Mechanism of Action
Huperzine A is a sesquiterpene alkaloid isolated from the Chinese club moss Huperzia serrata that functions as a reversible, selective inhibitor of acetylcholinesterase (AChE). By inhibiting the enzymatic breakdown of acetylcholine in the synaptic cleft, huperzine A increases cholinergic neurotransmission in the central nervous system (Wang et al., 2006). For a comprehensive overview of huperzine A's cognitive effects, see our complete guide to huperzine A benefits.
The compound demonstrates selectivity for AChE over butyrylcholinesterase (BuChE), which may contribute to its tolerability profile compared to non-selective cholinesterase inhibitors. Additionally, preclinical studies suggest huperzine A may act as a weak antagonist at N-methyl-D-aspartate (NMDA) receptors (Wang et al., 2006). However, this effect has not been validated in human studies and should not be considered a rationale for combination protocols.
Understanding this mechanism is essential for evaluating combination protocols: any compound that similarly affects acetylcholine levels—whether through synthesis, release, or degradation—will interact with huperzine A's pharmacological effects. This forms the theoretical basis for both potentially beneficial combinations and contraindicated pairings, though clinical trial data supporting specific combination efficacy are lacking.
Pharmacokinetic Considerations for Combination Use
Rational combination therapy requires understanding huperzine A's pharmacokinetic profile. In a study of 12 healthy volunteers (age 20-25 years) administered a single 0.4 mg oral dose, huperzine A demonstrated the following parameters (Li et al., 2007):
| Parameter | Value | Clinical Significance |
|---|---|---|
| Elimination half-life (t½β) | 716.25 ± 130.18 min (~11.9 hours) | Extended action; accumulation with daily dosing |
| Time to peak (Tmax) | 58.33 ± 3.89 min | Rapid absorption; effects begin within 1 hour |
| Peak concentration (Cmax) | 2.59 ± 0.37 ng/mL | At 0.4 mg dose |
| Onset of detection | 5-10 minutes | Rapid appearance in plasma |
The extended half-life of approximately 12 hours has important implications for combination therapy. With once-daily dosing, steady-state conditions would result in significant accumulation. This prolonged activity window means that any compound administered concurrently will interact with sustained elevated acetylcholine levels for an extended period. For guidance on optimal dosing schedules, see our article on huperzine A dosage.
In elderly subjects, the area under the curve (AUC) has been reported to increase by approximately 75% compared to younger adults, suggesting reduced clearance in this population (Sheng et al., 2016). This age-related pharmacokinetic change warrants dose adjustment considerations in older individuals.
Contraindicated Combinations: Acetylcholinesterase Inhibitors
The concurrent use of huperzine A with prescription acetylcholinesterase inhibitors represents a strict contraindication due to pharmacodynamic redundancy and significantly increased risk of cholinergic adverse effects.
Contraindicated Drug Combinations
Concurrent use of huperzine A with the following medications may result in excessive cholinergic stimulation, potentially leading to bradycardia, respiratory depression, gastrointestinal distress, and in severe cases, cholinergic crisis. These combinations should be avoided.
| Medication | Mechanism | Risk |
|---|---|---|
| Donepezil (Aricept) | High-affinity AChE inhibition | Additive AChE inhibition; increased cholinergic adverse effects |
| Galantamine (Razadyne) | AChE inhibition + nicotinic receptor modulation | Dual mechanism increases interaction potential |
| Rivastigmine (Exelon) | AChE and BuChE inhibition | Broader cholinesterase inhibition amplifies effects |
| Physostigmine | Reversible AChE inhibition | Overlapping mechanism; avoid completely |
Population-based studies of cholinesterase inhibitors have demonstrated that these medications are associated with increased rates of hospitalization for bradycardia (Gill et al., 2009). A study in the French Pharmacovigilance Database found that 54.5% of drug-drug interactions involving cholinesterase inhibitors were with bradycardic medications, and cardiovascular adverse events (bradycardia, AV block, hypotension) accounted for the most serious outcomes, including fatalities (Tavassoli et al., 2007).
Antagonistic Interactions
Anticholinergic medications functionally oppose huperzine A's effects by blocking muscarinic acetylcholine receptors. While not inherently dangerous, these combinations render huperzine A therapeutically ineffective.
Antagonistic Medications
The following medications may reduce or negate the therapeutic effects of huperzine A through anticholinergic activity: diphenhydramine (Benadryl), first-generation antihistamines, tricyclic antidepressants, and certain antipsychotics with anticholinergic properties.
Choline Precursor Combinations
Combining huperzine A with choline precursors such as alpha-glycerylphosphorylcholine (alpha-GPC) or citicoline (CDP-choline) represents a mechanistically plausible approach: choline precursors increase acetylcholine synthesis while huperzine A decreases its degradation. However, no controlled human trials have specifically evaluated this combination in healthy adults, and claims of synergy remain theoretical rather than clinically validated.
Alpha-GPC
Alpha-GPC (choline alfoscerate) is a cholinergic compound that crosses the blood-brain barrier and serves as a precursor for acetylcholine synthesis. In clinical trials for Alzheimer's disease, alpha-GPC has been administered at doses of 400 mg three times daily (1,200 mg/day total) for periods up to 180 days (De Jesus Moreno, 2003).
The ASCOMALVA trial investigated the combination of alpha-GPC with the cholinesterase inhibitor donepezil in patients with Alzheimer's disease and found that combination therapy may delay cognitive decline compared to donepezil alone, without a significant increase in adverse events (Amenta et al., 2014). However, this trial used a prescription cholinesterase inhibitor rather than huperzine A, and results may not be directly generalizable.
Choline Precursor Considerations
When combining huperzine A with alpha-GPC or citicoline, conservative dosing of both compounds is advisable. Symptoms suggesting excessive cholinergic activity include: headache, nausea, gastrointestinal discomfort, muscle tension, and depressed mood. If these symptoms occur, the combination should be discontinued or doses reduced.
Practical Considerations
No controlled clinical trials have specifically evaluated the combination of huperzine A with choline precursors in healthy individuals. Anecdotal reports from the nootropic community suggest that many individuals tolerate low-dose huperzine A (50-100 mcg) without added choline, and that symptoms of cholinergic excess often emerge when combining higher doses of both compounds. These observations reflect community practice rather than clinical evidence and should be interpreted accordingly. For more information on combining huperzine A with other supplements, see our guide on brain fog supplement stacking.
Combination Comparison Table
| Combination | Theoretical Rationale | Risk Considerations | Practical Guidance |
|---|---|---|---|
| HupA + Alpha-GPC | ↑ ACh synthesis + ↓ ACh degradation | Cholinergic overload symptoms | Halve choline dose (e.g., 250 mg GPC + 100-200 mcg HupA) |
| HupA + CDP-Choline | Nucleotide + choline support | Similar to Alpha-GPC | Monitor for headache, insomnia |
| Standalone HupA | Pure AChE inhibition | Headaches if dietary choline insufficient | Ensure adequate dietary choline (eggs, lecithin) |
| HupA + ALCAR | ACh preservation + mitochondrial support | Additive cholinergic effects | Limited trial data available (see below) |
Evidence from Combination Trials
Two randomized controlled trials have evaluated huperzine A as part of multi-compound nootropic formulations in healthy adults:
Wesnes and Reynolds (2019) conducted a 28-day, double-blind, placebo-controlled trial (n=90) evaluating a combination of acetyl-L-carnitine (1,500 mg), vinpocetine (15 mg), and huperzine A (150 mcg). The combination significantly improved a validated global score derived from six tests of working and episodic memory, with effect sizes comparable to approved Alzheimer's medications. No serious adverse events were reported.
Stough et al. (2011) evaluated a five-compound combination (huperzine A, vinpocetine, acetyl-L-carnitine, Rhodiola rosea, and alpha-lipoic acid) in 60 healthy adults over 4 weeks. The treatment group showed significant improvement on Raven's Advanced Progressive Matrices compared to placebo (p = 0.009).
While these trials provide preliminary evidence that huperzine A-containing combinations may improve cognitive measures in healthy adults, important limitations apply: both studies used multi-compound formulations, making it impossible to attribute effects to huperzine A specifically; sample sizes were modest; and neither study evaluated long-term safety or the specific combination of huperzine A with choline precursors alone.
Phosphatidylserine and Benfotiamine Considerations
Some combination protocols pair huperzine A with phosphatidylserine (PS) for membrane support and benfotiamine (fat-soluble vitamin B1) for mitochondrial energy metabolism—a framework sometimes described as addressing "signal, structure, and energy" pathways. This rationale is mechanistically plausible: huperzine A supports cholinergic signaling, PS contributes to neuronal membrane integrity, and benfotiamine supports thiamine-dependent enzymes in energy metabolism. However, no clinical trials have specifically evaluated this three-component combination. PS and benfotiamine have independent evidence for cognitive support in certain populations, but their interaction with huperzine A remains unstudied. For more on cycling strategies that may reduce accumulation risk, see our article on cycling huperzine A.
Recommended Stacking Protocols
This section separates protocols with clinical trial evidence from those derived from community practice and mechanistic reasoning. Users seeking maximum defensibility should stick to trial-tested protocols; those comfortable with informed self-experimentation may consider community-derived options with appropriate caution.
Trial-Tested Protocols
The following combinations have been evaluated in randomized, placebo-controlled trials in healthy adults.
Evidence Level: RCT Data Available
These exact formulations showed statistically significant cognitive improvements vs placebo. Doses and durations match trial parameters.
Wesnes Protocol (2019)
A 28-day, double-blind, placebo-controlled trial (n=90 healthy adults, mean age 48.3 years) demonstrated significant improvement on a validated global memory score derived from six tests of working and episodic memory. Effect sizes were comparable to approved Alzheimer's medications (Wesnes & Reynolds, 2019).
| Compound | Daily Dose | Mechanism |
|---|---|---|
| Huperzine A | 150 mcg | AChE inhibition |
| Acetyl-L-Carnitine (ALCAR) | 1,500 mg | Mitochondrial support; acetyl group donor |
| Vinpocetine | 15 mg | Cerebral blood flow; PDE1 inhibition |
Trial duration: 28 days continuous dosing (no cycling used in trial)
Adverse events: No serious adverse events reported
Limitation: Single trial; effects of individual components cannot be isolated
Note: Vinpocetine has regulatory restrictions in some countries (prescription-only in parts of Europe; banned in Australia)
Stough Protocol (2011)
A 4-week, double-blind, placebo-controlled trial (n=60 healthy adults, mean age 45.4 years) showed significant improvement on Raven's Advanced Progressive Matrices, a measure of fluid intelligence (p=0.009, partial η²=0.113) (Stough et al., 2011).
| Compound | Daily Dose | Mechanism |
|---|---|---|
| Huperzine A | Not specified in abstract | AChE inhibition |
| Acetyl-L-Carnitine | Not specified | Mitochondrial support |
| Vinpocetine | Not specified | Cerebral blood flow |
| Rhodiola rosea | Not specified | Adaptogen; fatigue reduction |
| Alpha-lipoic acid | Not specified | Antioxidant; mitochondrial cofactor |
Trial duration: 4 weeks continuous dosing
Limitation: Proprietary formula (Ceretrophin™); exact doses not disclosed in published abstract; 5-compound stack makes attribution impossible
Note: If using this framework, the Wesnes Protocol provides more specific dosing guidance for the overlapping components
Community-Derived Protocols
Evidence Level: No Clinical Trial Data
The following protocols are derived from pharmacological reasoning and nootropic community practice. They have NOT been evaluated in controlled trials. Efficacy is unproven and safety in combination is unstudied. Use at your own risk with appropriate monitoring.
Foundational Stack (Beginner)
Rationale: Conservative starting point to assess individual response before adding complexity. Based on principle of starting low and titrating.
| Compound | Dose | Timing | Reasoning |
|---|---|---|---|
| Huperzine A | 50-100 mcg | Morning with food | Sub-clinical-trial dose; assess tolerance |
| Dietary choline | 2-3 eggs or equivalent | With breakfast | Substrate support without supplemental load |
Cycling: 5 days on, 2 days off (based on 12-hour half-life accumulation logic, not trial data)
Evidence: None for this combination. Huperzine A monotherapy has trial data in AD patients but not healthy adults at this dose.
Cholinergic Enhancement Stack
Rationale: Combines AChE inhibition with choline precursor and complementary memory-supporting herb. Common in nootropic community.
| Compound | Dose | Timing | Reasoning |
|---|---|---|---|
| Huperzine A | 100-200 mcg | Morning | AChE inhibition |
| Alpha-GPC | 300 mg | Morning | Choline precursor; crosses BBB |
| Bacopa monnieri | 300 mg (50% bacosides) | With food | Independent memory evidence; non-cholinergic |
Evidence: None for this combination. Alpha-GPC has been studied with donepezil (ASCOMALVA trial) but not huperzine A. Bacopa has independent RCT evidence for memory but not in combination with AChE inhibitors.
Signal-Structure-Energy Stack
Rationale: Addresses three theoretical pathways—cholinergic signaling, membrane integrity, and mitochondrial energy. Components have independent evidence but combination is unstudied.
| Compound | Dose | Pathway | Independent Evidence |
|---|---|---|---|
| Huperzine A | 100-200 mcg | Signal | AD trials only |
| Phosphatidylserine | 100-300 mg | Structure | Meta-analysis positive for memory in elderly (Kang et al., 2022) |
| Benfotiamine | 150-300 mg | Energy | Diabetic neuropathy trials; no cognitive trials in healthy adults |
Evidence: None for this combination. PS has systematic review support for age-related memory decline. Benfotiamine lacks cognitive trials. Interaction effects unknown.
Focus/Study Stack
Rationale: Acute cognitive enhancement pairing cholinergic boost with calming agent to reduce overstimulation. Popular in student/productivity communities.
| Compound | Dose | Timing | Reasoning |
|---|---|---|---|
| Huperzine A | 50-100 mcg | 60 min before task | Tmax ~60 min per Li et al. PK data |
| L-Theanine | 100-200 mg | With huperzine A | Alpha wave promotion; anxiety reduction |
| Caffeine (optional) | 50-100 mg | With stack | Alertness; theanine-caffeine combo has RCT support |
Evidence: None for huperzine A + theanine. Caffeine + theanine combination has independent RCT support for attention. Adding huperzine A to this is community practice, not science.
Stacking Principles Summary
| Principle | Application | Evidence Basis |
|---|---|---|
| Start low | Begin with 50 mcg huperzine A | General pharmacology principle |
| Cycle huperzine A | 5:2 or every-other-day | Extrapolated from 12-hour t½ (Li et al., 2007); no cycling trials exist |
| Monitor cholinergic load | Watch for headache, nausea, mood changes | Known AChE inhibitor side effect profile |
| One variable at a time | Add compounds with 1-2 week gaps | Basic experimental design principle |
| Respect contraindications | Never combine with Rx AChE inhibitors | Pharmacovigilance data (Tavassoli et al., 2007) |
Adverse Effects by System
In a systematic review of 20 randomized controlled trials (n=1,823), Yang et al. (2013) reported that no trials documented severe adverse events attributable to huperzine A. However, the methodological quality of included trials was assessed as having high risk of bias, and adverse event reporting was incomplete in many studies.
In the Phase II trial conducted by the Alzheimer's Disease Cooperative Study (n=210), huperzine A was generally well-tolerated at doses up to 400 mcg twice daily for 24 weeks. Notably, 57% of enrolled subjects had previously discontinued other cholinesterase inhibitors due to adverse events, most commonly nausea (Rafii et al., 2011).
Gastrointestinal Effects (Mild)
Gastrointestinal symptoms represent the most commonly reported adverse effects of cholinergic compounds. In clinical trials of huperzine A and related cholinesterase inhibitors, nausea, diarrhea, and abdominal discomfort have been reported as mild and transient in most cases (Yang et al., 2013; Rafii et al., 2011).
Central Nervous System Effects (Mild)
Vivid dreams and sleep disturbances have been associated with huperzine A use, likely related to increased cholinergic activity during sleep. Headache has also been reported. These effects are typically self-limiting (Rafii et al., 2011). For detailed information on this topic, see our article on huperzine A and lucid dreaming.
Cardiovascular Effects (Moderate)
Cholinesterase inhibitors as a class may exert vagotonic effects on the sinoatrial and atrioventricular nodes, potentially resulting in bradycardia or heart block. While this has been more extensively documented with prescription cholinesterase inhibitors, it represents a theoretical concern with huperzine A, particularly at higher doses or in combination with other bradycardic agents. Individuals with pre-existing cardiac conduction abnormalities should exercise caution. Intermittent dosing may reduce accumulation risk—see our guide on cycling huperzine A (Park-Wyllie et al., 2009).
Cholinergic Crisis (Serious - Rare)
Excessive cholinergic stimulation can manifest as the "SLUDGE" syndrome: Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress, and Emesis. Additional signs include muscle fasciculations, weakness, and respiratory compromise. This represents a medical emergency requiring immediate discontinuation and potentially medical intervention. While no cases have been reported in clinical trials of huperzine A at therapeutic doses, risk increases with supratherapeutic dosing or contraindicated combinations. For detailed information on recognizing and managing adverse effects, see our article on huperzine A side effects.
Dosing and Cycling Protocols
Clinical trials have employed varying doses of huperzine A, with 200-400 mcg twice daily being common in Alzheimer's disease studies (Rafii et al., 2011). For healthy individuals seeking cognitive support, substantially lower doses (50-200 mcg) are typically discussed, though controlled efficacy data in this population are lacking.
Given the extended half-life of approximately 12 hours, continuous daily dosing leads to accumulation. Intermittent dosing schedules may help minimize tolerance development and reduce steady-state accumulation. For detailed guidance on cycling schedules, see our article on cycling huperzine A.
Proposed Cycling Approaches
While no controlled trials have compared different cycling regimens, several approaches are commonly discussed:
- 5:2 Protocol: Five consecutive days of use followed by two days off
- Every-other-day dosing: Allows for more complete clearance between doses
- Weekday-only dosing: Use on workdays, rest on weekends
- Cyclical blocks: 3-4 weeks on, 1 week off
These approaches have not been validated in controlled studies, and optimal cycling protocols remain undetermined.
Limitations of Current Evidence
Critical Appraisal
The available evidence on huperzine A combinations and safety should be interpreted with significant caution. The 2013 systematic review by Yang et al. concluded that the methodological quality of most included trials had a high risk of bias, and findings regarding both efficacy and safety require confirmation in better-designed studies.
Key limitations of the current evidence base include:
- Incomplete adverse event reporting: Many trials did not systematically collect or report adverse event data
- Short trial duration: Most trials lasted 8-16 weeks; long-term safety data are limited
- Sample sizes: Individual trials were generally small, limiting power to detect uncommon adverse effects
- Study quality: High risk of bias in most trials due to inadequate randomization, blinding, and allocation concealment
- Population studied: Most data come from older adults with cognitive impairment; generalizability to healthy young adults is uncertain
- Product variability: As a dietary supplement, quality control and standardization vary between manufacturers
- Combination data: No controlled trials have specifically evaluated huperzine A in combination with choline precursors, racetams, noopept, or other nootropic compounds in any population
Clinical Evidence vs. Community Practice
It is essential to distinguish between evidence derived from controlled clinical trials and practices that have emerged within the nootropic community. Many combination protocols discussed online are based on theoretical mechanisms, individual experimentation, and anecdotal reports rather than systematic scientific evaluation. While such practices may inform hypothesis generation, they do not constitute clinical evidence of safety or efficacy. Readers should interpret claims about "synergistic" effects or optimal stacking protocols with appropriate skepticism when controlled trial data are absent.
For the full context of huperzine A's benefits and limitations, see our comprehensive huperzine A guide.
Frequently Asked Questions
The only huperzine A stacks with RCT evidence are the Wesnes Protocol (huperzine A 150 mcg + ALCAR 1,500 mg + vinpocetine 15 mg) and Stough Protocol (5-compound formula). Both showed significant cognitive improvement in healthy adults. Popular community stacks like huperzine A + alpha-GPC or huperzine A + L-theanine have no trial data—they're based on theoretical mechanisms, not proven efficacy.
Due to the extended elimination half-life of approximately 12 hours (Li et al., 2007), daily dosing without cycling may lead to systemic accumulation. Clinical trials have primarily assessed durations of 8-16 weeks. While no severe long-term adverse events have been reported in available studies, long-term safety data are limited. Intermittent dosing protocols may help minimize potential tolerance development, though optimal cycling regimens have not been established in controlled trials.
Both compounds affect cholinergic neurotransmission: caffeine has been shown to increase acetylcholine release, while huperzine A inhibits its breakdown. This combination has not been systematically studied in controlled trials. Given the theoretical potential for additive cholinergic effects, individuals considering this combination should use conservative doses of huperzine A and monitor for signs of cholinergic excess such as headache, nausea, or muscle tension.
Clinical trial data predominantly come from older adults with Alzheimer's disease or mild cognitive impairment. The systematic review by Yang et al. (2013) encompassing 20 RCTs (n=1,823) showed cognitive benefits in this population. Pharmacokinetic data suggest that clearance may be reduced in elderly individuals, with AUC increased by approximately 75% (Sheng et al., 2016). Efficacy in healthy young adults has not been established in controlled trials, and doses used in cognitive impairment studies (400 mcg twice daily) may not be appropriate for healthy individuals.
Early signs of cholinergic excess may include headache, nausea, diarrhea, excessive salivation, muscle tension (particularly jaw clenching), and depressed mood. More significant symptoms include muscle fasciculations, bradycardia, and respiratory symptoms. If any of these occur, the compound should be discontinued and medical attention sought if symptoms are severe or persistent. For a detailed discussion of adverse effects, see our article on huperzine A side effects.
Racetams (such as piracetam, aniracetam, or oxiracetam) are a class of compounds that modulate neurotransmission through mechanisms that may include effects on acetylcholine. No controlled clinical trials have evaluated combinations of huperzine A with any racetam compound in humans. The practice of combining these substances is based entirely on theoretical mechanisms and anecdotal reports from the nootropic community, not clinical evidence. Theoretically, racetams that increase acetylcholine release or receptor sensitivity could have additive effects with huperzine A's mechanism, potentially increasing both benefits and risks. Individuals considering such combinations should recognize that safety and efficacy are unestablished, start with low doses of each compound, and monitor carefully for adverse effects.
Noopept (N-phenylacetyl-L-prolylglycine ethyl ester) and similar synthetic nootropics have proposed mechanisms involving cholinergic modulation, among other pathways. No clinical trials have examined the safety or efficacy of combining huperzine A with noopept or comparable compounds. Such combinations are practiced within the nootropic community based on theoretical rationales and personal experimentation, but this should not be conflated with clinical evidence. The absence of safety data means that potential interactions, including additive or unexpected effects, remain unknown.
Given the elimination half-life of approximately 12 hours, approximately 5-6 half-lives (60-72 hours, or roughly 3 days) would be required for near-complete elimination. However, this question should be addressed with a prescribing physician who can consider individual factors and provide appropriate medical guidance.
References
- Amenta F, Carotenuto A, Fasanaro AM, et al. The ASCOMALVA (Association between the Cholinesterase Inhibitor Donepezil and the Cholinergic Precursor Choline Alphoscerate in Alzheimer's Disease) Trial: interim results after two years of treatment. J Alzheimers Dis. 2014;42 Suppl 3:S281-288. PubMed
- De Jesus Moreno M. Cognitive improvement in mild to moderate Alzheimer's dementia after treatment with the acetylcholine precursor choline alfoscerate: A multicenter, double-blind, randomized, placebo-controlled trial. Clin Ther. 2003;25(1):178-193. PubMed
- Gill SS, Anderson GM, Fischer HD, et al. Syncope and its consequences in patients with dementia receiving cholinesterase inhibitors: a population-based cohort study. Arch Intern Med. 2009;169(9):867-873. PubMed
- Li YX, Zhang RQ, Li CR, Jiang XH. Pharmacokinetics of huperzine A following oral administration to human volunteers. Eur J Drug Metab Pharmacokinet. 2007;32(3):183-187. PubMed
- Park-Wyllie LY, Mamdani MM, Li P, et al. Cholinesterase inhibitors and hospitalization for bradycardia: a population-based study. PLoS Med. 2009;6(9):e1000157. PMC2745757
- Rafii MS, Walsh S, Little JT, et al. A phase II trial of huperzine A in mild to moderate Alzheimer disease. Neurology. 2011;76(16):1389-1394. PMC3269774
- Tavassoli N, Sommet A, Lapeyre-Mestre M, et al. Drug interactions with cholinesterase inhibitors: an analysis of the French Pharmacovigilance Database and a comparison of two national drug formularies (Vidal, British National Formulary). Drug Saf. 2007;30(11):1063-1071. PubMed
- Wang R, Yan H, Tang XC. Progress in studies of huperzine A, a natural cholinesterase inhibitor from Chinese herbal medicine. Acta Pharmacol Sin. 2006;27(1):1-26. PubMed
- Yang G, Wang Y, Tian J, Liu JP. Huperzine A for Alzheimer's disease: A systematic review and meta-analysis of randomized clinical trials. PLoS One. 2013;8(9):e74916. PMC3781107
- Wesnes KA, Reynolds J. The effects on the cognitive function of healthy volunteers of a combination of acetyl-L-carnitine, vinpocetine and huperzine A administered over 28 days. Int J Neurol Neurother. 2019;6(2):089. ClinMedJournals
- Stough C, Downey LA, Lloyd J, et al. Improving general intelligence with a nutrient-based pharmacological intervention. Intelligence. 2011;39(2-3):100-107. ScienceDirect
- Kang EY, Cui F, Kim HK, et al. Effect of phosphatidylserine on cognitive function in the elderly: A systematic review and meta-analysis. Korean J Food Sci Technol. 2022;54(1):52-58. KoreaScience
