Nootropic

Nootropic

Nootropics (play /n.ɵˈtrɒpɨks/ no-eh-tro-pik), also referred to as smart drugs, brain steroids, memory enhancers, and cognitive enhancers as well as intelligence enhancers, are drugs, supplements, nutraceuticals, and functional foods that improve mental functions such as cognition, memory, intelligence, motivation, attention, and concentration.[1][2] The word nootropic was coined in 1972[3][4] by the Romanian Dr. Corneliu E. Giurgea, 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. However the efficacy of nootropic substances, in most cases, has not been conclusively determined. This is complicated by the difficulty of defining and quantifying cognition and intelligence.

Contents

Nootropics vs. cognitive enhancers

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

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 difficulties such as Alzheimer's disease, Parkinson'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 many of the claims attributed to most nootropics have not been formally tested.

In academia, modafinil has been used to increase productivity, although its long-term effects have not been assessed in healthy individuals.[7] Stimulants such as methylphenidate 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 in the past year, and on some campuses the number is as high as 25%.[8]

Recreational drugs

Many recreational substances that are currently illegal or heavily controlled have effects on the brain or long-term functions that are typically considered secondary to their effects on perception. Note that this list is not intended to be exhaustive. This list includes substances that are illegal, or not completely illegal, but are not controlled or exempt under a Drug schedule.

Traditional herbs

A 2007 survey online databases for herbs used in traditional herbal medicine to treat cognitive decline found over 150 plant species, such as Ginkgo biloba.[11]

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 wide therapeutic window;[12] however, any substance ingested could produce harmful effects. An unapproved drug or dietary supplement does not have to have safety or efficacy approval before being sold.[13] (This mainly applies to the USA, but may not apply in the EU or elsewhere.)

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.[14] 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.[15] A systematic review of trials found "little evidence of a beneficial impact" from supplements on cognitive function later in life.[16]
  • Omega-3—linked to the maintenance brain function. A study done in Norway,[17] demonstrated a potential link between Omega-3 consumption during pregnancy and child intelligence test scores.[18]
  • Isoflavones—may be related to cognitive function[19]

Racetams

The word nootropic was coined upon discovery of the effects of piracetam, developed in the 1960s.[20] Although piracetam is the most commonly taken nootropic,[20] 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.[21] Although aniracetam and nebracetam show affinity for muscarinic receptors, only nefiracetam shows it at the nanomolar range. Racetams have been called "pharmacologically safe" drugs.[12]

Other substances sometimes classified as nootropics include hydergine, vinpocetine, bifemelane, huperzine A (cholinergic activator below), and dimethylaminoethanol (DMAE).[12]

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] They generally have a very substantial side-effect profile and are not considered classical "nootropic" drugs. 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][22]

Dopaminergics

Dopaminergics are substances that affect the neurotransmitter dopamine or the components of the nervous system that use dopamine. Attributable effects of dopamine are enhancement of attention, alertness, and antioxidant activity. Dopamine is the primary activity of stimulants like methylphenidate (Ritalin) or amphetamine. Dopaminergic nootropics include dopamine synthesis precursors, dopamine reuptake inhibitors, monoamine oxidase inhibitors, and other compounds:


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
  • Suritozole—α5 partial inverse agonist

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.[36]

  • Guanfacine is an α2A receptor agonist, FDA approved for and frequently used to treat ADHD symptoms.[1][2] 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.[37]

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:

Anti-depression, adaptogenic (antistress), and mood stabilization

Stress, depression, and depressed mood negatively affect cognitive performance.[citation needed] It is reasoned that counteracting and preventing depression and stress may be an effective nootropic strategy.[citation needed] The term adaptogen applies to most herbal anti-stress claims.[citation needed]

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

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.

  • Blessed Thistle—increases blood circulation, improving memory
  • 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.[51]
  • Vinpocetine—increases blood circulation (vasodilator) and metabolism in the brain; 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.[52] Vinpocetine may therefore induce or exasperate depressive symptoms as an adverse effect.
  • Vincamine—presumably increases blood circulation (vasodilator) and metabolism in the brain; related to vinpocetine; used in sustained release (example of a brand is Oxybral SR (note that this example is not meant to insinuate superiority over other preparations, nor advertise it; it is given due to it's popularity in some regions, inspite of sometimes being more expensive (possibly due to the mechanism which implements it's sustained release form) than other available drugs with the same active ingredient))

Experimental histamine antagonists

The H3-receptor decreases neurotransmitter release: histamine, acetylcholine, norepinephrine, serotonin. Thus, H3-receptor-antagonists increases cognition 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.[53]
  • A-349,821—It has nootropic effects in animal studies.[54]

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.

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
  • Pregnenolone—increases neurogenesis
  • Orexin—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:

  • Bacopa monniera (Brahmi)—shown to possess adaptogenic properties and enhance memory and concentration.[65] Folk use in Ayurvedic medicine purports "enhancement of curiosity"; Brahmi rasayana has been shown to improve learning and memory in mice[66]
  • Fipexide—drug for Dementia
  • 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[67] and object recognition tests[68]
  • Royal Jelly—Increases brain cell growth and diversity, only demonstrated in-vitro, improbable in-vivo
  • Curcumin—significant in-vitro activity, but in-vivo activity limited by low bioavailability

Other nootropics

These substances have been linked to better cognitive function, but may not be the cause. See correlation does not imply causation.

See also

References

  1. ^ "Dorlands Medical Dictionary". Archived from the original on 2008-01-30. http://web.archive.org/web/20080130031824/http://www.mercksource.com/pp/us/cns/cns_hl_dorlands.jspzQzpgzEzzSzppdocszSzuszSzcommonzSzdorlandszSzdorlandzSzdmd_n_10zPzhtm. 
  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. pp. 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")" (in French). Actual Pharmacol (Paris) 25: 115–56. PMID 4541214. 
  5. ^ "Dorlands Medical Dictionary". Archived from the original on 2008-01-30. http://web.archive.org/web/20080130031824/http://www.mercksource.com/pp/us/cns/cns_hl_dorlands.jspzQzpgzEzzSzppdocszSzuszSzcommonzSzdorlandszSzdorlandzSzdmd_n_10zPzhtm. 
  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. ^ a b c d Sahakian B; Morein-Zamir S (December 2007). "Professor's little helper". Nature 450 (7173): 1157–9. doi:10.1038/4501157a. PMID 18097378. 
  8. ^ a b c ""Towards responsible use of cognitive-enhancing drugs by the healthy" in Nature: International Weekly Journal of Science". http://www.nature.com/nature/journal/vaop/ncurrent/full/456702a.html. Retrieved December 2008. 
  9. ^ "Smart Drugs and Should We Take Them?". Dolan DNA Learning Center. http://blogs.dnalc.org/g2conline/2009/09/21/smart-drugs-and-should-we-take-them/. Retrieved 2009-09-21. 
  10. ^ 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. http://www.jci.org/articles/view/25509. Retrieved 2011-03-02. 
  11. ^ 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. 
  12. ^ a b c 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. http://www.bentham-direct.org/pages/content.php?CMC/2007/00000014/00000002/0001C.SGM. 
  13. ^ Goldman P (2001). "Herbal medicines today and the roots of modern pharmacology". Ann. Intern. Med. 135 (8 Pt 1): 594–600. PMID 11601931. 
  14. ^ 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. 
  15. ^ 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. 
  16. ^ 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. 
  17. ^ Pediatrics. 2003 Jan;111(1):e39-44
  18. ^ Prevention [0032-8006] Chillot yr.2004 vol.56 iss.1 pg.122 -9
  19. ^ 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. 
  20. ^ a b 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)' 3 (1): 957–75. doi:10.1016/S0899-9007(03)00024-8. PMID 14624946. 
  21. ^ 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. 
  22. ^ Szalavitz, Maia (2009-01-06). "Popping Smart Pills: The Case for Cognitive Enhancement - TIME". Time. http://www.time.com/time/health/article/0,8599,1869435,00.html. Retrieved 2010-05-20. 
  23. ^ 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. 
  24. ^ Kiefer, I. (2007). "Brain Food". Scientific American Mind 18 (5): 58–63. doi:10.1038/scientificamericanmind1007-58. http://www.nature.com/scientificamericanmind/journal/v18/n5/full/scientificamericanmind1007-58.html. Retrieved 2009–11- 01. 
  25. ^ 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. 
  26. ^ 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. 
  27. ^ 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. PMID 14563489. 
  28. ^ 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. doi:10.1126/science.6168019. PMID 6168019. 
  29. ^ a b 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. 
  30. ^ 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. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1908237. 
  31. ^ 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. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=548494. 
  32. ^ "Supplement naturally boosts ageing brain power". Sydney Morning Herald. 2008-02-25. http://www.smh.com.au/articles/2008/02/24/1203788130776.html. Retrieved 2009-07-28. 
  33. ^ 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. 
  34. ^ 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. 
  35. ^ 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. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2562334. 
  36. ^ 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. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2518387. 
  37. ^ Arnsten, A. & Dudley, A. (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. 1:2. http://www.behavioralandbrainfunctions.com/content/1/1/2
  38. ^ 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. 
  39. ^ 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. 
  40. ^ 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. 
  41. ^ 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. 
  42. ^ 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. 
  43. ^ 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. 
  44. ^ 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. 
  45. ^ Cite error: Invalid <ref> tag; no text was provided for refs named mp09; see Help:Cite errors/Cite error references no text
  46. ^ Cite error: Invalid <ref> tag; no text was provided for refs named cns08; see Help:Cite errors/Cite error references no text
  47. ^ Panossian A., Wikman G."Evidence based efficacy of adaptogens in fatigue" Planta Medica 2009 75:9
  48. ^ 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. http://linkinghub.elsevier.com/retrieve/pii/S0091305704001935. 
  49. ^ Jesky R, Hailong C. "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." Phytother Res. 2011 Feb 9. doi: 10.1002/ptr.3388. [Epub ahead of print]
  50. ^ Morgan A, Stevens J"Does Bacopa monnieri improve memory performance in older persons? Results of a randomized, placebo-controlled, double-blind trial." J Altern Complement Med. 2010 Jul;16(7):753-9 Authors:
  51. ^ 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. 
  52. ^ 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. 
  53. ^ 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. 
  54. ^ 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. 
  55. ^ 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. 
  56. ^ 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. 
  57. ^ 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. 
  58. ^ http://www.biopsychiatry.com/article/sameart.htm
  59. ^ http://www.ajcn.org/content/76/5/1158S/F2.expansion.html
  60. ^ http://www.acetylcysteine.org/glutathione.htm
  61. ^ Nelson T, Cavallaro S, Yi C, McPhie D, Schreurs B, Gusev P, Favit A, Zohar O, Kim J, Beushausen S, Ascoli G, Olds J, Neve R, Alkon D (1996). "Calexcitin: a signaling protein that binds calcium and GTP, inhibits potassium channels, and enhances membrane excitability". PNAS 93 (24): 13808–13. doi:10.1073/pnas.93.24.13808. PMC 19433. PMID 8943017. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=19433. 
  62. ^ Deng, L.; Vysotski, ES.; Markova, SV.; Liu, ZJ.; Lee, J.; Rose, J.; Wang, BC. (Mar 2005). "All three Ca2+-binding loops of photoproteins bind calcium ions: the crystal structures of calcium-loaded apo-aequorin and apo-obelin.". Protein Sci 14 (3): 663–75. doi:10.1110/ps.041142905. PMID 15689515. 
  63. ^ http://www.proteotech.com/
  64. ^ http://www.jfponline.com/Pages.asp?AID=518
  65. ^ 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. http://ijp-online.com/article.asp?issn=0253-7613;year=1997;volume=29;issue=5;spage=359;epage=365;aulast=Singh;type=0. 
  66. ^ 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. http://ecam.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=16550227. 
  67. ^ 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. 
  68. ^ 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. 
  69. ^ Britton A, Singh-Manoux A, Marmot M (August 2004). "Alcohol consumption and cognitive function in the Whitehall II Study". Am. J. Epidemiol. 160 (3): 240–7. doi:10.1093/aje/kwh206. PMID 15257997. http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=15257997. 
  70. ^ Launer LJ, Feskens EJ, Kalmijn S, Kromhout D (February 1996). "Smoking, drinking, and thinking. The Zutphen Elderly Study". Am. J. Epidemiol. 143 (3): 219–27. PMID 8561155. http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=8561155. 
  71. ^ Galanis DJ, Joseph C, Masaki KH, Petrovitch H, Ross GW, White L (August 2000). "A longitudinal study of drinking and cognitive performance in elderly Japanese American men: the Honolulu-Asia Aging Study". Am J Public Health 90 (8): 1254–9. doi:10.2105/AJPH.90.8.1254. PMC 1446341. PMID 10937006. http://www.ajph.org/cgi/pmidlookup?view=long&pmid=10937006. 
  72. ^ Dufouil C, Ducimetière P, Alpérovitch A (September 1997). "Sex differences in the association between alcohol consumption and cognitive performance. EVA Study Group. Epidemiology of Vascular Aging". Am. J. Epidemiol. 146 (5): 405–12. PMID 9290500. http://aje.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=9290500. 
  73. ^ Rodgers B, Windsor TD, Anstey KJ, Dear KB, F Jorm A, Christensen H (September 2005). "Non-linear relationships between cognitive function and alcohol consumption in young, middle-aged and older adults: the PATH Through Life Project". Addiction 100 (9): 1280–90. doi:10.1111/j.1360-0443.2005.01158.x. PMID 16128717. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0965-2140&date=2005&volume=100&issue=9&spage=1280. 
  74. ^ Anstey KJ, Windsor TD, Rodgers B, Jorm AF, Christensen H (September 2005). "Lower cognitive test scores observed in alcohol abstainers are associated with demographic, personality, and biological factors: the PATH Through Life Project". Addiction 100 (9): 1291–301. doi:10.1111/j.1360-0443.2005.01159.x. PMID 16128718. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0965-2140&date=2005&volume=100&issue=9&spage=1291. 

External links


Wikimedia Foundation. 2010.

Игры ⚽ Нужно сделать НИР?

Look at other dictionaries:

  • nootropic — no·o·tro·pic .nō ə trō pik, träp ik adj of, relating to, or promoting the enhancement of cognition and memory and the facilitation of learning <nootropic drugs> nootropic n a nootropic substance and esp. a drug called also smart drug * * *… …   Medical dictionary

  • nootropic — noun Etymology: International Scientific Vocabulary noo + tropic Date: 1976 a substance that enhances cognition and memory and facilitates learning • nootropic adjective …   New Collegiate Dictionary

  • nootropic — ˌnōəˈtrōpik, ˈträp noun ( s) Etymology: International Scientific Vocabulary noo + tropic; originally formed as French nootrope : a substance that enhances cognition and memory and facilitates learning • nootropic adjective …   Useful english dictionary

  • Nootropic — Nootropikum (gr. νόος „Verstand“, τρόπος „Wendung, Richtung“) ist ein unscharf definierter Begriff, der sowohl in der Pharmakologie als auch in anderen Bereichen wie Komplementärmedizin, Wellness und Anti Aging Anwendung findet. Im weitesten… …   Deutsch Wikipedia

  • nootropic — noun /ˌnoʊəˈtroʊpik,ˌnoʊəˈtrɑːpik/ a) Any substance purported to increase cognitive abilities. b) A drug that enhances learning and memory and lacks the usual pharmacology of other psychotropic drugs (e.g. sedation, motor stimulation) and… …   Wiktionary

  • nootropic — [ˌnəʊə trəʊpɪk, trɒpɪk] adjective denoting drugs used to enhance memory or other cognitive functions. Origin 1970s: from Fr. nootrope (from Gk noos mind + tropē turning ) + ic …   English new terms dictionary

  • nootropic — no·o·tro·pic …   English syllables

  • nootropic — /ˈnoʊətrɒpɪk/ (say nohuhtropik) adjective 1. of or relating to a drug which affects the brain, affording improvements in alertness, memory, etc. –noun 2. such a drug. {Greek noos mind + tropic} …  

  • Piracetam — Systematic (IUPAC) name 2 oxo 1 pyrrolidineacetamide Clinical data …   Wikipedia

  • Corneliu E. Giurgea — Piracetam Corneliu E. Giurgea was a Romanian psychologist and chemist. In 1964, he synthetised Piracetam, which he has described as a nootropic.[1] Giurgea coined the term nootropic …   Wikipedia

Share the article and excerpts

Direct link
Do a right-click on the link above
and select “Copy Link”