Nootropics NSI-189 Recovery

NSI-189: A Nootropic Antidepressant That Promotes Neurogenesis

The use of antidepressant medications in America is a rapidly growing portion of the pharmaceutical industry. The number of people who take antidepressants has increased by almost 400% from 1990 through 2008.[1] In addition, eleven percent of Americans aged 12 years and older take some form of antidepressant medication.

Antidepressants have long been a troubled group of drugs in terms of side-effects, with even the most recent class of antidepressants (SSRIs) exhibiting potential side-effects like insomnia, sexual dysfunction, or even worsened depression. These troublesome side-effects have displayed a clear need for more effective treatment options.

Prozac capsules and packaging anti depression medication

Despite the apparent need for a more effective class of antidepressants, no new major milestones have occurred regarding antidepressants since 1987, the year fluoxetine (Prozac) was approved by the FDA.[2] Since the beginning of Prozac’s use to treat depression, SSRIs have dominated the area of medical treatment for depression. This era of depression treatment has been going on for about 29 years. However, some progress is being made in the development of new antidepressants. One of the newest experimental drugs for depression, NSI-189, also displays nootropic properties. Here we will be examining some of the claims surrounding the purported benefits of NSI-189.

Origins of NSI-189

NSI-189 is an experimental drug currently being developed and studied by Neuralstem Inc., a biotechnology company that commercially produces neural stem cells for therapy.[3] The research and development of NSI-189 began in the 1990s, during the years of Bill Clinton’s presidency.

The Clinton administration contracted Neuralstem to research the possibilities of creating a “super soldier,” one that was able to stay awake and alert for extended periods of time.[4] The researchers at Neuralstem recognized that a drug targeting the hippocampus could possibly alleviate the effects of sleep deprivation and exhaustion, and set out to find a drug that could induce neurogenesis. Neuralstem, finding their prospects to be promising, continued research in this vein even after the government program was canceled.

This preliminary research would eventually result in the drug NSI-189. Clinical research on NSI-189 has been in the works since 2011, and a phase 1b trial was completed in July of 2014.[5] Clinical phase 1 trials typically focus on finding the correct dosage range of the drug, which has been placed around 40 to 80 mg per day in the treatment of Major Depressive Disorder (MDD) and cognitive decline.

NSI-189 structure

Chemically speaking, NSI-189 is classified as a small-molecule benzylpiperazine-aminopyridine drug, making it structurally unique among other antidepressants. However, the drug has also seen increased interest in terms of its ability to stimulate nerve growth in the hippocampus.

According to the official Neuralstem, Inc. press release concerning the phase 1b trial, “[NSI-189] is a proprietary new chemical entity that stimulates new neuron growth in the hippocampus, a region of the brain believed to be implicated in MDD, as well as other diseases and conditions such as traumatic brain injury (TBI), Alzheimer’s disease, and post-traumatic stress disorder (PTSD).”[6]

The phase 1b trial of NSI-189 was “a randomized, double-blind, placebo-controlled, multiple-dose escalating trial evaluating the safety, tolerability, pharmacokinetics and pharmacodynamic effect of NSI-189 in the treatment of MDD.” Now that the trial has been completed, the results have been released, and they appear quite promising.

The study, which was conducted on 24 patients over the course of 28 days, found that NSI-189 administration reduced the symptoms of depression and cognitive decline significantly more than placebo. The drug was tolerated well by the subjects, and it “may also exhibit pro-cognitive properties associated with increases in prefrontal alpha coherence.” [7] [8]

Mechanism of Action

Selective serotonin reuptake inhibitors (SSRIs) attempt to treat depression by increasing levels of serotonin in the brain. This model of depression, known as the “monoamine hypothesis,” states that depression is caused by a shortage or imbalance of certain neurotransmitters in the depressed patient, mainly serotonin. However, this model has been quite drastically debunked in recent years.[9] Many researchers and psychiatrists now recognize that depression is far more complex than a simple chemical imbalance. New theories have emerged that recognize factors such as emotional trauma, environmental factors, glutamatergic dysfunction, and inflammation as potential causes of depression.

In short, depression is a complex web of interweaving causes and effects, both psychological and physiological. While scientists know from research that SSRIs and other antidepressants certainly have an effect in alleviating depression, the actual pharmacology behind the medications is far more unclear. Why do some respond to medication negatively? Why do some not respond at all? Because these questions are so intimately tied with genetic and biochemical factors, they are very difficult to address in a comprehensive manner.

These observations lead to two important points: First, depression is such a complex disorder that we don’t yet know the best way to treat it with medication. Second, SSRIs may be somewhat effective in alleviating depression, but we don’t completely understand why they work the way they do. Because the root causes of depression are still somewhat uncharted territory, exploration of new treatments that work differently than SSRIs is very important. By pioneering these treatments and observing their effects, the puzzle pieces that make up the full picture of depression can be pieced together into a comprehensive model.

NSI-189 vs Placebo Hippocampus
Topographs of average amplitude at 10-12 Hz showing increased high-frequency alpha in patients receiving NSI-189 at Day 28. Differences scores comparing conditions show most significant differences between total subjects receiving NSI-189 (left) vs. Placebo (right) in the left posterior temporal and parietal regions.

Some researchers, like those at Neuralstem, have noticed a correlation between reduced hippocampal volume and increased incidence of Major Depressive Disorder.[10] According to this theory, NSI-189 could potentially be a remedy to those suffering from depression by contributing to the growth of the patient’s hippocampus. Because the hippocampus is also so closely associated with memory, NSI-189 also has the potential to impact cognition.

This “hippocampal” model of depression is still in its infancy, and NSI-189 is one of the first drugs being researched that uses this specific form of treatment. Although it is known that NSI-189 increases hippocampal volume, the exact mechanism underlying this effect is still unsure. The results of the phase 1b trial even suggested that NSI-189s effect on hippocampal volume was not as drastic as that which was seen in animal studies.[11] Whether or not the increase of hippocampal volume persists after ceasing the medication remains to be determined. As the research and experimentation with NSI-189 continue, new research will shed light on this model for depression, and the medical community will be better able to understand the correlation between depression and hippocampal volume.

Purported Benefits

As mentioned above, the potential benefits of NSI-189 are:

    1. Improvement in behavioral responses associated with depression.[12]
    2. Reversal of hippocampal atrophy.[13]
    3. May enhance memory and cognition through increase neurogenesis, particularly in depressed subjects.
    4. Positive effects may persist after treatment ceases.[14]

    Subjective Experiences

    Because NSI-189 is still in its infancy as a clinical treatment for MDD and cognitive disorders, anecdotal information is important for those determining if they want to try NSI-189. This community poll conducted by /u/MisterYouAreSoDumb on /r/nootropics is useful for seeing various users’ experiences with NSI-189

    A Reddit user, Code_of_Error, relayed his experience with NSI-189 in a post on reddit[15]:

    I have been on NSI-189 Phosphate for three weeks now. I take 40mg orally once per day. I used to take it sublingually, but I learned that doing so may be counterproductive due to the possibility that too much is absorbed. Apparently, 40mg-80mg ORALLY was the sweet spot in clinical trials, so sublingual administration has too many unknowns to be worth it. Albeit, the freebase form is a different story.
    Anyway, I started exploring this substance in hopes of counteracting my chronic brain fog, slight depersonalization, anhedonia, general feelings of haziness, and slow cognition.
    Most notably, I have noticed an intensification of emotions, as well as pleasure. The first few days, I felt the inclination to tear up at every positive emotion. It felt ridiculous, but that has mostly leveled out. Although I am only three weeks in, I notice I am more inclined to look forward to plans. I am quicker to laugh and socialize.
    Prior to NSI-189, every emotion I experienced felt like nothing more than background noise. Now a days, all of my emotions feel more genuine, as if they’re at the forefront of my brain. When I experience anxiety, I no longer feel so dissociated from it. When I feel joy, it tends to last longer. Although these new perspectives are scary, I welcome the change. My default state of mind tends to be slightly perkier as well.
    I will admit that I am more guided by my emotions than I have been in years, and I am totally enabling it. I don’t recommend falling in love while on this substance. However, this substance is bringing me closer to my long-lost inner feelings. The effects aren’t perfect, and I still often feel that irritating haze (i.e., brain fog/dulled-out sensation/whatever ambiguous symptoms) to a degree, but I hope that my mental issues continue to improve as I stay on this. I’ve certainly made strides.
    Interestingly, I have noticed that I better able to “feel” the effects of nootropics while on this as well. Caffeine has a much more profound effect on me (comparable to when I first started using it), and the effects of tianeptine are as potent as ever. Again, I feel as if this speaks MORE to NSI-189’s ability to make you feel and less to its ability to reduce tolerance.
    Lastly, I would venture to say I am bit sharper mentally, and less likely to experience “cluttering” when I go to speak.
    Side effect wise, I only experience a mild fluttering (almost like a twitch) directly behind the inner half of my right eyebrow. Other than that, no headaches. I may have a mild reduction in sex drive, but nothing too troubling.
    Overall, I am looking forward to staying on this drug for a while. My mental symptoms are nowhere near gone, but I see enough benefits to keep going. Like many people who try an under-researched compound intended for depression, I feel as if I have little to lose.

    This is the experience of flare1028us, another reddit user:[16]

    Personally, I’ve found NSI-189 to be very useful. I’m taking 50mg freebase once daily in the morning. The acute effects for me are a gentle wave of calmness, improved long-term memory, and notably improved vision.
    The improved vision, as another redditor put it, is like my vision being “zoomed out” by 5%, like having a slightly larger field of view. Improved memory is the strong point of this substance. I find myself having vivid recollection of memories going back to my single digit ages. This has also allowed me to remember times when I encountered some of the same struggles I have to this day, and how I handled them – I feel better equipped to tackle them with better memory of what did and didn’t work in the past.
    As far as side effects, child-like emotions are coming on fairly strong. This is both good and bad. The good is that the sense of wonderment that we experience as children has come forth again, the bad being somewhat immature initial emotional responses. For example, jealousy – on a very childish level. It’s not debilitating, but it’s something to be mindful of.
    Speaking of being mindful, it has gotten a whole lot easier to practice mindfulness meditation and commit experiences I’ve gained through it to long(er) term memory.
    Interactions: Cannabis now gives me a mild headache, but if the high is balanced well (sometimes I’ll add some sublingual CBD), it is a very useful state of mind – for me it’s like being high with a better ability to remember the observations I make about my decisions and behavior that I may not come to so quickly in other states of mind. I tried taking piracetam once on NSI, and I’m never doing it again. Total dysphoria for most of the day from 3.5g piracetam in the morning. This stuff is supposed to reset piracetam tolerance, but I won’t be testing that until I’m off NSI-189 for a while.
    Tianeptine (sodium and sulfate) feels like it meshes really well with NSI-189, along with neurogenic peptides – took 200ug NA-Semax Amidate (sub-q) with NSI and went to yoga class (pretty intense class too). That was a level of control I would love to be able to gain every time I exercise in general.
    Hope this helps, I’m still waking up – I’ll answer questions if you have them


    If NSI-189 proves to be an effective treatment for Major Depressive Disorder, it could have a potentially large impact on the direction of depression medication in the upcoming years. The long-standing dominance of SSRI drugs in the treatment of depression has left many wondering just how much longer it will be before the next major breakthrough occurs in depression treatment.

    A novel drug like NSI-189 could be the answer, and the studies concerning NSI-189 also give us a useful glimpse into the correlations between depression, hippocampal volume, and cognition. As we move further into the 21st century, the scientific community will undoubtedly continue to map more accurately the territory that is the human mind.

    References   [ + ]

    Cognitive Health Nootropics

    Can We Really Increase Our Intelligence?

    According to the psychological literature available, there are two general prospects of intelligence: the uniform one, evaluated in school, which basically addresses linguistic & logical-mathematical intelligence; and the Pluralistic View of Mind, proposed by Howard Gardner in his acclaimed theory of Multiple Intelligences. Two different theories that demand two very different -and eventually opposed- answers to the inquiry of intelligence enhancement.

    Intelligence Quotient (IQ) is a certain type of measurement of intellectual ability that came in due to devotion to universal formal education. Thus, IQ tests have been shown to be moderately correlated with grades in elementary, primary, and high school; job performance; professional status; and number of years in school[1]. In this way, the prevalence of IQ tests imply a certain Hereditarian Theory of Intelligence that is rather invariable and stable across time among healthy individuals. According to this approach, intelligence is a unitary entity, an abstraction of an all-purpose system that permeates uniformly in all intellectual activity. Therefore, according to this prospect, the primary basis of intelligence is primarily genetically determined.

    Indisputably, IQ tests are limited in some of its applications and have interpretation problems. They do not appropriately assess the role of motivation (it is likely that motivated individuals put more effort in IQ tests and hence score higher), creativity, social skills, practical intelligence, or wisdom, just for mentioning some relevant variables. Nevertheless, Charles Spearman has demonstrated[2], interestingly, that the various subsets that conform the IQ inventory are positively correlated, labeled as the factor G to stand for the general factor that underlies all intellectual ability. This generic problem solving system is what is popularly called “fluid intelligence”, an empirical argument that  rather supports a hereditarian or genetic theory of intelligence.

    Indeed, available data from twins research suggest that genes are a primary determinant of this view of intelligence[3]. Thus, there is an important group of psychologists and brain & mind scientists who do not think that it is possible to modify your factor G, even though it is not completely clear how this factor and the environment interact with each other[4]. For instance, Jack Naglieri, an intelligence expert from University of Virginia, prevents us to not confuse ability with knowledge. The right way of measuring intelligence, he argues, is to quantify those abilities that underlie the acquisition of knowledge, independently from the knowledge itself. Thus, this psychologist is implying that intelligence is something relatively independent of the learning experience.

    Nonetheless, a renowned article published in the journal Nature by Price and her colleagues challenged this immutable view of intelligence[5]. The study had 33 adolescents, who were 12 to 16-years-old when the study initiated. Price and her team gave them IQ tests, tracked them for four years, and then tested them again with the same measurement tools. The fluctuations in IQ were outstanding: not about a couple points, but 20-plus IQ points. These changes in IQ scores, according to the researchers, were not random — they tracked elegantly with structural and functional brain imaging. Thus, there is also an important group of scientists that maintain that many of the changes in IQ are correlated to changes in the environment, particularly schooling.

    It’s analogous to fitness. A teenager who is athletically fit at 14 could be less fit at 18 if they stopped exercising. Conversely, an unfit teenager can become much fitter with exercise.

    Furthermore, there is also a certain number of studies that have shown brain changes after several kinds of educational regimens. The study about Tokyo taxi drivers is a especially distinguished one[6]. Scientists conducted memory, visual and spatial information tests and took brain scans using MRI of 79 male trainee Tokyo taxi drivers at the beginning of their training regimen. At the beginning of the study, no variance was found in their brain structure or memory. Three to four years later, however, scientists found a considerable increase in grey matter in the posterior hippocampi, among the 39 trains who performed as taxi drivers. Naturally, this change was not observed in the non-taxi drivers. Thus, this kind of studies suggest that the brain can change to accommodate new knowledge, so future programs for lifelong learning are possible[7].

    To sum up, it is not fully clear What intelligence is[8], and hence How to directly increase it.[9] Nonetheless, we can consider intelligence, for practical purposes, as a starting point in life. Naturally, we are born with certain capacities and particular features, but it is later in life when we discover and develop them, regardless of our individual  genetic background. Thus, instead of frustratingly trying to increase your “G” factor (since we do not have a general consensus and determinant scientific evidence yet), what you can do is focus in your multiple crystallized intelligences: the ability to use skills, knowledge, and experience. If you are a scientist, observe and analyze information; if you are a philosopher, organize it and turn it into knowledge; if you are an artist, interpret it. Different areas of intelligence have different weights of importance in each person’s occupational life, and you can definitely get better at specific activities through practice and discipline.

    References   [ + ]

    1, 8. Intelligence and Achievement: Just how Correlated are they?
    2, 9. Summary of Psychology topic Intelligence g Factor
    3. McGue , M. Bouchard , T. J. , Jr Iacono , W. G. Lykken , D. T. (1993). Behavioral genetics of cognitive ability: A life-span perspective. In R. Plomin G. E. McClearn (Eds.), Nature, nurture, and psychology (pp. 59-76). Washington, DC: American Psychological Association
    4. Nature-nurture and intelligence.
    5. Brain scans support findings that IQ can rise or fall significantly during adolescence
    6. The Use of Geospatial Information and Spatial Cognition of Taxi Drivers in Tokyo
    7. Nurture net of nature: Re-evaluating the role of shared environments in academic achievement and verbal intelligence
    Cognitive Health Health Recovery

    9 Supplements To Counteract The Negative Effects of Alcohol

    Despite clinical proof that alcohol has detrimental effects on the human body, even more so than certain illegal substances, it still remains one of the world’s most readily available and favorite intoxicants. Alcohol has been a mainstay in nearly every society for thousands of years, and its commonality leads some people to not even recognize it as a drug. From sporting events to celebrations with family, it’s likely you will toss back a few drinks on occasion.

    However, even moderate alcohol use can carry negative side effects. Consequently, many people seek supplements that will help mitigate some of the deleterious effects on the human body caused by consumption. Whether it’s for an occasional night on the town or more frequent use, or even for recovering from years of alcoholism, there are natural herbs, supplements, and nootropics that have been proven effective for harm reduction with alcohol use.

    • Before consuming any substance along with alcohol, be careful to check for any known interactions. Some nootropics have not been extensively studied and may possess undocumented interactions.
    • GABAergic nootropics like phenibut should be avoided because they can boost the effect of alcohol by producing similar effects of intoxication. It is generally not a good idea to mix alcohol with other depressants.
    • Many ADHD medications that contain amphetamine salts or methylphenidate can delay the onset of alcohol effects leading to increased consumption and potential heart problems.

    Dihydromyricetin (DHM)

    dihydromyricetinDihydromyricetin, a flavonoid, increases metabolism of both alcohol and its primary metabolite, acetaldehyde, by increasing key enzymatic action. In addition to ridding your body of these toxins, it has demonstrated effectiveness at blocking alcohol at the neurological level by binding to GABA receptors in place of alcohol. [1] While this compound theoretically shows promise for hangover prevention, many clinical studies need to take place before it’s classified as a safe supplement for human use.

    Milk Thistle

    Milk_thistle_flowerMilk Thistle, used as a natural medicine for over 2000 years, can accelerate the regeneration of liver cells and reduce fatty liver deposits that build up with alcohol use. It has been hypothesized that milk thistle increases the rate of protein synthesis in the liver, allowing it to more readily repair itself from alcohol-induced damage. [2] Milk thistle contains silibinin, which is thought to be the main active constituent of the plant.[3] Many users take milk thistle as a daily supplement, but it can also be consumed after a night of drinking to aid the liver in detoxification.

    N-Acetylcysteine (NAC)

    NAC is a nutritional supplement that is able to increase levels of the endogenous peptide glutathione [4], an important antioxidant. If you take NAC before a session of drinking, it can potentially reduce the oxidant side effects of alcohol. [5] It can also decrease the acetaminophen toxicity induced by alcohol. [6]
    NAC also has anti-addictive properties.


    emoxypineEmoxypine (also known as Mexidol) is an antioxidant drug that is molecularly similar to pyroxidine, a form of vitamin B6. Emoxypine was first synthesized in Russia, where it is used in the medical field for its anxiolytic, nootropic, neuroprotective, and anti-inflammatory effects, among others. [7] Emoxypine possesses general antioxidant properties, but also can specifically counteract the negative effects of alcohol. It displays therapeutic effects against health issues caused by chronic alcohol use and acute intoxication. In experiments, emoxypine administration reversed the learning deficits caused by chronic alcohol use in rats. [8] Emoxypine also lowers lipofuscin amounts in the cerebrum, much like piracetam. In terms of acute alcohol use (one night of heavy drinking), emoxypine significantly reduces the physical and mental feelings of intoxication that alcohol produces, specifically improving muscle coordination and mental clarity.[9]

    Tauroursodeoxycholic Acid (TUDCA)

    TUDCATUDCA is a bile acid that is found in trace amounts within humans. However, additional supplementation may be beneficial for those who are attempting to recover from alcoholism. TUDCA is used in some countries to treat gallstones and cirrhosis of the liver, but it is not FDA approved for this purpose in the United States.[10] TUDCA has been demonstrated to increase healing rates in unhealthy livers, specifically ones that have been damaged by alcohol. [11] TUDCA should not be consumed before drinking, as it carries the possibility of potentiating liver damage. Rather, TUDCA should be supplemented after drinking, or could be used on a regular basis by former alcoholics who wish to promote healing in their liver. [12]


    HER-ASH01-2Ashwagandha is an herbal supplement that contains various chemicals known collectively as withanolides. These chemicals have been found to be effective at decreasing social anxiety when paired with alcohol, and ineffective threshold doses of either appear to be highly effective when combined. [13] However, the social disinhibition produced by alcohol alone may make this combination unnecessary for some users. Another use of this popular supplement is to aid in quitting alcohol consumption altogether. Indeed, alcohol cessation cold turkey can lead to an increase in anxiety. Ashwagandha has been clinically proven to reduce spikes in anxiety from abstinence. [14]


    Agmatine is an amino acid and neurotransmitter derived from the amino acid, L-Arginine. It has been noted for its positive effects on neuropathic pain and drug addiction. Agmatine appears to reduce symptoms of alcohol withdrawal and dependence, such as anxiety and tremors. [15] [16] One note of caution: Agmatine is known to be a gastro-protective agent but when co-ingested with alcohol it can enhance ulcer formation. [17]


    piracetam_structure_500pxWhile moderate alcohol use does not typically cause damage to the brain, cognitive functions are significantly impaired following the consumption of alcohol, and can continue to be impaired the next day or so after it is consumed. Nootropics that possess cholinergic mechanisms are potentially effective in improving cognition against alcohol-induced impairment. [18] Alcohol consumption increases neuronal lipofuscin, which contributes to age-related neurodegenerative disorders. [19] Piracetam and other racetams, in general, inhibit the accumulation of neuronal lipofuscin, counteracting neurodegeneration. [20]


    Matcha is a Japanese green tea with a very high content of L-Theanine

    The amino acid theanine, which is naturally found in green tea, is another important supplement that may provide liver protection from alcohol consumption. In one study, mice treated with L-theanine prior to alcohol consumption had lower ethanol concentrations in their blood after one hour compared to mice that were administered only alcohol. [21] This implies that L-Theanine could help the body recover faster from the negative effects of alcohol. (Consequently, this also implies Theanine could also decrease the duration of alcohol’s “positive” recreational effects.) Alcohol use typically impairs the antioxidant capabilities of hepatocytes (liver cells), and L-theanine has been found to restore the antioxidant capabilities of these cells. [22]


    Alcohol has maintained its status as society’s drug of choice throughout history. As a result, it will continue to be used extensively and excessively by many despite its potential health risks. Those who are well armed with the knowledge of the aforementioned substances can use them to counteract and overcome the neurological and physical difficulties caused by alcohol consumption.

    At the end of the day, supplements and nootropics can only do so much to prevent the negative effects of alcohol. A cautious and responsible approach to alcohol consumption is ultimately the most important component of using alcohol safely.

    References   [ + ]

    1. Dihydromyricetin As A Novel Anti-Alcohol Intoxication Medication (2012)
    2. Biochemical effects of the flavonolignane silibinin on RNA, protein and DNA synthesis in rat livers. (1986)
    3. Silibinin protects OTA-mediated TNF-alpha release from perfused rat livers and isolated rat Kupffer cells. (2009)
    4. Alcohol and thermally oxidized pufa induced oxidative stress: role of N-acetyl cysteine (2004)
    5. Antioxidant therapy attenuates deficient bone fracture repair associated with binge alcohol exposure (2011)
    6. Clinical course of repeated supratherapeutic ingestion of acetaminophen.
    7. Comparative Analysis of the Anxiolytic Effects of 3-Hydroxypyridine and Succinic Acid Derivatives (2015)
    8, 9. Antioxidant Mexidol. The main neuropsychotropic effects and the mechanism of action. mechanism of action. (2009)
    10. The clinical profiles of primary biliary cirrhosis with a suboptimal biochemical response to ursodeoxycholic acid. (2011)
    11. Endoplasmic reticulum stress inhibition protects steatotic and non-steatotic livers in partial hepatectomy under ischemia-reperfusion. (2010)
    12. Toxicity of ethanol and acetaldehyde in hepatocytes treated with ursodeoxycholic or tauroursodeoxycholic acid. (2004)
    13. Effect of Withania somnifera Dunal in ethanol-induced anxiolysis and withdrawal anxiety in rats. (2008)
    14. Evaluation of Ashwagandha in alcohol withdrawal syndrome (2012)
    15. Effects of agmatine on ethanol withdrawal syndrome in rats. (2000)
    16. Agmatine, an endogenous imidazoline receptor ligand modulates ethanol anxiolysis and withdrawal anxiety in rats. (2010)
    17. Investigation on the mechanism involved in the effects of agmatine on ethanol-induced gastric mucosal injury in rats. (2000)
    18. Can nootropic drugs be effective against the impact of ethanol teratogenicity on cognitive performance? (2001)
    19. Chronic alcohol consumption induces lipofuscin deposition in the rat hippocampus. (1986)
    20. The effects of piracetam on lipofuscin of the rat cerebellar and hippocampal neurons after long-term alcohol treatment and withdrawal: a quantitative study. (1991)
    21. Effects of theanine on alcohol metabolism and hepatic toxicity. (2005)
    22. L-Theanine prevents alcoholic liver injury through enhancing the antioxidant capability of hepatocytes. (2012)
    Cognitive Health

    Why Do I Find Stimulants Calming?

    ADHD drugs enhance human focus by expanding the levels of neurotransmitters from the prefrontal cortex of the brain which coordinate attention and behavior: norepinephrine and dopamine. Psychostimulants like methylphenidate (Ritalin) amphetamines (Adderall) encourage focus and attention, both in ADHD-diagnosed and non-ADHD-diagnosed people[1], regardless of one’s initial intellectual baseline.

    Thus, giving stimulants to a person with a learning disability is like giving more time on a test: an advantage that might help anybody, but assists especially the ones in need (rather than fixing their brains).

    In spite of the positive evidence[2], stimulant users do report different subjective realities: while ones get anxiety, others remain calm and relaxed. From a psychological point of view, it is assumed that part of the problem in ADHD is that the patient’s environment doesn’t stimulate their brains enough as it does in people without the disorder. As a result, ADHD-sufferers feel constantly bored and hence look for various ways to stimulate themselves by rapidly shifting their attention to something new. Therefore, in theory, by providing the missing excitement to the brain, these medicines allow ADHD people calm down and stay focused in a single activity.

    Despite this highly plausible explanation, the neurological mechanism by which psychostimulants act as calming agents in humans with attention-deficit hyperactivity disorder or hyperkinetic disorder is currently unknown. Mice lacking the gene encoding the plasma membrane dopamine transporter (DAT) have elevated dopaminergic tone and are hyperactive[3], particularly when facing a novel environment. Furthermore, these mice are appreciably impaired in spatial cognitive function, and they display a decrease in locomotion in response to psychostimulants[4]. The behavioural resemblance between the DAT knockout mice and individuals with ADHD bring to mind that common mechanisms may underlie some of their conducts and responses to psychostimulants, and that dopamine D4 receptor gene might be abnormal on these individuals.[5]
    In contrast to the classical dopamine transporter (DAT)-dependent enhancement of the dopaminergic signal observed at concentrations of cocaine lower than 3 μM, the inhibitory effect of cocaine was found at concentrations higher than 3 μM. The paradoxical inhibitory effect of cocaine and methylphenidate was associated with a decrease in synapsin phosphorylation [] Interestingly, a cocaine-induced depression of DA release was only present in cocaine-insensitive animals (DAT-CI). Similar effects of cocaine were produced by methylphenidate in both wild-type and DAT-CI mice. On the other hand, nomifensine only enhanced the dopaminergic signal either in wild-type or in DAT-CI mice. Overall, these results indicate that cocaine and methylphenidate can increase or decrease DA neurotransmission by blocking reuptake and reducing the exocytotic release, respectively. The biphasic reshaping of DA neurotransmission could contribute to different behavioural effects of psychostimulants, including the calming ones, in attention deficit hyperactivity disorder.[6]
    Thus, SUNY’s researcher David Erlij and his group of researchers sustain to have recognized a network of nerve terminals where stimulation of dopamine D4 receptors exhaust motor activity.[7] This network seem to be localized deep in the brain, in the basal ganglia and the thalamus and its responses may explain the reduction in motor activity caused by psychostimulants. In this way, these results suggest that enhancing dopamine D4 transmission in the basal ganglia and the thalamus is likely part of the mechanism of the therapeutic effects of psychostimulants on ADHD patients.
    In conclusion, because of genetic anomalies, people with ADHD might encounter stimulants antagonistically. While further research is required to clear up the mechanisms behind the cognitive enhancement itself (why does it also works for the healthy ones then?) at a neurological level, taking into account the subjective outcome of the individual -calm vs. nervous- becomes significant when choosing a treatment.

    References   [ + ]

    Cognitive Health Nootropics

    Contraceptives: a Nootropic for Women?

    As you might already know, the nervous system uses neurotransmitters as its chemical signals; the endocrine system, hormones. In this way, the pituitary gland secretes factors into the blood that operate on the endocrine glands to either raise or drop hormone production, establishing a major communication system between the body and the brain. This process is known as a feedback loop, and it involves chemical transmission from the brain to the pituitary to an endocrine gland, and back to the brain. When this process is comprehended, it does not become a surprise that hormonal medication may rapidly change the structure and function of our brains.

    Birth control pills are on the market now for more than five decades, used by more than one hundred million of women who report high levels of contentment. However, the repercussions of the synthetic steroids contained in the pill on brain and cognition have scarcely been studied. Thus, 2014 has been a year in which neuroscientists just found the topic particularly appealing.[1] Here we summarize for you the latest findings, which might be of special interest among female nootropic users.

    According to a new UC Irvine research[2], women who take contraceptives may experience memory changes. These changes are not from a quantitative nature, but rather a qualitative one: women who are taking the pill were found to be more effective at recalling the gist of an emotional event, while the women who were not using it performed better at retaining details. This cognitive change makes perfect sense, argues researcher Nielsen, since contraceptives suppress sex hormones such as estrogen and progesterone to prevent pregnancy, and these hormones were previously linked to women’s strong “left brain”.

    Thus, birth control medication is nowadays presumed of being “masculinizing” brain patterns activation. In this trial[3], women’s number processing was analyzed and male-like brain activation patterns were recognized in women who were taking the pill, and a small but significant enhancement in processing social cues[4]. Nevertheless, the most consistent finding was the sustained improvement of verbal memory with birth control use, and a statistically significant enhancement in visuospatial ability as well. Interestingly, these cognitive changes seem to present a long-term nature, which results predict better cognitive outcomes later in life, even years after discontinued use. In this line of thought, this study[5] found that contraceptive ever users performed significantly better than never users in the domain of visuospatial ability, and speed & flexibility, with duration-dependent increases in performance, especially in ever users with ≥ 15 years of use.

    Furthermore, an apparent effect of oral contraceptives on emotion recognition was observed, strengthening the theory of brain masculinization. While it is well known in neuropsychology that females tend to score higher at recognizing faces and emotions; in this clinical trial[6], users of oral contraceptives detected significantly fewer facial expressions of sadness, anger and disgust than non-users.

    A few years back, a study discovered that users of oral contraceptives had larger volumes of grey matter[7] in certain areas of the brain. Thus, these past neuroatomical findings seem to correlate pretty well with the neurobehavioral changes recognized nowadays in the cited studies.

    In conclusion,  the mechanisms in which the brain responds to hormones point out that the organ is capable of responding effectively, in a flexible manner, to environmental signals from the endocrine system. This creates a strong demand for additional studies about how the pill affects indirectly & directly the nervous system from a molecular to a behavioural level.

    References   [ + ]

    Cognitive Health Memantine Nootropics Recovery

    Can Nootropics Help With Drug Abuse and Addiction?

    In recent years, evidence has compiled suggesting a common pathologic mechanism underlying addictive behaviours of several substances. Dysregulation of glutamatergic neurotransmission within the prefrontal cortex (PFC) and nucleus accumbens (NA) appears to predispose to a higher tendency towards drug-seeking behaviour.

    Thus far, this mechanism has been associated with the addiction potential of cocaine, heroin, nicotine, cannabis, & alcohol, with possible implications for other substances and even non-drug-related compulsive habits such as pathological gambling. Discovery of this shared pathology has led to the investigation of the potential application of existing agents, such as Memantine and n-acetylcysteine.

    Could nootropics targeting elements in this key glutamatergic circuit reduce symptoms and complications of substance use disorders?

    Glutamate Spillover

    «Glutamate spillover» refers to the pathologic cascade in brain chemistry that occurs with chronic abuse of certain substances that results in reinforcement of the behaviour[1].

    McClure EA, Gipson CD, Malcolm RJ, Kalivas PW, Gray KM. Potential role of N-acetylcysteine in the management of substance use disorders. CNS Drugs. 2014 02;28(2):95-106.

    Prolonged exposure to substances of abuse leads to several maladaptive changes in the glutamatergic PFC-NA pathway, specifically:

    • Downregulation of glial glutamate transporter-1 (GLT1) expression in the nucleus accumbens. By removing glutamate from the extrasynaptic space, GLT1 prevents inappropriate excitatory stimulation due to an accumulation of the excitatory neurotransmitter.
    • Decreased ability of presynaptic metabotropic glutamate receptor 2 (mGluR2) to inhibit glutamate release. In normal physiology, mGluR2 autoreceptors manage a feedback loop where increased extracellular glutamate levels trigger a reduction in the presynaptic release of glutamate. This auto-regulatory mechanism also serves to prevent an extracellular accumulation of glutamate.

    When glutamate spillover within the non-synaptic extracellular space does occur as a result of the combination of these processes, the following sequelae are may manifest:

    • Stimulation of postsynaptic mGluR5, AMPA and NMDA receptors.
    • Upregulation of AMPA and NMDA receptors (increased synaptic plasticity).
    • Stimulation of extrasynaptic glutamate receptors may also occur.

    Increased excitatory tone due to these two processes culminates in impaired inhibition with regard to drug-seeking behaviour as well as increased risk of relapse. Furthermore, persistently elevated glutamatergic tone may lead to neurotoxicity secondary to excessive Ca2+ ion influx. This pathology has also been associated in neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s disease.


    n-acetylcysteine (NAC) is a cysteine precursor that has a long history of use for indications ranging from bronchopulmonary disorders to paracetamol overdose. It produces many beneficial effects through a variety of mechanisms ranging from supporting antioxidant processes to suppressing over-reactive immune responses to inhibiting apoptosis. NAC’s glutamatergic modulation, however, is of key interest in managing substance use disorders[2].

    Brown RM, Kupchik YM, Kalivas PW. The story of glutamate in drug addiction & of n-acetylcysteine as a potential pharmacotherapy. JAMA Psychiatry. 2013 09;70(9):895-7.

    NAC is converted to L-cysteine in vivo, which enhances the activity of the cysteine/glutamate exchange transporter positioned near the pre-synaptic terminal. This increases the concentration of extracellular glutamate, resulting in increased tonic activation of pre-synaptic mGluR2 autoreceptors. This causes a subsequent decrease in glutamate release. NAC also increases expression of GLT1 and the cysteine/glutamate exchange transporter, promoting the removal of glutamate from the extrasynaptic space and ‹putting it back› in the pre-synaptic area. These effects in concert have been shown to mitigate the complications from glutamate spillover, & have been tested in several small trials with promising results.

    • When administered in patients with a history of cocaine addiction, NAC was shown to decrease self-reported cocaine use within the 28 days of treatment (mean 8.1 days out of 28 days before treatment & 1.1 days during treatment, p = 0.001)[3], desire to use cocaine (F = 5.07; df = 1,13; p = 0.05), & response to cocaine cues (F = 4.79, df = 1,13, p = 0.05)[4]. A magnetic resonance spectroscopy study confirmed elevated glutamate levels in the dorsal anterior cingulate cortex of cocaine users when compared against non-users (t(7) = 3.08, p = 0.02), and also showed a reduction 1 hour after a single 2.4 g dose of NAC[5].
    • With regard to cannabis, 2.4 g/day NAC decreased craving in one 4-week open label study of 24 patients[6]; in a double-blind placebo-controlled trial, subjects given 2.4 g/day NAC in addition to counselling were 2.4 times more likely to test negative on urinalysis (95%CI 1.1 to 5.2) but there was no difference in number of reported days of cannabis use[7].

    The dosage for managing consequences of substance use disorders in trials ranged from 1.2 to 2.4 g by mouth daily. Benefits on neurochemistry may occur with single doses although significant alterations in behaviour may take days to weeks. The pharmacodynamic effect also depends upon the history of substance use and individual predisposition to addictive behaviour.

    NAC is significantly protein-bound (80%). It is metabolised in the liver via non-CYP450 pathways. NAC and its metabolites are primarily eliminated in the urine, with a half-life of 5.6 hours in adults[8].

    NAC is generally well-tolerated. Nausea, vomiting, rash, and fever have been reported.


    Memantine (Namenda®) is an uncompetitive NMDA receptor antagonist most commonly used in the management of moderate-to-severe Alzheimer’s disease. In addition to its glutamatergic modulation, memantine also acts as an agonist at the D2 and nicotinic acetylcholinergic receptors (nAChR). Memantine binds and inhibits NMDA receptors with low-to-moderate affinity, most effectively in states of excess glutamatergic activity (such as in substance use disorder). By blocking NMDA receptors, memantine decreases glutamatergic tone[9].

    Clapp P, Bhave SV, Hoffman PL. How adaptation of the brain to alcohol leads to dependence: a pharmacological perspective. Alcohol Res Health. 2008;31(4):310-39.
    Neurochemical effects of alcohol intoxication in various contexts.

    Upregulation of NMDA receptors has been observed with chronic alcohol consumption. Abrupt discontinuation of alcohol removes GABAergic suppression, resulting in the characteristic acute sequelae of alcohol withdrawal (symptoms of excitotoxicity): seizures, hallucinations, tachycardia, and shock. By inhibiting these receptors, memantine may theoretically attenuate symptoms of alcohol withdrawal.

    • In one RCT of 18 moderate alcohol drinkers (10-30 drinks/week), 30 mg/day memantine significantly decreased alcohol craving before alcohol consumption in comparison to 15 mg/day and placebo[10]. Another placebo-controlled RCT with 10-40 mg/day showed no difference[11].
    • A subsequent study of 38 patients utilising 20-40 mg/day memantine showed dose-dependent reductions in cue-induced craving[12].
    • In another RCT of 127 male patients undergoing alcohol withdrawal, administration of 10 mg memantine three times a day decreased apparent withdrawal symptom severity, dysphoria, and need for diazepam[13].
    • Administration of 60 mg significantly alleviated subjectively-rated symptoms of naloxone-induced opioid withdrawal in 8 heroin-dependent patients[14].
    • In a study of 67 heroin-dependent subjects, 10-30 mg/day memantine significantly reduced heroin craving, depression, and state & trait anxiety compared to placebo after 3 weeks of use. A separate treatment arm using amitriptyline 75 mg/day achieved similar results but with a higher incidence of side effects and a higher dropout rate[15].
    • Clinical data on application in cocaine[16],[17] and nicotine abuse[18] is less promising.

    The dosage for mitigating substance use disorders in trials ranged from 5 to 60 mg, with 30 mg by mouth once daily showing the best effects for alcohol abuse and 30 to 60 mg by mouth once daily shown to be most effective in limited trials for opioid dependence. Safety is best characterised at doses up to 30 mg, as this dosage is used in Alzheimer’s disease. Memantine is typically initiated at 5 mg daily then titrated by 5 mg per week up to the goal dose (30 to 60 mg depending upon the indication).

    Memantine undergoes favourable non-hepatic metabolism; its metabolites are minimally active. Individuals with a history of kidney disease should consult a doctor or pharmacist before use, as memantine undergoes significant renal elimination (74% is excreted in the urine). The half-life of memantine ranges from 60-80 hours.

    The most common side effects noted at therapeutic doses higher than 7 mg/day are dizziness, headache, confusion, anxiety; increased blood pressure; cough; & constipation[19].


    • Disrupted regulation of glutamatergic pathways in the prefrontal cortex-nucleus accumbent pathway has been implicated as an underlying pathology among several substance use disorders, including cocaine, alcohol, and opioid dependence.
    • Therapies such as n-acetylcysteine (NAC) and memantine have demonstrated efficacy in attenuating the symptoms of some of these disorders in small trials.

    References   [ + ]

    1. McClure EA, Gipson CD, Malcolm RJ, Kalivas PW, Gray KM. Potential role of n-acetylcysteine in the management of substance use disorders. CNS Drugs. 2014 02;28(2):95-106.
    2. Brown RM, Kupchik YM, Kalivas PW. The story of glutamate in drug addiction & of n-acetylcysteine as a potential pharmacotherapy. JAMA Psychiatry. 2013 09;70(9):895-7.
    3. Mardikian PN, LaRowe SD, Hedden S, Kalivas PW, Malcolm RJ. An open-label trial of n-acetylcysteine for the treatment of cocaine dependence: a pilot study. Prog Neuropsychopharmacol Biol Psychiatry. 2007;31:389-94.
    4. LaRowe SD, Myrick H, Hedden S, Mardikian P, Saladin M, McRae A, et al. Is cocaine desire reduced by n-acetylcysteine? Am J Psychiatry. 2007;164:1115-7.
    5. Schmaal L, Veltman DJ, Nederveen A,van den Brink W, Goudriaan AE. n-acetylcysteine normalizes glutamate levels in cocaine- dependent patients: a randomized crossover magnetic resonance spectroscopy study. Neuropsychopharmacology. 2012;37:2143-52.
    6. Gray KM, Watson NL, Carpenter MJ, LaRowe SD. n-acetylcysteine (NAC) in young marijuana users: an open-label pilot study. Am J Addict. 2010;19:187-9.
    7. Gray KM, Carpenter MJ, Baker NL, DeSantis SM, Kryway E, Hartwell KJ, et al. A double-blind randomized controlled trial of n-acetylcysteine in cannabis-dependent adolescents. Am J Psychiatry. 2012;169:805-12.
    8. Medscape® 5.1.2, (electronic version). Reuters Health Information, New York, New York.
    9. Zdanys K, Tampi RR. A systematic review of off-label uses of memantine for psychiatric disorders. Prog Neuro-Psychopharmacol Biol Psychiatry. 2008 8/1;32(6):1362-74.
    10. Bisaga A, Evans SM. Acute effects of memantine in combination with alcohol in moderate drinkers. Psychopharmacology 2004;172:16–24.
    11. Evans SM, Levin FR, Brooks DJ, Garawi F. A pilot double-blind treatment trial of memantine for alcohol dependence. Alcoholism: Clin Exp Res 2007;31(5):775–82.
    12. Krupitsky EM, Neznanova O, Masalov D, Burakov AM, Didenko T, Romanova T, et al. Effect of memantine on cue-induced alcohol craving in recovering alcohol-dependent patients. Am J Psychiatry 2007a;164(3):519–23.
    13. Krupitsky EM, Rudenko AA, Burakov AM, Slavina TY, Grinenko AA, Pittman B, et al. Antiglutamatergic strategies for ethanol detoxification: comparison with placebo & diazepam. Alcoholism: Clin Exp Res 2007b;31(4):604–11.
    14. Bisaga A, Comer SD, Ward AS, Popik P, Kleber HD, Fischman MW. The NMDA antagonist memantine attenuates the expression of opioid physical dependence in humans. Psychopharmacology 2001(157):1–10.
    15. Krupitsky EM, Masalov DV, Burakov AM, Didenko TY, Romanova TN, Bespalov AY, et al. A pilot study of memantine effects on protracted withdrawal (syndrome of anhedonia) in heroin addicts. Addict Disord Treat 2002;1(4):143–6.
    16. Collins ED, Vosburg SK, Ward AS, Haney M, Foltin RW. Memantine increases cardiovascular but not behavioral effects of cocaine in methadone-maintained humans. Pharmacol Biochem Behav 2006;83(1):47–55.
    17. Collins ED, Ward AS, McDowell DM, Foltin RW, Fischman MW. The effects of memantine on the subjective, reinforcing, & cardiovascular effects of cocaine in humans. Behav Pharmacol 1998;9(7):587–98.
    18. Thuerauf N, Lunkenheimer J, Lunkenheimer B, Sperling W, Bleich S, Schlabeck M, et al. Memantine fails to facilitate partial cigarette deprivation in smokers—no role of memantine in the treatment of nicotine dependency? J Neural Transm 2007;114:351–7.
    19. Micromedex® 1.0 (Healthcare Series), (electronic version). Truven Health Analytics, Greenwood Village, Colorado, U.S.A. Available at:
    Biohacking Cognitive Health

    The Shocking Truth about tDCS and its Effects

    Developed as an answer to the problem of brain injuries and certain mental illnesses, tDCS has truly made an 180° turn, heading towards a place no one could have ever predicted. For decades, it has been used as a last resort to help patients suffering from mental illnesses. It has also proven to be a highly efficient method in helping stroke patients regain control over their mental functions, including walking and talking. But its recent application as a cognitive enhancer tool has created a stir in the field of neuroscience. In the attempt to pinpoint the exact effect tDCS has on our mental powers, we have to start from the beginning: the brain.

    Your Brain in the Fast Lane!

    Arguably the most complex organ in the human body, the brain has baffled scientists for centuries. Aside from a few things we have learned, like its size, shape and consistency, much about it is still unknown and undiscovered. The workings of the brain are still as much of a mystery as they were a hundred years ago. What we do know is that its founding blocks, impulse-conducted cells, make up only about 10% of it, and the glia (the glue that binds the neurons together) makes up as much as 90%. It all looks a lot like a highway, with millions and millions of lanes – pathways, each going in different directions. The pathways, or synapses, are the brain’s response to outer stimuli. These pathways get created whenever a person learns something new – a language, sport, how to tie a shoelace, etc. This superpower that our brain has of creating new synapses whenever we are exposed to new stimuli is something called plasticity, and it is directly proportional to the number of synapses the brain has. The more synapses there are, the higher the plasticity of the brain. How fast you learn a second language, master a new skill, solve a math problem, etc. depends not only on the number of neurons you have but also on your brain’s plasticity.

    Some simple math here: number of neurons + brain’s plasticity = degree of intelligence

    Studies have shown that the higher the number of neurons and synapses you have, the higher your IQ will be.
    And while the number of neurons is not something we can change (it’s written in our genetics), the plasticity of the brain is actually something we can control – through constant stimulation, or being exposed to new situations, problems, and difficulties. This often requires quite a bit of effort, and, what’s even more important: time.
    But, there seems to be a shortcut to the whole story, in the form of tDCS. An electrifying shortcut indeed!

    back to the future tdcs

    tDCS as an outer stimulus

    Studies conducted on tDCS have shown that stimulating a certain part of the brain through very low-level currents of up to 2mA, can cause an “excitability” of the brain in healthy individuals. This excitability of the brain is seen as a number of cortical changes that can last even after the stimulation is done. How long the changes last is directly linked to how long an individual has been exposed to a stimulus, the number of tDCS sessions, as well as the intensity of the stimulus.

    There are two types of changes that tDCS can cause: depolarization or hyperpolarization. Namely, when the anodal tDCS is conducted, which is positive stimulation, the resting membrane potential depolarizes. This, in turn, increases the neuronal excitability and allows for more spontaneous cell firing. On the other hand, when cathodal tDCS is performed, which is negative stimulation, the resting membrane potential gets hyper-polarized, thus decreasing spontaneous cell firing, a.k.a. neuron excitability.

    tDCS takes advantage of two concepts, LTP and LTD. Long-term potentiation (LTP) refers to the strengthening the connection between two neurons. LTD, or long-term depression, refers to the weakening of the same connection, thus causing the transmission between two neurons to be enhanced or hindered.


    One of the studies conducted on a group of 60 participants researched the effects of tDCS on creativity. Test participants were given a number of everyday objects, such as a baseball bat, for which they needed to come up with another use (for example, using that bat as a rolling pin). Thinking about unconventional uses of simple everyday objects requires “thinking outside the box”, which requires thinking about the size and material of the object as well as eliminating the usual things that the object is used for. This all required a high level of creativity.
    The participants were presented with 60 different objects, one every nine seconds. The researchers noted down the answers, the lack of answers, as well as the time it took the participants to come up with an answer.
    The study showed that the participants who received tDCS to their left prefrontal cortex didn’t know 8 answers on average. Those who received placebo or tDCS to their right prefrontal cortex missed about 15 answers out of 60. The group whose left prefrontal cortex was inhibited through tDCS was also faster in coming up with the answers – a whole one second quicker than the other two groups, which is a lot when it comes to psychological research, as the director of Penn’s Center for Cognitive Neuroscience and lead researcher Sharon Thompson-Schill concluded.

    Another study on the stimulation of the left dorsolateral prefrontal cortex in patients with depression showed that 48% of participants responded well to the treatment. They received tDCS every weekday, 30 treatments in total. A majority of them noted a substantial difference in their cognitive powers, i.e. better working memory and verbal fluency.

    A number of studies suggest that tDCS may improve learning, vigilance, intelligence, and working memory. However, many of these studies have been small and heterogeneous, and meta-analyses have failed to prove conclusive effects, and long-term risks have not been established. Consequently, the F.D.A. does not regulate the use of tDCS.

    tDCS-distributing machine

    brain_types_directcurrentA tDCS – DTC (direct-to-consumer) device consists of a main operating unit, one battery, and two electrodes: an anode and cathode with conductive sponges that can be applied to the head, held in place with a band. The principle behind it is to place the electrodes on brain regions of interest on the skull and let the low-level direct current induce intracerebral current flow which will either decrease or increase excitability of the neurons. The treatment lasts twenty to thirty minutes with the current level individually adjusted, but limited to a maximum of 2mA.

    The specific placement of the electrodes is called a montage based on the “10-20 International System of Electrode Placement”. This is a mapping point for the brain with coordinates that point to specific regions of the brain. Montages vary, depending on what effects the individual would like to have. For a comprehensive list of possible montages as well as links to the studies conducted for various conditions, like mood improvement, accelerated learning, pain management, working memory improvement, etc. please check this article, which also contains brain electrode placement maps for your reference.

    Should you or shouldn’t you?

    Though tDCS has taken the world of neuroscience by storm, it is not the only place of its application. Scientists are not the only ones intrigued by it. Army and military forces are currently conducting many experiments in the hope that one day they’ll be able to create a “super soldier” – one with the heightened concentration, improved cognitive powers, and enhanced working memory.
    So, the final question of whether to supercharge the brain or not is completely left to the reader, but with the benefits heavily outweighing the drawbacks, it seems only logical that there are many potential benefits to tDCS use.

    One thing is for certain, tDCS should not be dismissed so easily! It is definitely one form of treatment that will shape our future.