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Neuropharmacological Review of the Nootropic Herb Bacopa Monnieri

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Neuropharmacological Review of the Nootropic Herb Bacopa Monnieri REJUVENATION RESEARCH Volume 16, Number 4, 2013 ª Mary Ann Liebert, Inc. DOI: 10.1089/rej.2013.1431 Neuropharmacological Review of the Nootropic Herb Bacopa monnieri Sebastian Aguiar and Thomas Borowski Abstract This review synthesizes behavioral research with neuromolecular mechanisms putatively involved with the low- toxicity cognitive enhancing action of Bacopa monnieri (BM), a medicinal Ayurvedic herb. BM is traditionally used for various ailments, but is best known as a neural tonic and memory enhancer. Numerous animal and in vitro studies have been conducted, with many evidencing potential medicinal properties. Several randomized, double-blind, placebo-controlled trials have substantiated BM’s nootropic utility in humans. There is also evidence for potential attenuation of dementia, Parkinson’s disease, and epilepsy. Current evidence suggests BM acts via the following mechanisms—anti-oxidantneuroprotection(viaredoxandenzymeinduction),acetylcholinesteraseinhibitionand/or choline acetyltransferase activation, b-amyloid reduction, increased cerebral blood flow, and neurotransmitter modulation (acetylcholine [ACh], 5-hydroxytryptamine [5-HT], dopamine [DA]). BM appears to exhibit low toxicity in model organisms and humans; however, long-term studies of toxicity in humans have yet to be conducted. This review will integrate molecular neuroscience with behavioral research. Introduction agents,15 BM is only beginning to undergo rigorous experi- mental research. ognitive enhancement typically exacts a toxico- Bacopa monnieri (also known as brahmi, water hyssop, Clogical and psychological toll.1–4 The milieu of nootropic Bacopa monniera, and Herpestis monniera), is a creeping pe- phytochemicals found within Bacopa monnieri (BM), primar- rennial with small oblong leaves and purple flowers, found ily triperpenoid saponins called bacosides, exhibit minimal in warm wetlands, and native to Australia and India. Com- observable adverse effects at standard dosages. BM demon- monly found as a weed in rice fields, BM grows throughout strates anti-oxidant,5 hepatoprotective,6 and neuroprotective7 East Asia and the United States.16 The entire plant is used activity. Emerging research demonstrates several mechanisms medicinally. of action—acetylcholinesterase inhibition, choline acetyl- Unlike the potentially addictive and forceful action of transferase activation, b-amyloid reduction, increased cerebral widely used psychostimulants, chronic and moderate ad- blood flow, and monoamine potentiation. ministration of BM appears to nourish rather than deplete Herbal medicine is regularly used by 80% of the world neurons, an action compatible with 1400 years of Ayurvedic population and is increasing in popularity in Europe and study. BM was initially described around the 6th century North America. 8 In 2008, the National Institutes of Health A.D. in texts such as the Charaka Samhita, Athar-Ved, and (NIH) found 4 in 10 adults reported using complementary Susrutu Samhita as a medhya rasayana–class herb taken to and alternative medicine (CAM) in the last 12 months, 17.7% sharpen intellect and attenuate mental deficits. The herb was of such treatments being herbal medicine.9 Those with higher allegedly used by ancient Vedic scholars to memorize education are most likely to use CAM,10 which may partially lengthy sacred hymns and scriptures. BM is colloquially reflect the fact that public health insurance used by poor called Brahmi, after the Hindu creator-god Brahma, espe- individuals tends not to cover CAM.11 Herbal medicine cially when combined with other alleged intellect-sharpening tends to be cheaper than pharmaceuticals, albeit less stan- herbs like Centella asiatica (Gotu Kola). BM is consistently dardized.12,13 Western biomedicine is in the midst of inves- found in the many Ayurvedic preparations prescribed for tigating the potential value of the Eastern pharmacopeia. Of cognitive dysfunction. the 150 most used pharmaceutical drugs in the United States, An estimated 3.4 million people are affected by dementia in 118 were derived from plants.14 Traditional medical systems the United States,17 most prevalently in the elderly. The el- offer a vast library of potentially therapeutic neurological derly population (aged over 65) is expected to double by 2030, Department of Neuroscience, Pitzer College, Claremont, California. 313 314 AGUIAR AND BOROWSKI reaching 72 million, or 20% of the total U.S. population.18 BM clinical studies cited focus on memory, omitting other facets shows great clinical potential in attenuating dementia via of cognition like fluid intelligence or creativity. Past clinical several mechanisms, most notably dose-dependent acetyl- studies were not longitudinal, typically lasting only 12 choline potentiation and free radical scavenging. weeks. The long-term effect of BM on humans is unknown, In a 90-day oral administration trial in rats, BM exhibited a but animal models suggest considerable protection against no-observed adverse effect level (NOAEL) of 500 mg/kg and age-related neurodegeneration rather than progressive tox- 5 a median lethal dose (LD50) of 2400 mg/kg. The standard icity or tolerance formation. experimental human dose is between 150 and 3000 mg equivalent per day. The most common clinical side effect of Putative mechanisms of action BM is mild gastrointestinal upset, but long-term clinical trials are lacking. Several research groups formulate bacoside- The following mechanisms will be discussed: Anti-oxidant/ standardized BM extract for clinical use, and the herb is neuroprotection, acetylcholinesterase inhibition, choline acet- widely used in India, the United States, and Australia. BM yltransferase activation, b-amyloid reduction, increased cere- has been applied in rodents and cell culture for the following bral blood flow, and monoamine potentiation and modulation. uses, which will not be detailed in this review: Anti-oxidant/neuroprotection. Oxidative stress (OS) oc- anti-convulsant19–21 curs when free radicals (chemical species with unpaired anti-depressant22 electrons, produced during normal metabolism) overcome analgesic23–25 the cell’s homeostatic defense mechanisms.49 Protective, free anti-inflamatory26 radical–quenching enzymes include superoxide dismutase, anti-microbial27 catalase, glutathione peroxidase (GPx), glutathione reductase anti-ulcerogenic28/anti-H. pylori29 (GSR), and others. Anti-oxidant compounds also play a key anxiolytic30 protective role, including vitamins A, C, E, and myriad adaptogenic31,32 phytonutrients (particularly phenols).50,51 OS plays a role in anti-neoplastic33,34 many diseases, even aging itself,52 by degrading ligands, hepatoprotective6 peroxidizing lipids, disrupting metabolic pathways, dena- immunostimulatory35–37 turing proteins, and breaking DNA strands.53 Past reviews have focused on the broad therapeutic uses The brain is especially susceptible to OS because it is of BM, including the above uses. This review will elucidate metabolically active, possesses high levels of pro-oxidant the neuropharmacological mechanisms underlying the noo- iron, and is composed of unsaturated lipids (prone to lipid tropic effects of the herb, summarize pre-clinical and clinical peroxidation).54 Furthermore, the blood–brain barrier pre- studies, outline putative mechanisms of action, and address vents many exogenous anti-oxidants from quenching reac- issues of toxicity. tive oxygen species (ROS) in the brain.55 Anbarasi et al.56 assessed the neuroprotective role of ba- Chemical Constituents coside A against OS in the brains of rats exposed to cigarette smoke by measuring concentrations of enzymatic and non- The main nootropic constituents of BM are believed to be enzymatic anti-oxidants as well as trace elements. The dammarane types of triterpenoid saponins known as baco- researchers administered 10 mg/kg aqueous bacoside A ga- sides, with jujubogenin or pseudo-jujubogenin moieties as vage daily and found that BM significantly increased brain aglycone units.38 Bacosides comprise a family of 12 known levels of glutathione, vitamin C, vitamin E, and vitamin A in analogs.39 Novel saponins called bacopasides I–XII have rats exposed to cigarette smoke (perhaps an anti-oxidant been identified more recently.40–42 The alkaloids brahmine, conservation effect). Bacoside A administration increased the nicotine, and herpestine have been catalogued, along with activities of superoxide dismutase (SOD), catalase, GPx, and D-mannitol, apigenin, hersaponin, monnierasides I–III, cu- GSR. As a result, the levels of glutathione (primary endog- curbitacins and plantainoside B.43–50 The constituent most enous anti-oxidant conjugate) in the brain were significantly studied has been bacoside A, which was found to be a blend increased as well. The researchers found that cigarette smoke of bacoside A , bacopacide II, bacopasaponin C, and a juju- 3 depletes zinc and selenium levels in the brain, which is es- bogenin isomer of bacosaponin C.48 These assays have been pecially problematic because zinc is a SOD co-factor and conducted using whole plant extract, and bacoside concen- selenium is a GPx co-factor. Administration of bacoside A trations may vary depending upon the part from which they also restored zinc and selenium levels. are extracted. In a related study, Anbarasi et al.57 also showed that In one BM sample, Rastogi et al. found this bacoside 10 mg/kg aqueous gavage administration of bacoside A in- profile—bacopaside I (5.37%), bacoside A3 (5.59%), bacopa- hibited lipid peroxidation, improved the activities
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