annals of Internal Medicine 135 (8 Pt 1): 594–600. doi:10.7326/0003-4819-135-8_Part_1-200110160-00010. PMID 11601931. 
  13. ↑ 13.0 13.1 McDaniel, M.A., Maier, S.F., and Einstein, G.O. (2002). "Brain-Specific Nutrients: A Memory Cure?". Psychological Science in the Public Interest (American Psychological Society) 19 (11): 957–75. doi:10.1016/S0899-9007(03)00024-8. PMID 14624946. 
  14. ↑ Gualtieri F, Manetti D, Romanelli MN, Ghelardini C (2002). "Design and study of piracetam-like nootropics, controversial members of the problematic class of cognition-enhancing drugs". Curr. Pharm. Des. 8 (2): 125–38. doi:10.2174/1381612023396582. PMID 11812254. 
  15. ↑ Selhub J, Bagley L, Miller J, Rosenberg I (2000). "B vitamins, homocysteine, and neurocognitive function in the elderly". American Journal of Clinical Nutrition 71 (2): 614S–620s. PMID 10681269. 
  16. ↑ Huskisson E, Maggini S, Ruf M (2007). "The influence of micronutrients on cognitive function and performance". J. Int. Med. Res. 35 (1): 1–19. PMID 17408051. 
  17. ↑ Jia X, McNeill G, Avenell A (August 2008). "Does taking vitamin, mineral and fatty acid supplements prevent cognitive decline? A systematic review of randomized controlled trials". J Hum Nutr Diet 21 (4): 317–36. doi:10.1111/j.1365-277X.2008.00887.x. PMID 18721399. 
  18. ↑ Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, Oulhaj A, Bradley KM, Jacoby R, Refsum H (September 2010). "Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial.". PLoS ONE 8 (5(9)). Bibcode:2010PLoSO...512244S. doi:10.1371/journal.pone.0012244. PMC 2935890. PMID 20838622. 
  19. ↑ NCBI. The relation of dietary choline to cognitive performance and white-matter hyperintensity in the Framingham Offspring Cohort. 
  20. ↑ Times of India. Eating beef liver improves long-term memory. 
  21. ↑ Sheila M. Innis (April 2007). "Dietary (n-3) fatty acids and brain development". the journal of nutrition 137 (4). 
  22. ↑ Pediatrics. 2003 Jan;111(1) e39–44
  23. ↑ Prevention [0032-8006] Chillot yr.2004 vol.56 iss.1 pg. 122–129
  24. ↑ Kalmijn S, van Boxtel MP, Ocké M, Verschuren WM, Kromhout D, Launer LJ (January 2004). "Dietary intake of fatty acids and fish in relation to cognitive performance at middle age.". Neurology 62 (2): 275–80. PMID 14745067. 
  25. ↑ J.R. Burgess, L. Steens, W. Zhang, L. Peck (2000). "long-chain polyunsaturated fatty acids in children with attention-deficit hyperactivity disorder". am. j. clin. nutr 71: 327–330. 
  26. ↑ Wong MC, Emery PW, Preedy VR, Wiseman H (October 2008). "Health benefits of isoflavones in functional foods? Proteomic and metabonomic advances". Inflammopharmacology 16 (5): 235–9. doi:10.1007/s10787-008-8023-x. PMID 18815737. 
  27. ↑ Thorp AA, Sinn N, Buckley JD, Coates AM, Howe PR (November 2009). "Soya isoflavone supplementation enhances spatial working memory in men.". Br J Nutr 102 (9): 1348–54. doi:10.1017/S0007114509990201. PMID 19480732. 
  28. ↑ Gleason CE, Carlsson CM, Barnet JH, Meade SA, Setchell KD, Atwood CS, Johnson SC, Ries ML, Asthana S (January 2009). "A preliminary study of the safety, feasibility and cognitive efficacy of soy isoflavone supplements in older men and women". Age Ageing 38 (1): 86–93. doi:10.1093/ageing/afn227. PMC 2720778. PMID 19054783. 
  29. ↑ Buell JS, Scott TM, Dawson-Hughes B, Dallal GE, Rosenberg IH, Folstein MF, Tucker KL (Aug 2009). "Vitamin D is associated with cognitive function in elders receiving home health services.". J Gerontol A Biol Sci Med Sci. 64 (8): 888–95. doi:10.1093/gerona/glp032. PMC 2981461. PMID 19377013. 
  30. ↑ Thomas H. J. Burne, PhD (May 2013). "vitamin d and the brain". http://chemistry.beloit.edu/Ordman/nutrition/aln13/1305lpi.htm. 
  31. ↑ Roc Ordman (June 2012). "AGE meeting June, 2012". http://chemistry.beloit.edu/Ordman/nutrition/aldo/1206AGE.htm. 
  32. ↑ Roc Ordman (October 2009). "VITAMIN C MAY REDUCE STROKE (COMA and TRAUMATIC BRAIN INJURY) DAMAGE". http://chemistry.beloit.edu/Ordman/nutrition/stroke.htm. 
  33. ↑ Adams M, Gmünder F, Hamburger M (September 2007). "Plants traditionally used in age related brain disorders--a survey of ethnobotanical literature". J Ethnopharmacol 113 (3): 363–81. doi:10.1016/j.jep.2007.07.016. PMID 17720341. 
  34. ↑ Cheng, N.; Maeda, T.; Kume, T.; Kaneko, S.; Kochiyama, H.; Akaike, A.; Goshima, Y.; Misu, Y. (Dec 1996). "Differential neurotoxicity induced by L-DOPA and dopamine in cultured striatal neurons.". Brain Res 743 (1–2): 278–83. doi:10.1016/S0006-8993(96)01056-6. PMID 9017256. 
  35. ↑ Maeda, T.; Cheng, N.; Kume, T.; Kaneko, S.; Kouchiyama, H.; Akaike, A.; Ueda, M.; Satoh, M. et al. (Oct 1997). "L-DOPA neurotoxicity is mediated by glutamate release in cultured rat striatal neurons.". Brain Res 771 (1): 159–62. doi:10.1016/S0006-8993(97)00908-6. PMID 9383020. 
  36. ↑ Lee, JJ.; Kim, YM.; Yin, SY.; Park, HD.; Kang, MH.; Hong, JT.; Lee, MK. (Nov 2003). "Aggravation of L-DOPA-induced neurotoxicity by tetrahydropapaveroline in PC12 cells.". Biochem Pharmacol 66 (9): 1787–95. doi:10.1016/S0006-2952(03)00421-0. PMID 14563489. 
  37. ↑ Kapatos, G.; Kaufman, S.; Weller, JL.; Klein, DC. (Sep 1981). "Biosynthesis of biopterin: adrenergic cyclic adenosine monophosphate-dependent inhibition in the pineal gland.". Science 213 (4512): 1129–31. Bibcode:1981Sci...213.1129K. doi:10.1126/science.6168019. PMID 6168019. 
  38. ↑ 38.0 38.1 van Diermen, D.; Marston, A.; Bravo, J.; Reist, M.; Carrupt, PA.; Hostettmann, K. (Mar 2009). "Monoamine oxidase inhibition by Rhodiola rosea L. roots.". J Ethnopharmacol 122 (2): 397–401. doi:10.1016/j.jep.2009.01.007. PMID 19168123. 
  39. ↑ Giménez R, Raïch J, Aguilar J (November 1991). "Changes in brain striatum dopamine and acetylcholine receptors induced by chronic CDP-choline treatment of aging mice". British Journal of Pharmacology 104 (3): 575–8. PMC 1908237. PMID 1839138. 
  40. ↑ Teather LA, Wurtman RJ (2005). "Dietary CDP-choline supplementation prevents memory impairment caused by impoverished environmental conditions in rats". Learning & Memory 12 (1): 39–43. doi:10.1101/lm.83905. PMC 548494. PMID 15647594. 
  41. ↑ "Supplement naturally boosts ageing brain power". Sydney Morning Herald. 2008-02-25. Retrieved 2009-07-28. 
  42. ↑ Silveri MM, Dikan J, Ross AJ, et al. (November 2008). "Citicoline enhances frontal lobe bioenergetics as measured by phosphorus magnetic resonance spectroscopy". NMR in Biomedicine 21 (10): 1066–75. doi:10.1002/nbm.1281. PMID 18816480. 
  43. ↑ Szalavitz, Maia (2009-01-06). "Popping Smart Pills: The Case for Cognitive Enhancement – TIME". Time. Retrieved 2010-05-20. 
  44. ↑ Heishman SJ, Kleykamp BA, Singleton EG (June 2010). "Meta-analysis of the acute effects of nicotine and smoking on human performance". Psychopharmacology (Berl). 210 (4): 453–69. doi:10.1007/s00213-010-1848-1. PMC 3151730. PMID 20414766. Retrieved 2012-03-23. 
  45. ↑ Rogers, P. (2007). "Caffeine, mood and mental performance in everyday life.". Psychology Today 32 (1): 84–89. doi:10.1111/j.1467-3010.2007.00607.x. 
  46. ↑ Kiefer, I. (2007). "Brain Food". Scientific American Mind 18 (5): 58–63. doi:10.1038/scientificamericanmind1007-58. Retrieved 2009-11-01. 
  47. ↑ Tang, L., Wang, R., Tang, X. (2005). "Effects of huperzine A on secretion of nerve growth factor in cultured rat cortical astrocytes and neurite outgrowth in rat PC12 cells". Acta Pharmacologica Sinica 26 (6): 673–678. doi:10.1111/j.1745-7254.2005.00130.x. PMID 15916732. 
  48. ↑ Eubanks, LM.; Rogers, CJ.; Beuscher, AE.; Koob, GF.; Olson, AJ.; Dickerson, TJ.; Janda, KD. (2006). "A molecular link between the active component of marijuana and Alzheimer's disease pathology.". Mol Pharm 3 (6): 773–7. doi:10.1021/mp060066m. PMC 2562334. PMID 17140265. 
  49. ↑ Wen Jiang; Yun Zhang; Lan Xiao; Jamie Van Cleemput; Shao-Ping Ji; Guang Bai; Xia Zhang (2005-11-01). "Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects". Journal of Clinical Investigation 115 (11): 3104–16. doi:10.1172/JCI25509. PMC 1253627. PMID 16224541. Retrieved 2011-03-02. 
  50. ↑ http://www.smarternootropics.com/coluracetam/
  51. ↑ http://pantogam.ru/preparaty/pantogam-tabletki-instrukcija
  52. ↑ Kolar, D.; Keller, A; Golfinopoulos, M; Cumyn, L; Syer, C; Hechtman, L (2008). "Treatment of adults with attention-deficit/hyperactivity disorder". Neuropsychiatric Disease and Treatment 4 (2): 389–403. PMC 2518387. PMID 18728745. 
  53. ↑ Compositions and Methods for Treating Cognitive Disorders. United States Patent Application 20090221610.
  54. ↑ "Shire Receives FDA Approvable Letter For INTUNIV (guanfacine) ER, A Nonstimulant ADHD Treatment". Medical News Today. 24 June 2007. 
  55. ↑ Arnsten, A. F.; Dudley, A. G. (2005). "Methylphenidate improves prefrontal cortical cognitive function through α2 adrenoceptor and dopamine D1 receptor actions: Relevance to therapeutic effects in Attention Deficit Hyperactivity Disorder". Behavioral and Brain Functions 1 (1): 2. doi:10.1186/1744-9081-1-2. PMC 1143775. PMID 15916700. 
  56. ↑ Müller, U; Clark, L; Lam, ML; Moore, RM; Murphy, CL; Richmond, NK; Sandhu, RS; Wilkins, IA et al. (2005). "Lack of effects of guanfacine on executive and memory functions in healthy male volunteers". Psychopharmacology 182 (2): 205–13. doi:10.1007/s00213-005-0078-4. PMID 16078088. 
  57. ↑ Hansl, NR; Nikolaus R. Hansl, Beverley T. Mead (1978). "PRL-8-53: Enhanced learning and subsequent retention in humans as a result of low oral doses of new psychotropic agent". Psychopharmacology 56 (3): 249–253. doi:10.1007/BF00432846. PMID 418433. 
  58. ↑ Hansl, N. R. (1974). "A novel spasmolytic and CNS active agent: 3-(2-benzylmethylamino ethyl) benzoic acid methyl ester hydrochloride". Experientia 30 (3): 271–272. doi:10.1007/BF01934822. PMID 4824605. 
  59. ↑ Calderón-Guzmán, D.; Hernández-Islas, JL.; Espitia-Vázquez, I.; Barragán-Mejía, G.; Hernández-García, E.; Santamaría-del Angel, D.; Juárez-Olguín, H. "Pyridoxine, regardless of serotonin levels, increases production of 5-hydroxytryptophan in rat brain.". Arch Med Res 35 (4): 271–4. doi:10.1016/j.arcmed.2004.03.003. PMID 15325498. 
  60. ↑ Lee, NS.; Muhs, G.; Wagner, GC.; Reynolds, RD.; Fisher, H. (Mar 1988). "Dietary pyridoxine interaction with tryptophan or histidine on brain serotonin and histamine metabolism.". Pharmacol Biochem Behav 29 (3): 559–64. doi:10.1016/0091-3057(88)90020-2. PMID 3362950. 
  61. ↑ Stafford, GI.; Pedersen, ME.; van Staden, J.; Jäger, AK. (Oct 2008). "Review on plants with CNS-effects used in traditional South African medicine against mental diseases.". J Ethnopharmacol 119 (3): 513–37. doi:10.1016/j.jep.2008.08.010. PMID 18775771. 
  62. ↑ Yáñez, M.; Fraiz, N.; Cano, E.; Orallo, F. (Jun 2006). "Inhibitory effects of cis- and trans-resveratrol on noradrenaline and 5-hydroxytryptamine uptake and on monoamine oxidase activity.". Biochem Biophys Res Commun 344 (2): 688–95. doi:10.1016/j.bbrc.2006.03.190. PMID 16631124. 
  63. ↑ Xu, Y.; Ku, BS.; Yao, HY.; Lin, YH.; Ma, X.; Zhang, YH.; Li, XJ. (Jul 2005). "The effects of curcumin on depressive-like behaviors in mice.". Eur J Pharmacol 518 (1): 40–6. doi:10.1016/j.ejphar.2005.06.002. PMID 15987635. 
  64. ↑ Rahman, T.; Rahmatullah, M. (Jan 2010). "Proposed structural basis of interaction of piperine and related compounds with monoamine oxidases.". Bioorg Med Chem Lett 20 (2): 537–40. doi:10.1016/j.bmcl.2009.11.106. PMID 19969454. 
  65. ↑ Herraiz, T.; González, D.; Ancín-Azpilicueta, C.; Arán, VJ.; Guillén, H. (Mar 2010). "beta-Carboline alkaloids in Peganum harmala and inhibition of human monoamine oxidase (MAO).". Food Chem Toxicol 48 (3): 839–45. doi:10.1016/j.fct.2009.12.019. PMID 20036304. 
  66. ↑ 66.0 66.1 McEwen, B. S.; Chattarji, S.; Diamond, D. M.; Jay, T. M.; Reagan, L. P.; Svenningsson, P.; Fuchs, E. (March 2010). "The neurobiological properties of tianeptine (Stablon): from monoamine hypothesis to glutamatergic modulation". Molecular Psychiatry 15 (3): 237–249. doi:10.1038/mp.2009.80. PMC 2902200. PMID 19704408. 
  67. ↑ Kasper S, McEwen BS (2008). "Neurobiological and clinical effects of the antidepressant tianeptine". CNS Drugs 22 (1): 15–26. doi:10.2165/00023210-200822010-00002. PMID 18072812. 
  68. ↑ Invernizzi R, Pozzi L, Garattini S, Samanin R (March 1992). "Tianeptine increases the extracellular concentrations of dopamine in the nucleus accumbens by a serotonin-independent mechanism". Neuropharmacology 31 (3): 221–7. doi:10.1016/0028-3908(92)90171-K. PMID 1630590. 
  69. ↑ "( Stablon, Coaxil ) and the dopamine D(2) and D(3) receptors". Tianeptine. Retrieved 2010-08-13. 
  70. ↑ Lupien S, Lecours AR, Lussier I, Schwartz G, Nair NP, Meaney MJ (May 1994). "Basal cortisol levels and cognitive deficits in human aging.". J Neurosci. 14 (5pt1): 2893–903. PMID 8182446. 
  71. ↑ 71.0 71.1 71.2 71.3 PALMER, L. K. (2013). The Relationship between Stress, Fatigue, and Cognitive Functioning. College Student Journal, 47(2), 312-325.
  72. ↑ 72.0 72.1 72.2 72.3 Singh, Y, Ratna, A (2012). "Immediate and Long-term Effects of Meditation on Acute Stress Reactivity, Cognitive Functions, and Intelligence." Alternative Therapies in Health & Medicine 18, no. 6: 46-53.
  73. ↑ 73.0 73.1 Howe, M. L., & Malone, C. (2011). Mood-congruent true and false memory: Effects of depression. Memory, 19(2), 192-201. doi:10.1080/09658211.2010.544073
  74. ↑ Tyrer P (January 1992). "Anxiolytics not acting at the benzodiazepine receptor: beta blockers.". Prog Neuropsychopharmacol Biol Psychiatry 16 (1): 17–26. doi:10.1016/0278-5846(92)90004-X. PMID 1348368. 
  75. ↑ Awad, R.; Levac, D.; Cybulska, P.; Merali, Z.; Trudeau, V.L.; Arnason, J.T. (September 2007). "Effects of traditionally used anxiolytic botanicals on enzymes of the γ-aminobutyric acid (GABA) system". Can J Physiol Pharmacol. 85 (9): 933–42. doi:10.1139/Y07-083. PMID 18066140. 
  76. ↑ Wake G, Court J, Pickering A, Lewis R, Wilkins R, Perry E (February 2000). "CNS acetylcholine receptor activity in European medicinal plants traditionally used to improve failing memory". J Ethnopharmacol. 69 (2): 105–14. doi:10.1016/S0378-8741(99)00113-0. PMID 10687867. 
  77. ↑ Kennedy DO, Little W, Scholey AB (Jul–Aug 2004). "Attenuation of laboratory-induced stress in humans after acute administration of Melissa officinalis (Lemon Balm)". Psychosom Med. 66 (4): 607–13. doi:10.1097/01.psy.0000132877.72833.71. PMID 15272110. 
  78. ↑ Panossian A., Wikman G."Evidence based efficacy of adaptogens in fatigue" Planta Medica 2009; 75:9
  79. ↑ Niederhofer, H. (2007). "St. John's wort may diminish methylphenidate's efficacy in treating patients suffering from attention deficit hyperactivity disorder". Medical Hypotheses 68 (5): 1189–2007. doi:10.1016/j.mehy.2005.11.004. PMID 17254717. 
  80. ↑ Soman I, Mengi SA, Kasture SB (September 2004). "Effect of leaves of Butea frondosa on stress, anxiety, and cognition in rats". Pharmacol. Biochem. Behav. 79 (1): 11–6. doi:10.1016/j.pbb.2004.05.022. PMID 15388278. 
  81. ↑ Kennedy DO, Wightman EL (Jan 2011). "Herbal extracts and phytochemicals: plant secondary metabolites and the enhancement of human brain function.". Adv Nutr. 2 (1): 32–50. doi:10.3945/an.110.000117. PMID 22211188. 
  82. ↑ Jesky, R.; Hailong, C. (August 2011). "Are Herbal Compounds the Next Frontier for Alleviating Learning and Memory Impairments? An Integrative Look at Memory, Dementia and the Promising Therapeutics of Traditional Chinese Medicines". Phytotherapy Research 25 (8): 1105–1118. doi:10.1002/ptr.3388. PMID 21305632. 
  83. ↑ Morgan, A.; Stevens, J. (July 2010). "DoesBacopa monnieriImprove Memory Performance in Older Persons? Results of a Randomized, Placebo-Controlled, Double-Blind Trial". The Journal of Alternative and Complementary Medicine 16 (7): 753–759. doi:10.1089/acm.2009.0342. PMID 20590480. 
  84. ↑ Mondal, Shankar; Mirdha, Bijay R.; Mahapatra, Sushil C. (October–December 2009). "The science behind sacredness of Tulsi (Ocimum sanctum Linn.)". Indian journal of physiology and pharmacology 53 (4): 291–306. PMID 20509321. 
  85. ↑ Fehske, CJ.; Leuner, K.; Müller, WE. (Jul 2009). "Ginkgo biloba extract (EGb761) influences monoaminergic neurotransmission via inhibition of NE uptake, but not MAO activity after chronic treatment.". Pharmacological Research 60 (1): 68–73. doi:10.1016/j.phrs.2009.02.012. ISSN 1043-6618. PMID 19427589. 
  86. ↑ Hindmarch I (1986). "[Activity of Ginkgo biloba extract on short-term memory].". Presse Med (in French) 15 (31): 1592–94. PMID 2947108. 
  87. ↑ Kaschel R (2009). "Ginkgo biloba: specificity of neuropsychological improvement--a selective review in search of differential effects.". Hum Psychopharmacol 24 (5): 345–70. doi:10.1002/hup.1037. PMID 19551805. 
  88. ↑ Kennedy DO, Scholey AB, Wesnes KA (2000). "The dose-dependent cognitive effects of acute administration of Ginkgo biloba to healthy young volunteers.". Psychopharmacology (Berl) 151 (4): 416–23. doi:10.1007/s002130000501. PMID 11026748. 
  89. ↑ Szilágyi G, Nagy Z, Balkay L, et al. (2005). "Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study". Journal of the Neurological Sciences. 229–230: 275–84. doi:10.1016/j.jns.2004.11.053. PMID 15760651. 
  90. ↑ Dézsi L, Kis-Varga I, Nagy J, Komlódi Z, Kárpáti E (2002). "[Neuroprotective effects of vinpocetine in vivo and in vitro. Apovincaminic acid derivatives as potential therapeutic tools in ischemic stroke]". Acta Pharmaceutica Hungarica (in Hungarian) 72 (2): 84–91. PMID 12498034. 
  91. ↑ "Vinpocetine. Monograph". Alternative Medicine Review 7 (3): 240–3. 2002. PMID 12126465. 
  92. ↑ Trejo, F.; Nekrassov, V.; Sitges, M. (Aug 2001). "Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings.". Brain Res 909 (1–2): 59–67. doi:10.1016/S0006-8993(01)02621-X. PMID 11478921. 
  93. ↑ Jeon, KI; Xu, X; Aizawa, T; Lim, JH; Jono, H; Kwon, DS; Abe, J; Berk, BC et al. (2010). "Vinpocetine inhibits NF-kappaB-dependent inflammation via an IKK-dependent but PDE-independent mechanism.". Proceedings of the National Academy of Sciences of the United States of America 107 (21): 9795–800. Bibcode:2010PNAS..107.9795J. doi:10.1073/pnas.0914414107. PMC 2906898. PMID 20448200. 
  94. ↑ Medina, AE (2010). "Vinpocetine as a potent antiinflammatory agent.". Proceedings of the National Academy of Sciences of the United States of America 107 (22): 9921–2. Bibcode:2010PNAS..107.9921M. doi:10.1073/pnas.1005138107. PMC 2890434. PMID 20495091. 
  95. ↑ Fioravanti M, Flicker L (2001). "Efficacy of nicergoline in dementia and other age associated forms of cognitive impairment". Cochrane Database Syst Rev (4): CD003159. doi:10.1002/14651858.CD003159. PMID 11687175. 
  96. ↑ Le S, Gruner JA, Mathiasen JR, Marino MJ, Schaffhauser H (June 2008). "Correlation between ex vivo receptor occupancy and wake-promoting activity of selective H3 receptor antagonists". J. Pharmacol. Exp. Ther. 325 (3): 902–9. doi:10.1124/jpet.107.135343. PMID 18305012. 
  97. ↑ Esbenshade, TA; Fox, GB; Krueger, KM; Baranowski, JL; Miller, TR; Kang, CH; Denny, LI; Witte, DG et al. (2004). "Pharmacological and behavioral properties of A-349821, a selective and potent human histamine H3 receptor antagonist". Biochemical pharmacology 68 (5): 933–45. doi:10.1016/j.bcp.2004.05.048. PMID 15294456. 
  98. ↑ Ohsawa, Toshiko. "Sesamol and sesaminol as antioxidants." New Food Industry (1991), 33(6), 1-5.
  99. ↑ Kolotushkina EV, Moldavan MG, Voronin KY, Skibo GG (2003). "The influence of Hericium erinaceus extract on myelination process in vitro". Fiziol Zh 49 (1): 38–45. PMID 12675022. 
  100. ↑ Mori K, Obara Y, Hirota M, et al. (September 2008). "Nerve growth factor-inducing activity of Hericium erinaceus in 1321N1 human astrocytoma cells". Biol. Pharm. Bull. 31 (9): 1727–32. doi:10.1248/bpb.31.1727. PMID 18758067. 
  101. ↑ Mori K, Inatomi S, Ouchi K, Azumi Y, Tuchida T (March 2009). "Improving effects of the mushroom Yamabushitake (Hericium erinaceus) on mild cognitive impairment: a double-blind placebo-controlled clinical trial". Phytotherapy Research 23 (3): 367–72. doi:10.1002/ptr.2634. PMID 18844328. 
  102. ↑ The Way SAMe Works
  103. ↑ Mischoulon, D.; Fava, M. (November 2002). "Role of S-adenosyl-L-methionine in the treatment of depression: A review of the evidence". The American journal of clinical nutrition 76 (5): 1158S–1161S. PMID 12420702. 
  104. ↑ "glutathione". "In short words: N-acetylcysteine (NAC) is precursor of glutathione (GSH)." 
  105. ↑ "Medications for dementia: New drugs, mechanisms are coming for Alzheimer's disease". The Journal of Family Practice 1 (6). June 2002. "PTI-00703 is a beta-amyloid inhibitor derived from the cat's claw, a woody vine found in the Peruvian rain forest. It is being tested in patients with mild-to-moderate AD [Alzheimer's disease]." , which cites:
    "OSHU Researchers Investigate Substance Derived From Amazon Rainforest Plant as Possible treatment For Alzheimer's Disease". Oregon Health & Science University. March 2, 2000. "Researchers at OHSU are interested in a particular extract, derived from the bark of the vine, called PTI-00703. It has been shown to stop the formation of, and break up beta-amyloid deposits in both a test tube and animal models." 
  106. ↑ Hampson, A. J.; Grimaldi, M.; Axelrod, J.; Wink, D. (1998). "Cannabidiol and (−)Δ9-tetrahydrocannabinol are neuroprotective antioxidants". Proceedings of the National Academy of Sciences of the United States of America 95 (14): 8268–8273. Bibcode:1998PNAS...95.8268H. doi:10.1073/pnas.95.14.8268. PMC 20965. PMID 9653176. "The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate." 
  107. ↑ Hamburger-Bar R, Eisenberg J, Belmaker RH (Jan–Feb 1987). "Animal and clinical studies of vasopressin effects on learning and memory.". Isr J Med Sci. 23 (1–2): 12–8. PMID 2952619. 
  108. ↑ Lee J.-Y., Kim K.Y., Shin K.Y., Won B.Y., Jung H.Y., Suh Y.H. (2009). "Effects of BT-11 on memory in healthy humans". Neuroscience Letters 454 (2): 111–114. doi:10.1016/j.neulet.2009.03.024. PMID 19429065. 
  109. ↑ Shin K.Y., Lee J.-Y., Won B.Y., Jung H.Y., Chang K.-A., Koppula S., Suh Y.-H. (2009). "BT-11 is effective for enhancing cognitive functions in the elderly humans". Neuroscience Letters 465 (2): 157–159. doi:10.1016/j.neulet.2009.08.033. 
  110. ↑ Singh, H.K. and Dhawan, B.N. (1 September 1997). "Neuropsychopharmacological effects of the Ayurvedic nootropic Bacopa monniera Linn. (Brahmi)". Indian Journal of Pharmacology 29 (5): 359–65. 
  111. ↑ Joshi H, Parle M (March 2006). "Brahmi rasayana improves learning and memory in mice". Evid Based Complement Alternat Med 3 (1): 79–85. doi:10.1093/ecam/nek014. PMC 1375237. PMID 16550227. 
  112. ↑ Micheau J, Durkin TP, Destrade C, Rolland Y, Jaffard R (1985). "Chronic administration of sulbutiamine improves long term memory formation in mice: possible cholinergic mediation". Pharmacol Biochem Behav 23 (2): 195–8. doi:10.1016/0091-3057(85)90555-6. PMID 4059305. 
  113. ↑ Bizot JC, Herpin A, Pothion S, Pirot S, Trovero F, Ollat H (2005). "Chronic treatment with sulbutiamine improves memory in an object recognition task and reduces some amnesic effects of dizocilpine in a spatial delayed-non-match-to-sample task". Prog Neuropsychopharmacol Biol Psychiatry 29 (6): 928–35. doi:10.1016/j.pnpbp.2005.04.035. PMID 15951087. 
  114. ↑ Hashimoto, M.; Kanda, M.; Ikeno, K.; Hayashi, Y.; Nakamura, T.; Ogawa, Y.; Fukumitsu, H.; Nomoto, H. et al. (April 2005). "Oral administration of royal jelly facilitates mRNA expression of glial cell line-derived neurotrophic factor and neurofilament H in the hippocampus of the adult mouse brain". Bioscience, Biotechnology, and Biochemistry 69 (4): 800–805. doi:10.1271/bbb.69.800. PMID 15849420. 
  115. ↑ Hattori, N.; Nomoto, H.; Fukumitsu, H.; Mishima, S.; Furukawa, S. (October 2007). "Royal jelly and its unique fatty acid, 10-hydroxy-trans-2-decenoic acid, promote neurogenesis by neural stem/progenitor cells in vitro". Biomedical research (Tokyo, Japan) 28 (5): 261–266. PMID 18000339. 

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