Neurocognitive · synthetic proline-glycine dipeptide nootropic · investigational research only · oral study-reference only · injection blocked
NoopeptGVS-111 · Omberacetam — a proline-glycine dipeptide nootropic and prodrug of cycloprolylglycine, not a classical injectable peptide
Noopept is a synthetic nootropic compound related to proline-glycine peptide chemistry, studied mainly for memory, cognition, and neuroprotection. Some clinical research used it in people with mild cognitive impairment related to stroke, cerebrovascular disease, or traumatic brain injury, but the evidence isn't strong enough for Intrasigna to publish a public self-use protocol. In the U.S. it is an unapproved new drug, not a lawful dietary-supplement ingredient, so this page is a study reference — not a recommendation.
Noopept (GVS-111, omberacetam; N-phenylacetyl-L-prolylglycine ethyl ester) is a synthetic dipeptide-derived nootropic investigated for nootropic, anxiolytic, neuroprotective, antioxidant, and anti-inflammatory effects. Mechanistic and clinical literature links it to NGF/BDNF expression, amyloid-β toxicity reduction, calcium/glutamate neurotoxicity modulation, and cognitive, anxiolytic, and vegetostabilizing effects in cerebrovascular/post-traumatic mild cognitive impairment. Dosing output is restricted to study-arm reference with provider review.
Noopept is a prodrug of the endogenous neuropeptide cycloprolylglycine (cPG), designed at the Zakusov Institute as a dipeptide analog of piracetam. Its mechanism is multi-component: positive allosteric modulation of AMPA-type and modulation of NMDA glutamate receptors, NGF/BDNF upregulation, a proposed HIF-1-positive transcriptional effect, and antioxidant, anti-inflammatory, anti-calcium/glutamate-neurotoxic activity. It is roughly 1,000× more potent than piracetam by weight.
GVS-111Omberacetam (INN)
~1,000×Potency vs piracetam (by weight)
oralStudy-reference only
BLOCKEDPersonalized / healthy-user dosing
Status
Investigational research only · oral clinical-study reference · personalized dosing blocked
Synthetic dipeptide nootropic (peptide-like small molecule)
U.S. status
Unapproved new drug; not a lawful supplement
Evidence grade
C (human cognitive impairment) · B/C (preclinical)
INVESTIGATIONAL · ORAL STUDY-REFERENCE ONLY · personalized & healthy-user dosing BLOCKED
Noopept is a CNS-active investigational nootropic, not a routine supplement page. The FDA has stated products including Noopept are not dietary supplements or conventional foods, and it is an unapproved new drug whose use in supplements, food, or medicine is unlawful in the U.S. Intrasigna displays clinical-study dose records only as source-backed references with provider review; self-use, productivity/student/trading stacks, injection protocols, supplement-sales claims, and dementia-prevention claims are blocked. Intrasigna classifies Noopept as an advanced neurocognitive research compound with provider review required and a regulatory warning enabled.
01 · At a glance
A dipeptide nootropic, graded honestly.
Noopept occupies an unusual position: a peptide-derived molecule that behaves like an orally available small-molecule nootropic. Its preclinical neuroprotection literature is broad and mechanistically rich, but human evidence is older, region-specific, and limited to mild cognitive impairment of vascular/traumatic origin. The engine reflects that — it surfaces study-arm dose references and mechanism source cards, while blocking personalized dosing, healthy-user enhancement, and supplement claims.
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What it is
Pro-Gly dipeptide
N-phenylacetyl-L-prolylglycine ethyl ester (GVS-111, omberacetam). Grade B.
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Prodrug
→ cycloprolylglycine
Converts in the body to cyclo-Pro-Gly, identical to an endogenous neuropeptide. Grade B/C.
⚖️
Potency
~1,000× piracetam
Active at 10–30 mg vs piracetam's 1,200–4,800 mg. Grade B.
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Oral
Brain-penetrant
Chemical modifications give it oral bioavailability uncommon for peptides. Grade B.
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Human lane
Vascular/TBI MCI
Studied in mild cognitive impairment of cerebrovascular/post-traumatic origin. Grade C.
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Preclinical
Neuroprotection
Antioxidant, anti-inflammatory, anti-Ca²⁺/glutamate-neurotoxicity in animal/cell models. Grade B/C.
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Blocked
Self-use protocols
Healthy-user enhancement, student/trading stacks, injection, and supplement claims are blocked. Admin rule.
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Regulatory
Unapproved (US)
U.S. unapproved new drug; AU prescription-only (S4). Grade B.
02 · Mechanism of action
Not one receptor — a multi-component nootropic.
Noopept's effects don't come from a single target. It is a prodrug that converts to an endogenous neuropeptide, modulates glutamate receptors, raises neurotrophins, engages a hypoxia-response transcriptional program, and protects neurons from oxidative, calcium, and amyloid stress. That breadth is its strength preclinically and the reason its human translation is graded cautiously — many mechanisms are demonstrated in cells and animals, not in modern human trials.
Grade B/C
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1 · Prodrug → cycloprolylglycine
It is largely a delivery vehicle for an endogenous brain peptide.
Mechanism: Noopept is a prodrug of cyclic glycine-proline (cycloprolylglycine, cPG), an endogenous neuropeptide, and was designed as a dipeptide analog of piracetam built on a rational peptide-design hypothesis at the Zakusov Institute.
Detail: In rats, GVS-111 itself was undetectable in brain 1 h after dosing while cyclo-Pro-Gly rose ~2.5-fold, and cPG formation from GVS-111 was shown with plasma/brain enzymes — evidence the parent converts to a cyclopeptide identical to the endogenous one. Its human metabolism and elimination half-life were noted as not well understood as of 2017. The endogenous metabolite cyclo-Pro-Gly has itself shown anxiolytic activity in the elevated plus-maze, supporting the prodrug rationale.
Grade C
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2 · AMPA / NMDA glutamate modulation
It tunes the brain's main excitatory signaling for learning and memory.
Mechanism: Its mechanism involves modulation of both AMPA and NMDA glutamate receptors — the receptor systems central to synaptic plasticity, learning, and memory, and also to excitotoxic injury.
Detail: It is described as a positive allosteric modulator of AMPA receptors, binding the S1-S2 extracellular domain interface and slowing receptor desensitization to amplify fast excitatory transmission in hippocampal/cortical circuits; earlier work also examined GVS-111 effects on neuronal voltage-gated calcium and potassium channels.
Grade C
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3 · NGF / BDNF neurotrophin upregulation
It raises the growth factors that support neuron survival and plasticity.
Mechanism: Noopept upregulates neurotrophic factor expression — nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) — a plausible substrate for memory and neuroplasticity effects.
Detail: Oral Noopept has been reported to increase the mature forms of BDNF and NGF in wild-type rat brain, the basis for a neurotrophin mechanism record — though this remains a preclinical mechanism, not a human protocol output.
It shields neurons from several overlapping forms of injury.
Mechanism: An oft-cited rat study attributes Noopept's action to an antioxidant effect, an anti-inflammatory action, the ability to inhibit neurotoxicity of excess calcium and glutamate, and improved blood rheology.
Detail: In rat cortical neurons exposed to hydrogen peroxide, GVS-111 increased neuronal survival across a wide concentration range (10 nM–100 µM), supporting an oxidative-stress neuroprotection lane — an in-vitro finding, not a human dosing lane.
Grade C
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5 · HIF-1 transcriptional program
A hypoxia-response pathway may be its primary upstream lever.
Mechanism: A molecular-mechanism study of the substituted Pro-Gly dipeptide proposed a HIF-1-positive effect as the primary mechanism of its activity, screening DNA-binding activity of transcription factors including CREB, NF-κB, p53, STAT1, VDR, HSF1, and HIF-1.
Detail: The work (Zakusov Institute, 2016) used HEK293 luciferase reporter constructs and molecular docking against HIF-prolyl hydroxylase 2, linking the Pro-Gly dipeptide structure to hypoxia-inducible-factor signaling and neuroprotection.
Grade C
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6 · Anti-amyloid / anti-tau / anti-aggregation
It counters several protein-misfolding injuries in cell models.
Mechanism: In a PC12 amyloid-β toxicity model, Noopept protected cells against amyloid-related toxicity, reducing oxidative damage and calcium overload.
Detail: In an Alzheimer-related cellular model its neuroprotection involved attenuation of apoptosis and tau hyperphosphorylation, and it has been reported to rescue α-synuclein amyloid cytotoxicity — all preclinical mechanism cards, never a treatment or prevention claim.
A clinical-study reference engine — not a self-use protocol.
Noopept does not get a peptide vial-reconstitution calculator. It gets a neurocognitive clinical-study-reference engine: it surfaces the doses actually used in human studies (as source-backed references), blocks personalized output, and hard-blocks healthy-user enhancement and supplement framing. Route is oral-only; any non-oral route returns BLOCKED. The lanes below mirror the human evidence — cerebrovascular/post-traumatic MCI, post-stroke MCI, preclinical neuroprotection — plus the explicitly blocked healthy-user and regulatory lanes.
Engine mode · neurocognitive clinical-study reference (oral only)
The engine is route-gated (oral only), regulatory-gated, and diagnosis-context-gated; it displays study-arm doses with source cards but blocks personalized dosing, cycles, and stacks. Human study doses (e.g., 20 mg/day for two months in stroke patients) are shown as references requiring provider review.
Quality-control warning
A 2021 analysis of cognitive-enhancement products sold online found unapproved drugs, including omberacetam/Noopept, supporting an adulteration and purity caution — another reason the engine refuses self-use protocol output.
Lane A — Cerebrovascular / post-traumatic MCI
Oral · clinical-study reference
Grade C
Study dose
10 mg twice daily (20 mg/day).
Duration
56 days, open-label comparative.
Comparator
Piracetam 400 mg three times daily.
Endpoints
MMSE, memory/attention, anxiety/vegetative symptoms, global assessment.
Noopept is a peptide-like neuroactive small molecule dosed in milligrams (human studies use fixed mg, not body-weight dosing; the mg/kg and human-equivalent-dose outputs are research conversions for context). This engine computes mg-per-dose, total daily mg, mg/kg/day, cumulative study-period exposure, and animal→human equivalent dose against the documented study arms and preclinical models. It does not generate personalized human protocols, cycles, stacks, healthy-user enhancement, injection/reconstitution, or supplement-sales output. Any non-oral route, or a healthy-user/dementia-prevention context, returns BLOCKED. Study-arm reference only — provider review required; not medical advice.
Total daily dose
—
Weight-normalized
—
Cumulative (study period)
—
Study-arm reference
—
Animal→human (HED) / model
—
Output status
—
04 · Interactions & stack logic
Stacking is blocked by default.
Noopept is CNS-active with too many neuropsychiatric and cardiovascular variables to allow casual stacking. Every combination below is provider-review-only or avoided — and healthy-user "enhancement stacks" are not permitted at all. The point of this section is the opposite of a stack builder: it documents why each combination needs medication review, psychiatric-risk screening, and blood-pressure/sleep monitoring before anyone considers it.
+ Racetams (piracetam etc.)
Avoid / provider-only
NoopeptRacetam
Same broad nootropic category with additive uncertainty; piracetam was the comparator in the main human study, not an established add-on. Provider-only.
Combo
Rule
Watch
Racetam
Provider-only
Additive CNS
+ Stimulants / modafinil
Caution / provider-only
NoopeptStimulant
CNS activation, sleep disruption, anxiety, and blood-pressure concerns. BP increase, sleep disturbance, and irritability are documented signals. Provider-only.
High-risk CNS drug class; default block pending specialist review. Block/provider-only.
Combo
Rule
Watch
MAOI
Block default
High-risk CNS
+ Benzodiazepines / sedatives
Provider-only
NoopeptSedative
Conflicting CNS effects (activation vs sedation); CNS review required. Provider-only.
Combo
Rule
Watch
Sedative
CNS review
Conflicting effects
+ Choline donors
Caution
NoopeptCholine
Cholinergic side effects (headache, GI) are possible; commonly paired anecdotally but unproven. Caution.
Combo
Rule
Watch
Choline
Caution
Cholinergic AEs
+ Semax / Selank / neuropeptides
Research-only
NoopeptSemax/Selank
Neuropeptide mechanism overlap (BDNF/neurotrophin lanes); research framing only, no human protocol. Research-only.
Combo
Rule
Watch
Neuropeptide
Research-only
Overclaim
+ Alcohol / cannabis
Avoid
NoopeptAlcohol/THC
Cognitive, sleep, and psychiatric confounding; avoid in any research-context use. Avoid.
Combo
Rule
Watch
Alcohol/THC
Avoid
CNS confounding
Stack safety note — Noopept stack output is blocked by default. Any CNS-active combination requires medication review, psychiatric-risk screening, blood-pressure and sleep monitoring, and a source-backed rationale. Healthy-user enhancement stacks (focus, study, trading, gaming, anti-aging) are not allowed. Dihexa and other neurotrophic "cognitive stacks" are blocked as overclaim/high-risk.
05 · Safety & screening
A neurocognitive, psychiatric & cardiovascular safety model.
Noopept is CNS-active, so its safety panel is neurocognitive/psychiatric/cardiovascular rather than a standard peptide lab panel. The decisive gates are route (oral only), regulatory (not a lawful supplement in the U.S.), psychiatric risk (mania/psychosis/seizure), blood pressure, and medication interactions — with hard blocks for pregnancy, pediatric use, and healthy-user self-dosing.
⛔ Investigational · not a supplement — In the U.S. Noopept is an unapproved new drug and not a lawful dietary-supplement ingredient. Reported safety signals include blood-pressure increases requiring treatment, sleep disturbance, and irritability. Intrasigna provides no self-use dosing, productivity protocols, injection protocols, or supplement claims.
Repeat MMSE/MoCA, attention, and memory measures over the study window. Endpoints are research-context only and apply to the defined MCI lanes, not to healthy-user enhancement.
Psychiatric & cardiovascular tolerability
Track sleep, anxiety/irritability, and blood pressure/heart rate — one 56-day study reported BP increases requiring treatment plus sleep disturbance and irritability. Watch for mood elevation/impulsivity (mania-spectrum) and medication changes.
Tolerability & interactions
Log headache and GI symptoms; review all CNS-active medications. Any combination is provider-review-only, and unknown-purity product is a block given documented adulteration of online cognitive-enhancement products.
Safety gates & claim boundaries
Condition / request
Concern
Action · grade
Pregnancy / breastfeeding
No safety basis
Block
Pediatric use
No clinical basis
Block
Bipolar / mania history
CNS activation / mood
Block / psychiatrist
Psychosis history
CNS-active
Block
Uncontrolled hypertension
BP signal
Block
Seizure disorder
Threshold uncertainty
Provider-only / block
Healthy-user / productivity self-use
Not evidence-supported
Block protocol
Supplement-sales claim (US)
Not a dietary supplement
Block
Injection / reconstitution request
Oral records only
Block
Dementia / Alzheimer prevention claim
No human prevention evidence
Block
Unknown product purity
Adulteration risk
Block
Active substance-use disorder
CNS misuse
Block / provider-only
MAOI use
High-risk CNS class
Block default
SSRI / SNRI / TCA use
Interaction uncertainty
Medication review
Antipsychotic use
Psychiatric interaction
Psychiatric review
Benzodiazepine / sedative use
Conflicting CNS effects
CNS review
ADHD stimulant use
BP/HR/activation
BP/HR + CNS review
Prior stroke / TBI
May match a study lane
Provider required
Older-adult polypharmacy
Interaction load
Provider review
Liver / kidney disease
Unknown PK
Caution
Dementia diagnosis
Specialist context
Neurology review
GRADE summary — Identity and chemistry are well established (B), and the preclinical neuroprotection mechanisms (oxidative, calcium/glutamate, amyloid, NGF/BDNF, HIF-1) are reasonably supported (B/C). Human evidence is limited to mild cognitive impairment of cerebrovascular/post-traumatic origin and post-stroke cognitive impairment (C, older/region-specific), and there is no high-quality evidence for healthy-user enhancement or dementia prevention (D/E). The decisive levers are route gating (oral only), the regulatory gate (unapproved new drug; not a lawful U.S. supplement), psychiatric/blood-pressure gates, and study-arm-reference-only output — never personalized dosing, cycles, stacks, or supplement claims.
06 · Evidence base & studies
Broad preclinical, narrow human.
Noopept's literature is lopsided: a deep preclinical record of neuroprotection and mechanism, but a thin, older human record confined to mild cognitive impairment of vascular/traumatic origin. The credibility of this page comes from not inflating the human evidence into healthy-user or prevention claims. Each study below is tied to its grade and to a specific allowed output.
Human · MCI
10 mg BID · 56 d
Noopept vs piracetam in vascular/traumatic MCI. Neznamov & Teleshova.
Human · stroke
20 mg/d · 2 mo
Improved cognition, high safety in stroke patients. Clinical report.
Preclinical
PC12 · Aβ
Protection vs amyloid toxicity, oxidative/calcium stress. Cell model.
Mechanism
HIF-1
HIF-1-positive effect proposed as primary mechanism. Zakusov 2016.
CHuman · MCI (vascular/traumatic)
Noopept vs piracetam in mild cognitive disorders
A comparative study evaluated Noopept and piracetam in patients with mild cognitive disorders of vascular and traumatic origin; an evidence review summarizes a 56-day study using Noopept 10 mg twice daily versus piracetam, reporting improvements in mood and cognition measures while classifying human dementia/cognitive-aging prevention evidence as absent.
A clinical report describes Noopept 20 mg daily over two months in stroke patients with mild cognitive impairment, reporting improved cognitive functions and a high level of safety — an important dose-basis record that nonetheless belongs in study-arm-reference-only output with provider review.
A 2016 Zakusov-Institute study screening transcription-factor DNA-binding activity proposed a HIF-1-positive effect as the primary mechanism of Noopept, and the same line of work links clinical study in cerebrovascular/post-traumatic MCI to decreased cognitive impairment, anxiolytic effect, and vegetostabilizing activity.
The major metabolite of GVS-111 in rat brain is cyclo-prolylglycine, which rose ~2.5-fold 1 h after dosing while the parent was undetectable, with cPG formation confirmed via plasma/brain enzymes — identifying Noopept as a prodrug converting to a cyclopeptide identical to the endogenous neuropeptide.
In differentiated PC12 cells exposed to amyloid-β, Noopept protected against amyloid-related toxicity via reduced oxidative damage and inhibited calcium overload; in a broader Alzheimer-related cellular model, neuroprotection involved attenuation of apoptosis and tau hyperphosphorylation — mechanism cards, not Alzheimer treatment claims.
In rat cortical neurons exposed to hydrogen peroxide, GVS-111 increased neuronal survival across a wide concentration range (10 nM–100 µM), supporting an oxidative-stress neuroprotection lane — an in-vitro concentration record with no human dose conversion.
Noopept has been reported to rescue α-synuclein amyloid cytotoxicity, and earlier work characterized GVS-111 effects on neuronal voltage-gated calcium and potassium channels — broadening the anti-aggregation and ion-channel mechanism record while remaining preclinical.
A 2022 experimental paper notes prior oral-Noopept work showing increases in the mature forms of BDNF and NGF in wild-type rat brain, and neurotrophin upregulation (NGF/BDNF) is part of Noopept's described cognitive-enhancing mechanism — supporting a plasticity record, not a human protocol.
The FDA has stated products including Noopept are not dietary supplements or conventional foods; it is an unapproved new drug whose use in supplements, food, or medicine is unlawful in the U.S. and a 2021 analysis found unapproved drugs, including omberacetam, in online cognitive-enhancement products.
In one 56-day study, two participants experienced systolic blood-pressure increases requiring treatment, and other reported effects included increased sleep disturbance and irritability — secondary-source safety signals that the screening engine tracks (BP, sleep, irritability), even though the human safety database is limited.
Noopept was developed in 1996 at the State Zakusov Institute of Pharmacology by Tatyana Gudasheva and colleagues and approved as a prescription nootropic in Russia in 2006, built on a hypothesis that reproduces psychotropic structures using appropriate amino acids — with piracetam as the non-peptide prototype.
A peptide-derived molecule with oral bioavailability
Though derived from cycloprolylglycine and designed as a peptide-based nootropic, the N-phenylacetyl group and C-terminal ethyl ester make Noopept technically a small molecule — giving it oral bioavailability uncommon among peptide drugs; its human metabolism and half-life were noted as not well understood as of 2017.
The endogenous nootropic dipeptide cycloprolylglycine — the active Noopept metabolite — showed anxiolytic activity in the elevated plus-maze test, and clinical study in cerebrovascular/post-traumatic MCI reported an anxiolytic and vegetostabilizing effect alongside cognitive improvement, though graded below modern large RCTs.
An oft-cited rat study attributes Noopept's action to an antioxidant effect, an anti-inflammatory action, inhibition of excess calcium- and glutamate-neurotoxicity, and improved blood rheology — the convergent neuroprotection profile underpinning the cerebrovascular research lane.
Intrasigna runs Noopept as an oral clinical-study-reference engine — blocking personalized dosing, healthy-user enhancement, student/trading/productivity stacks, injection/reconstitution, supplement claims, and dementia-prevention claims, with the peptide vial calculator disabled and psychiatric/blood-pressure gates and a regulatory warning enabled.
Noopept produces cognition-enhancing effects at concentrations roughly 1,000× lower than piracetam and is described as acting over a wider range of cognition disturbances and neuronal-damage models, with more pronounced anxiolytic and neuroprotective properties than its prototype — a breadth that is the basis for its preclinical interest, not a license for healthy-user protocols.
Noopept's defining contrast is with its parent class. It was conceived as a peptide-based nootropic and a more potent analog of piracetam, but chemical modification turned it into an orally bioavailable small molecule — a property most therapeutic peptides lack. Against the racetams it is far more potent by weight; against approved drugs it remains investigational.
L1 · Consumer — Noopept is a synthetic nootropic related to proline-glycine peptide chemistry, studied mostly for memory, cognition, and protecting brain cells. The clearest human research is in people with mild cognitive problems after stroke or brain injury — not in healthy people looking for a focus boost. In the U.S. it isn't an approved drug or a legal supplement, so Intrasigna shows study doses as references only, never as a self-use plan, and flags blood-pressure, sleep, and mood as things to watch.
L2 · Clinical — Noopept/GVS-111 (omberacetam) is a CNS-active dipeptide nootropic studied in mild cognitive disorders of cerebrovascular and post-traumatic origin (10 mg BID × 56 days vs piracetam) and post-stroke cognitive impairment (20 mg/day × 2 months), with preclinical neuroprotection across amyloid, oxidative, calcium/glutamate, and neurotrophin pathways. Dosing output is study-arm-reference-only with provider review; route is oral; healthy-user, injection, supplement, and dementia-prevention outputs are blocked. Screen psychiatric history, seizure history, blood pressure, and CNS-active medications.
L3 · Research — Noopept (N-phenylacetyl-L-prolylglycine ethyl ester) is a prodrug of cycloprolylglycine designed at the Zakusov Institute as a piracetam analog, ~1,000× more potent by weight. Mechanisms: AMPA positive allosteric modulation + NMDA modulation, NGF/BDNF upregulation, a proposed HIF-1-positive transcriptional program, antioxidant/anti-inflammatory and anti-Ca²⁺/glutamate neuroprotection, and anti-amyloid/anti-tau/anti-α-synuclein effects in cellular models. Human evidence is older/region-specific (vascular-traumatic MCI; post-stroke MCI; grade C). U.S. unapproved new drug; metabolism/half-life poorly characterized; documented BP/sleep/irritability signals.
08 · References & evidence
Source register.
Evidence grades reflect the strength of support for the specific claim cited, not the prestige of the journal. Noopept's identity and chemistry are firm; its mechanisms are well-supported preclinically; its human cognitive evidence is older and region-specific (grade C); and healthy-user enhancement and dementia prevention have no adequate human support. Regulatory and admin sources anchor the oral-only, study-reference-only gating.