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superstack

The Limitless Stack v2

eleven compounds aimed at learning and memory: acetylcholine supply, a stronger response to glutamate, and more growth-factor signaling at the synapse

  1. Nefiracetam
    racetam that potentiates nicotinic and NMDA receptors
    Human RCTs
  2. Pramiracetam
    racetam acting on brain choline
    Human RCTs
  3. Oxiracetam
    racetam that positively modulates AMPA receptors
    Human RCTs
  4. NSI-189
    neurogenic compound found by a neural-stem-cell screen
    Early human trials
  5. no structure on file
    ACD856
    Trk receptor positive allosteric modulator
    Early human trials
  6. BPN14770
    allosteric PDE4D inhibitor
    Human RCTs
  7. J-147
    partial inhibitor of mitochondrial ATP synthase
    Preclinical
  8. Semax
    heptapeptide analog of the ACTH(4-10) fragment
    Early human trials
  9. Citicoline
    choline source, plus cytidine
    Human RCTs
  10. Tropisetron
    α7 nicotinic partial agonist and 5-HT3 antagonist
    Human RCTs
  11. PRL-8-53
    phenethylamine-derived benzoate studied for verbal memory
    Early human trials

Protocol

as reported; not a recommendation
CompoundRouteDose rangeTiming
NefiracetamOral100–1,000 mg2–3x Daily, With Fat
PramiracetamOral500–5,000 mgMorning and Early Afternoon, With Fat
OxiracetamOral500–2,000 mg or moreMorning and Early Afternoon
NSI-189Oral20–80 mgDaily or 3x Weekly, Morning
ACD856Oral5–30 mgDaily, Morning
BPN14770Oral2.5–5 mg or more1–2x Daily
J-147Oral10–30 mgDaily, Morning
SemaxIntranasal100–1,000 µgDaytime
CDP-CholineOral100–900 mg1–2x Daily, Morning or Morning/Midday
TropisetronOral5–20 mgDaily
PRL-8-53Oral10–60 mgAs Needed, Morning or Before Learning

What to expect

CompoundHow it contributes
Learning
Taking in something new and keeping it. This is the whole process; attention, encoding, consolidation and recall below are its parts.
PRL-8-53Strengthens dopamine signaling in rats [1], which may help new material go in. In people, a word list was learned slightly faster after taking it [2].
OxiracetamRaises the brain's use of acetylcholine in rats [3], which may help learning. In people with mild to moderate dementia, it improved the learning of a 15-word list [4].
CDP-CholineSupplies choline, the raw material brain cells make acetylcholine from [5], which may help learning. In healthy older adults with age-related memory complaints, it raised overall memory-test scores [6].
TropisetronSwitches on the α7 nicotinic receptor, one of the receptors for acetylcholine [7], which may help learning. In people with schizophrenia, it raised overall scores on a battery of memory and attention tests [8].
NefiracetamRaises the release of acetylcholine and the enzyme that makes it, which may help learning. In rats that had lost the brain cells that make acetylcholine, it improved learning [9].
SemaxRaises BDNF, a growth factor that supports brain cells and their connections, which may help learning. Rats given a single dose through the nose more often acted on a learned warning signal to avoid something unpleasant [10].
Sensory gating
The brain's automatic filter. It turns down repeated or irrelevant sounds before they reach your attention.
TropisetronSwitches on the α7 nicotinic receptor [7], which may strengthen this filter. In people with schizophrenia, in whom the filter is weak, it improved it [8][11][12].
CDP-CholineSupplies choline, which itself switches on the α7 nicotinic receptor and may strengthen this filter. In healthy volunteers whose filtering was weak to begin with, a single dose strengthened it [13].
Attention
Staying on a task (attention span) and picking out what matters within it (selective attention).
CDP-CholineSupplies choline, the raw material for acetylcholine [5], which may sharpen attention. In healthy teenage boys, it improved attention-test scores [14].
PramiracetamActs on how the brain takes up choline, the raw material for acetylcholine, in rats [15], which may support attention. In healthy men, it partly reversed the loss of selective attention caused by scopolamine, a drug that blocks acetylcholine [16].
TropisetronSwitches on the α7 nicotinic receptor [7], which may sharpen attention. In people with schizophrenia, it improved a test of sustained visual attention [11].
OxiracetamRaises the brain's use of acetylcholine in rats [3], which may sharpen attention. In people with mild to moderate dementia, it improved a test of sustained attention to sounds [4][17].
NefiracetamRaises the release of acetylcholine in the front of the brain in rats [9] and makes the nicotinic receptors it acts on respond more strongly [18], which may sharpen attention.
Processing speed
How quickly the brain handles simple information: reacting, scanning, tracking. It measures speed, not memory.
CDP-CholineSupplies choline for acetylcholine and for the membranes around brain cells [5], which may help the brain work faster. In healthy teenage boys, it raised movement speed, measured by finger tapping [14].
OxiracetamMakes the receptors that carry the brain's fast glutamate signals respond more strongly [19], which may speed up processing. In the hippocampus of mice with Alzheimer's-like disease, those signals were larger and more frequent [20].
Working memory
Holding something in mind for a few seconds while you use it, like a phone number you are about to dial.
BPN14770Blocks PDE4D, an enzyme that breaks down the messenger cAMP, and so raises cAMP in the brain of mice [21], which may help hold information in mind. In healthy volunteers aged 60 and over, two weeks of it was reported to improve working memory [22].
OxiracetamMakes the receptors that carry the brain's fast glutamate signals respond more strongly [19], which may help hold information in mind. In people with mild to moderate dementia, it lengthened the sequence of locations they could repeat back [4][17].
J-147Raises the growth factors BDNF and NGF, which may help hold information in mind. In mice given scopolamine, a drug that blocks acetylcholine, it protected working memory [23].
NefiracetamMakes the NMDA receptor, one of the receptors for the messenger glutamate, respond more strongly in rat brain cells [24], which may help hold information in mind.
Encoding
Getting new information into memory at the moment you meet it. Processing speed is how fast you take it in; encoding is whether it gets stored.
PramiracetamActs on how the brain takes up choline in rats [15], which may help new memories form. In healthy men, it partly reversed the memory loss caused by scopolamine, a drug that blocks acetylcholine [16].
OxiracetamMakes the receptors that carry the brain's fast glutamate signals respond more strongly [19], which may help new memories form. In healthy volunteers given scopolamine, it improved their later recall of word lists [25].
CDP-CholineSupplies choline, the raw material for acetylcholine [5], which may help new memories form. In healthy older adults with age-related memory complaints, it improved a test of remembering which items go together [6].
TropisetronSwitches on the α7 nicotinic receptor [7], which may help new memories form. In people with schizophrenia, it improved immediate memory, the recall of information just presented [8][12].
NefiracetamMakes nicotinic and NMDA receptors respond more strongly in rat brain cells [18][24], which may help new memories form. In rats, it countered the memory loss caused by scopolamine [9].
Consolidation
Turning a fresh, fragile memory into a lasting one in the hours and days after learning.
BPN14770In mice, raises cAMP, a messenger inside brain cells, and with repeated dosing switches on CREB, a protein that turns on genes, which may help memories last; the mice remembered an object better a day later [21]. Mice kept awake after learning were spared the memory loss that sleep deprivation causes [26][27].
ACD856Makes brain cells respond more strongly to BDNF and related growth factors, which may help memories last. In mice with drug-induced amnesia it rescued the memory when given just after training, and one dose left old mice remembering a task as well as young ones 11 days later [28].
J-147Helped connections between brain cells strengthen after use, in slices of rat brain, which may help memories last. Mice fed it remembered a maze better six weeks after learning it [29].
NefiracetamStrengthens long-term potentiation, the lasting boost a connection between brain cells gets from use, in rat brain tissue [30], which may help memories last. In rats, it countered the memory loss caused by cycloheximide, a drug that stops brain cells making new proteins [9].
SemaxIn rats, a single dose through the nose raised the output of the genes for BDNF, a growth factor that supports brain cells and their connections, and for its receptor in the hippocampus [10], which may help memories last.
Recall and retention
Retention is how much of a memory is still there later; recall is getting it back out. Retention is the result of consolidation, so this row overlaps the one above.
PRL-8-53Reported to produce an acetylcholine response in animals, which may help memories stay. People who took it before learning a word list remembered more of the words a day later and a week later [2].
PramiracetamActs on how the brain takes up choline in rats [15], which may help recall. In young men with memory problems after a head injury, it improved delayed recall, remembering something after a gap [31].
TropisetronSwitches on the α7 nicotinic receptor [7], which may help recall. In people with schizophrenia, it improved delayed memory, the recall of information after a gap [8].
ACD856Makes brain cells respond more strongly to BDNF and related growth factors, which may help recall. In mice with drug-induced amnesia, a dose given shortly before the memory test improved recall [28].
Neuroplasticity
The brain's ability to grow and rewire: new cells, new connections and the materials they are built from. It is not a memory stage; it is the groundwork the stages above depend on.
NSI-189Makes stem cells from the human hippocampus divide in the lab [32], which may help the brain grow new nerve cells. In rats recovering from radiation, it raised the number of new nerve cells in the hippocampus [33].
OxiracetamMakes the receptors that carry the brain's fast glutamate signals respond more strongly [19], which may help connections between brain cells grow and hold. In mice with Alzheimer's-like disease, it reduced the loss of nerve cells in the hippocampus and restored proteins that nerve-cell branches and connections are built from [20].
ACD856Makes brain cells respond more strongly to growth factors [28], which may help connections between them grow. Old mice given it daily for four weeks had more BDNF in their brains [34].
BPN14770In mice, raises cAMP and CREB signaling, which may help connections between brain cells grow; it raised the proteins those connections are built from in the mouse hippocampus [21].
J-147Partly blocks ATP synthase, the enzyme that makes energy in mitochondria, switching on the energy sensor AMPK [35], which may help brain cells grow and repair. In mice with Alzheimer's-like disease, it raised the growth factors BDNF and NGF in the hippocampus [23].
SemaxRaises BDNF, a growth factor that supports brain cells and their connections, which may help the brain rewire. In rats, a single dose through the nose raised BDNF in the hippocampus and switched on its receptor [10], and raised BDNF in the basal forebrain [36].
NefiracetamActing through nicotinic receptors, raises the release of the messenger glutamate, which may help connections between brain cells strengthen. In hippocampal tissue, it gave a lasting boost to the signals passing between cells [37].
CDP-CholineA building block of phosphatidylcholine, the main fat in the membranes around every brain cell, which may support the growth of new branches and connections. In animal models of stroke, it slowed the breakdown of those membranes [5].

What everything does

CompoundWhat it does
NefiracetamPotentiates α4β2 nicotinic acetylcholine receptor currents through Gs proteins [18] and NMDA receptor currents through protein kinase Cα [24]. Enhances long-term potentiation in the hippocampus [30].
PramiracetamIn rats, prevents the scopolamine-induced rise in choline extraction across the blood-brain barrier and increases cerebral blood flow [15]. Partly reverses the memory and attention deficits caused by the acetylcholine blocker scopolamine [16].
OxiracetamRaises the response of AMPA receptors to glutamate, with no change to kainate or NMDA responses [19], and slows the desensitization of their GluA1 and GluA2 subunits [20]. In rats, raises acetylcholine use and high-affinity choline uptake in the hippocampus [3].
NSI-189Stimulates the proliferation of hippocampal neural stem cells [32] and raised the number of newly born hippocampal neurons in irradiated rats [33]. Raises BDNF and stem cell factor in oxygen- and glucose-deprived hippocampal cultures [38].
ACD856Makes the TrkA, TrkB and TrkC receptors respond more strongly to their neurotrophins NGF, BDNF and NT-3 [28]. In cortical neurons it raises ERK1/2 phosphorylation in the neurites and BDNF protein [34].
BPN14770Inhibits the PKA-activated long forms of phosphodiesterase-4D [39]. In mice carrying the human enzyme it raises brain cAMP and, with repeated dosing, CREB phosphorylation and BDNF in the hippocampus [21].
J-147Partly inhibits the mitochondrial ATP synthase, which raises cytosolic calcium and activates AMPK through the kinase CAMKK2 [35]. Raises BDNF and NGF in the hippocampus of Alzheimer's-model mice [23].
SemaxRaises BDNF protein and the phosphorylation of its receptor trkB in the rat hippocampus after a single intranasal dose [10]. Binds specific, calcium-dependent sites in rat basal forebrain membranes and raises BDNF there [36].
CDP-CholineAn intermediate in the synthesis of phosphatidylcholine, the main membrane phospholipid. Also supplies choline for acetylcholine synthesis [5].
TropisetronPartially activates α7 nicotinic acetylcholine receptors, with no effect at the α4β2 subtype [7], and blocks 5-HT3 serotonin receptors [40]. Improves impaired P50 auditory sensory gating in schizophrenia [11].
PRL-8-53Improved the retention of verbal information in people, with a smaller effect on its acquisition. Potentiates apomorphine-induced gnawing, a dopamine-dependent behavior, and promotes conditioned avoidance learning in rats [1]. Reported to produce a cholinergic response and partly inhibit serotonin in animals [2].

Why it works

Cholinergic signaling

Five compounds act on acetylcholine at different points. CDP-choline supplies the choline it is made from [5], and pramiracetam acts on the transport of choline across the blood-brain barrier [15]. Oxiracetam raises high-affinity choline uptake and acetylcholine use in the rat hippocampus [3], and increases evoked acetylcholine release from hippocampal slices [41]. Nefiracetam stimulates acetylcholine release in the frontal cortex and raises the activity of choline acetyltransferase, the enzyme that makes it [9], and potentiates the α4β2 nicotinic receptors acetylcholine acts on [18]. Tropisetron acts on a second nicotinic receptor, α7, as a partial agonist [7].

Sensory gating

Sensory gating is the suppression of the brain's P50 response to the second of two paired sounds. Tropisetron improved it in people with schizophrenia, in whom it is impaired [8][12], and CDP-choline strengthened it in healthy volunteers whose gating was low to begin with [13].

Glutamate receptors

Two compounds strengthen the response to glutamate, each at a different receptor. Oxiracetam raises the efficacy of glutamate at AMPA receptors, leaving kainate and NMDA responses unchanged [19], and slows the receptors' desensitization [20]. Nefiracetam potentiates NMDA receptors through protein kinase Cα, enhancing glycine binding and largely removing the channel's magnesium block [24].

Long-term potentiation

Three compounds favor the lasting strengthening of a synapse after it is used. Nefiracetam enhances long-term potentiation in the hippocampus through CaMKII, PKCα and the phosphorylation of AMPA receptors [30]. BPN14770 let a weak stimulus produce long-lasting potentiation in hippocampal slices from mice carrying the human PDE4D [21], and J-147 helped potentiation form in rat hippocampal slices [29].

cAMP–CREB signaling

BPN14770 inhibits PDE4D most strongly once PKA has activated the enzyme, so it acts where cAMP signaling is already under way [39]. In mice carrying the human enzyme it raised brain cAMP and, after two weeks, phosphorylation of the transcription factor CREB in the hippocampus [21]; a PKA inhibitor blocked its memory effects [42].

Neurotrophin signaling

Four compounds raise the growth factor BDNF and a fifth acts on its receptor. BPN14770 raised it in the hippocampus with repeated dosing [21], J-147 raises hippocampal BDNF and NGF [23], and NSI-189 raised BDNF and stem cell factor in oxygen- and glucose-deprived hippocampal cultures [38]. Semax raised BDNF protein and the mRNA for BDNF and its receptor trkB in the rat hippocampus, with more of the receptor phosphorylated [10], and raised BDNF in the basal forebrain but not the cerebellum [36]. ACD856 works on the receptor side: it makes the Trk receptors respond more strongly to BDNF, NGF and NT-3 [28].

Neurogenesis

NSI-189 was selected for making human hippocampus-derived neural stem cells proliferate [32]. In irradiated rats it raised the number of newly born granule neurons in the hippocampus [33].

Synapses and neurites

BPN14770 raised phosphorylated synapsin and the postsynaptic protein PSD95 in the hippocampus [21], and J-147 restored synaptic proteins in Alzheimer's-model mice [29]. In cultured cells ACD856 largely prevented the loss of the synaptic protein SNAP25 caused by amyloid-β and lengthened the neurites grown in response to NGF [34]. NSI-189 increased the neurite marker MAP2 in the hippocampus and cortex of rats after stroke [38], and oxiracetam restored MAP2, GAP43 and the synaptic protein synaptophysin in the hippocampus of Alzheimer's-model mice [20].

Cell membranes

CDP-choline is the direct precursor of phosphatidylcholine, the main phospholipid in cell membranes. In animal models of cerebral ischemia it also slows membrane breakdown by inhibiting phospholipases [5].

Energy metabolism

J-147 partly inhibits the mitochondrial ATP synthase, raises whole-cell ATP and activates AMPK through the calcium-sensing kinase CAMKK2 [35]. AMPK then inhibits ACC1, which raises acetyl-CoA in neurons and the acetylation of histone H3, a mark linked to memory formation [43]. ACD856 kept ATP levels up in cortical neurons deprived of glucose and pyruvate [34].

Monoamine balance

PRL-8-53 potentiates apomorphine-induced gnawing, a dopamine-dependent behavior, without blocking monoamine oxidase [1]. In animals it also partly inhibits serotonin and produces a cholinergic response, without amphetamine-like stimulation [2].

Learning and retention

PRL-8-53 improved the retention of verbal information in people, with a slight improvement in its acquisition; visual reaction time and motor control did not change [2]. In rats it promoted conditioned avoidance learning and maze performance [1]. Semax raised the number of conditioned avoidance responses rats made after a single intranasal dose [10].

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Not a recommendation to take or combine anything. Doses are reported, not prescribed. Read the individual entries, and talk to a clinician before taking any of this, particularly anything labeled prescription drug.