Memantine Noopept Nootropics Phenylpiracetam Piracetam Pramiracetam

Best Nootropics for ADD & ADHD: 10 Alternatives to Adderall®

WARNING: The substances mentioned in this article are not approved by the FDA, we only list them for information purposes. They should NOT, and I repeat NOT, be used as replacements for a true and tested ADHD treatment. Our website and all the websites listed in this article are not responsible for errors, omissions, or for any outcomes related to the use of the contents of this article.

Attention Deficit Disorder with or without hyperactivity (ADD, ADHD) is one of the most commonly diagnosed disorders in children between 6 and 12 years of age. It is especially problematic for those attending school, as it adds an extra barrier that both students and teachers must overcome. There are various popular forms of medication in the amphetamine class used to treat these attention disorders. These medications are typically quite effective in alleviating attention deficits, but they carry with them the possibility of addiction and dependence.[1]

Attention Deficit Disorders

Two of the most commonly used drugs for the treatment of ADHD in children and adolescents are Adderall (amphetamine/dextroamphetamine) and Ritalin (methylphenidate).[2] Many people seek alternatives to classical stimulants because they know of potential adverse effects or want to avoid using potent phenethylamine derivatives on their own children or themselves. For this reason, we will investigate the potential benefits of nootropics in the treatment of attention disorders.

The most common nootropics that people use as alternatives to amphetamines are racetam drugs, modafinil and noopept. These nootropics have been demonstrated to have positive effects on cognition, but it is necessary to personalize treatment for each individual, evaluating if the course of treatment is actually working for them. It should be noted that the onset and duration of action of nootropics (as well as their effectiveness) can vary greatly. It would be wise to keep a journal where you take notes about the dosage and administration of nootropics you are using. Many nootropic drugs can take more than a week to establish their full effect, and dosages may need to be adjusted to achieve maximum effect.

Not all nootropics will ultimately be beneficial to those who suffer from attention deficits. However, many nootropics are well-known for their ability to improve cognition, motivation, and concentration.[3] Always consult your doctor before making adjustments to medication. Because most cognitive supplements and nootropics are stable and safe to use indefinitely, individuals who fear health risks or addiction to amphetamines may want to consider using nootropics as an alternative form of treatment.

Top 10 Nootropics for ADD & ADHD

These are the best nootropics for Attention Deficit Disorder with or without Hyperactivity, according to scientific studies and our anecdotal experience. As we frequently say in the nootropics community, your mileage may vary.


piracetam nootropic adhdPiracetam is considered by many to be the father of all nootropic drugs. It has a history of being used to treat dementia, Alzheimer’s Disease and other cognitive diseases that come with old age. Most research conducted on piracetam has come to the consensus that it does not have much effect on individuals who are not experiencing cognitive decline. For this reason, piracetam does not seem like an ideal alternative treatment for attention deficits. However, piracetam is extremely safe to take, and supplementation by anyone will help prevent cognitive decline before it even starts. Thus, it might be worthwhile to take piracetam alongside another medication on this list. One small study mentions a combination of atomoxetine (an ADHD medication) and Piracetam.[4][5]

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Noopept11Noopept is a favorite among nootropic users due to its ability to improve cognition and increase the ability to focus. Although it is not technically a racetam, due to the fact that it does not contain a pyrrolidone nucleus, it is still quite similar in structure and effects. Noopept is commonly touted as having an effective dose 1000 times smaller than that or piracetam.[6] There is not very much information out there about noopept as a treatment for ADD, but experts at the Second International Congress on ADHD noted that noopept may be a very good alternative medication for attention deficits.[7] Many anecdotal reports from users have found that noopept is helpful for maintaining focus and concentration for extended periods of time.

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Phenylpiracetam nootropic for adhdPhenylpiracetam is a derivative of piracetam that has an additional phenyl group. It is noticeably more stimulating than piracetam, as well as more potent. An 800 mg dose of piracetam is comparable to about 100 mg of phenylpiracetam. It has been found to be effective at improving cognition and produces stimulation that may translate to improved focus.[8][9] One drawback of phenylpiracetam is that it cannot be used indefinitely, as tolerance develops relatively quickly. However, this might make it useful to cycle with another nootropic compound, or to use a few times a week alongside something else like noopept.

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pramistar-nootropic-pramiracetamPramiracetam is another derivative of piracetam. It is not as well researched as some of the more popular racetams, but it has a lot of potential as a cognitive enhancer. While there is no research that specifically addresses the issue of attention in the traditional sense, pramiracetam demonstrated and ability to help reverse scopolamine-induced attention deficits in humans[10], and anecdotal experiences on the web show that it’s effective in young subjects with ADD, but not in those with normal “baseline” performance. Even though pramiracetam still needs to see more research before anything definitive can be said, the fact that it is considered safe to use opens up the possibility of personal experimentation.

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Memantine NootropicMemantine is another drug commonly used to treat cognitive decline, such as moderate and severe Alzheimer’s Disease. Memantine works on the glutamatergic system as an antagonist to NMDA receptors, which works to combat excitotoxicity. One of the benefits of Memantine is that it avoid the development of tolerance to a number of substances, including stimulants, caffeine, cannabis, alcohol and so on. It is therefore frequently combined with stimulants to reduce their neurotoxic effects as well as reducing tolerance to the positive effects of Adderall and Ritalin. Some research has been done on memantine’s possible effectiveness in treating ADHD (by itself, not in combination). One study found that memantine was fairly beneficial for alleviating symptoms of ADHD, but concluded that there is not enough evidence to draw any real conclusions.[11] Because of this, memantine could be a good choice to use in low doses alongside another substance on this. It must be noted that memantine acts as a dissociative at supratherapeutic doses, so proceed with caution.

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provigil-modafinilModafinil is a wakefulness-promoting (eugeroic) drug that is classified in many places as a prescription medication. Armodafinil, a closely related drug, consists of only the active (−)-(R)-enantiomer of modafinil, meaning it is theoretically more potent. Because of this, both drugs work in a similar fashion. Modafinil has shown a good amount of promise as an alternative treatment of ADD/ADHD. One study conducted on children found that 48% of the participants felt a significant improvement in attentive skills while on modafinil.[12] Multiple other studies have found that modafinil provides moderate increases in cognition, memory, and motivation.[13] Although modafinil’s mechanism works through modulation of dopamine, it does not seem to carry an addiction potential to the same degree as amphetamines.

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selegiline adhd nootropicSelegiline (L-deprenyl) is a substituted phenethylamine drug commonly used to treat Parkinson’s disease and dementia. It has also seen some use as an alternative treatment for depression. There has not been a significant amount of research done on its efficacy in treating ADHD, but one study done on a small group of 28 children with ADHD studied the treatment effects of selegiline in comparison to methylphenidate. The children treated with selegiline displayed fewer symptoms of ADHD than those treated with methylphenidate while also displaying fewer side effects.[14] This research is preliminary, but it demonstrates the selegiline displays promise as an ADHD treatment.

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These supplements are not strong enough to treat ADD/ADHD on their own, but they can potentiate and work synergistically with the nootropic drugs mentioned above.


acetylcholineCholine is an essential nutrient and precursor to acetylcholine that can be obtained in various ways in different foods. However, the easiest way to consume ideal amounts of choline is through a supplement. CDP-Choline and Alpha GPC are generally considered to be the two most effective sources of choline for nootropic use. Because racetam drugs and noopept work through modulation of acetylcholine, taking them alongside a choline source can make them more effective.

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L-Tyrosine is an amino acid that acts as a precursor to the neurotransmitters noradrenaline and dopamine. One study found that supplementation of both Tyrosine and 5-HTP (a serotonin precursor) helped improve ADHD symptoms in 77% of the participants.[15] Taking these supplements can help improve attention deficits by increasing levels of neurotransmitters that play a significant role in attention. Tyrosine should be taken on an empty stomach to prevent it from competing for absorption with other amino acids found in food.

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uridineUridine is a nucleotide base that has been found to improve memory, attentiveness, cognition, and learning.[16] The majority of uridine’s cognitive benefits appear to occur with its supplementation alongside other nootropics, such as racetams and noopept. It is considered a safe substance to combine with other nootropics and medications. Although uridine can be found naturally in liver, fish, and beer, it is most commonly supplemented through a uridine compound like uridine monophosphate or triacetyluridine.

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There are many nootropics, pharmaceuticals, and supplements that show significant promise for treating attention deficits. These substances are definitely worth looking into for those who are wary of amphetamines and the side effects and addictive potential they entail. In the end, the efficacy of each of these substances will vary between each individual and cautious experimentation will maximize the potential of finding an effective treatment regimen.

References   [ + ]

1. What is Attention Deficit Hyperactivity Disorder (ADHD, ADD)?
2. Methylphenidate
3. Gouliaev, A. H., & Senning, A. (1994). Piracetam and other structurally related nootropics. Brain Research Reviews, 19(2), 180–222.
4. Zavadenko, N. N., & Suvorinova, N. I. (2008). [Atomoxetine and piracetam in the treatment of attention deficit hyperactivity disorder in children]. Zhurnal Nevrologii I Psikhiatrii Imeni S.S. Korsakova / Ministerstvo Zdravookhraneniia I Meditsinskoi Promyshlennosti Rossiiskoi Federatsii, Vserossiiskoe Obshchestvo Nevrologov [i] Vserossiiskoe Obshchestvo Psikhiatrov, 108(7), 43–47.
5. Baumgaertel, a. (1999). Alternative and controversial treatments for attention-deficit/hyperactivity disorder. Pediatric Clinics of North America, 46(5), 977–992.
6. [The original novel nootropic and neuroprotective agent noopept].
7. Thome, J., & Reddy, D. P. (2009). The current status of research into Attention Deficit Hyperactivity Disorder: Proceedings of the 2nd International Congress on ADHD: From Childhood to Adult Disease. Attention Deficit and Hyperactivity Disorders, 1(2), 165–74.
8. Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders.
9. Investigation into stereoselective pharmacological activity of phenotropil.
10. Pramiracetam effects on scopolamine-induced amnesia in healthy volunteers.
11. Memantine: a review of possible uses in child and adolescent psychiatry.
12. Efficacy and safety of modafinil film-coated tablets in children and adolescents with attention-deficit/hyperactivity disorder: results of a randomized, double-blind, placebo-controlled, flexible-dose study.
13. Modafinil
14. Selegiline in the treatment of attention deficit hyperactivity disorder in children: a double blind and randomized trial
15. Treatment of attention deficit hyperactivity disorder with monoamine amino acid precursors and organic cation transporter assay interpretation
16. Cognitex supplementation in elderly adults with memory complaints: an uncontrolled open label trial.
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: