Glossary
Plain-English definitions of the recurring terms in nootropic peptide research. Each entry is short enough to scan, long enough to give a meaningful answer, and linked to the peptide pages where the concept is most relevant.
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Definitions
ACTH(4-10)
A seven-amino-acid fragment of adrenocorticotropic hormone with cognitive-modulating activity; the parent sequence of Semax.
The 4-10 fragment of ACTH was observed in early research to influence learning and memory in animal models, independently of the parent hormone's effects on the adrenal axis. Semax is a synthetic heptapeptide engineered from this fragment to retain the neurotropic effects while removing the steroid-axis activity, producing a cognitive peptide without endocrine side effects.
AMPA receptor
A glutamate receptor mediating fast excitatory transmission and the maintenance of LTP.
AMPA receptors are glutamate-gated ion channels that mediate the bulk of fast excitatory neurotransmission. The insertion of additional AMPA receptors into the postsynaptic membrane is the principal mechanism by which a potentiated synapse stays potentiated. Noopept is reported to modulate AMPA receptor function alongside its NMDA effects.
BDNF
Brain-derived neurotrophic factor — the master regulator of activity-dependent synaptic plasticity.
Brain-derived neurotrophic factor is a small protein released by neurons during periods of activity. It binds the TrkB receptor and triggers signalling cascades that stabilise newly active synapses, support the survival of mature neurons, and enable the long-term potentiation that underwrites memory formation. Reduced BDNF expression is associated with depressive states and cognitive decline; almost every effective antidepressant treatment converges on raising BDNF. Several research peptides — Semax, Selank, Noopept, Cerebrolysin — share BDNF induction as their principal mechanistic endpoint, which is why they appear together in the cognitive-peptide family.
Blood-brain barrier
The selective permeability barrier that limits which molecules from the bloodstream can reach the brain.
The blood-brain barrier is formed by tight junctions between the endothelial cells of brain capillaries, restricting passage of polar and large-molecule solutes. Most peptides cross it poorly. Research strategies to deliver peptides to the CNS either choose molecules small and lipophilic enough to permeate it (Dihexa, Noopept), use the intranasal route to bypass it, or accept the limited central bioavailability of parenteral administration.
c-Met receptor
A receptor tyrosine kinase activated by hepatocyte growth factor (HGF), involved in tissue repair and neurogenesis.
c-Met (encoded by the MET gene) is a receptor tyrosine kinase whose physiological ligand is hepatocyte growth factor (HGF). Activation drives cell proliferation, motility, and survival in many tissues; in the CNS it promotes dendritic spine formation and synaptogenesis. Dihexa is a small-peptide HGF mimetic that activates c-Met at picomolar concentrations and is the principal research peptide acting through this pathway. The same pathway is implicated in tumour growth when dysregulated, which is the source of the theoretical safety concerns around chronic Dihexa administration.
Cerebral ischaemia
Reduced blood flow to brain tissue, the proximate cause of ischaemic stroke.
Ischaemia is the standard experimental model for testing neuroprotective compounds. Tissue downstream of an occluded vessel is deprived of oxygen and glucose, triggering excitotoxicity, oxidative stress, and apoptotic neuronal death. Several research peptides are studied for protective effects in ischaemia models — Semax has the most-developed clinical-research record in this indication, with Cerebrolysin not far behind.
Cortisol
The principal glucocorticoid hormone in humans, released by the adrenal cortex under HPA-axis stimulation.
Cortisol mobilises energy substrates and suppresses the immune system during stress. Acute elevation is adaptive; chronic elevation is associated with cognitive impairment, anxiety, depression, sleep disruption, and metabolic dysregulation. Peptides that attenuate stress-induced cortisol elevation (DSIP, Pinealon, indirectly Selank) are studied in the context of stress resilience.
Dendritic spine
The small protrusion on a neuron's dendrite where most excitatory synapses form.
Dendritic spines are the structural unit of excitatory synaptic input. Spine density and morphology are dynamic — they grow and shrink with learning, stress, and ageing — and serve as a microscopic correlate of synaptic plasticity. Compounds that promote spine formation (Dihexa, FGL) are studied as candidates for cognitive enhancement and neural-repair research.
Endogenous opioid system
The system of enkephalins, endorphins, and dynorphins that act on opioid receptors to modulate pain, mood, and stress.
The endogenous opioid system comprises three peptide families — enkephalins, endorphins, dynorphins — and three receptor classes — mu, delta, kappa. Activation modulates pain, mood, stress response, and reward. Selank's anxiolytic mechanism works by raising enkephalin tone without administering an exogenous agonist; this is a fundamentally different pharmacology from morphine or fentanyl-class drugs.
Enkephalinase
An enzyme that degrades endogenous enkephalin peptides, terminating their signalling.
The term covers a small family of peptidases — principally neutral endopeptidase (neprilysin) and aminopeptidase N — that cleave endogenous enkephalin peptides and end their action at opioid receptors. Inhibiting these enzymes raises endogenous enkephalin tone without administering an exogenous opioid agonist, producing analgesic and anxiolytic effects with a different side-effect profile from direct receptor agonism. Selank and its acetylated analogue are research peptides that achieve their anxiolytic effects principally via this pathway.
Excitotoxicity
Neuronal injury caused by overactivation of glutamate receptors, particularly NMDA receptors.
When neurons are deprived of energy (ischaemia, hypoxia, severe metabolic stress) they release glutamate uncontrollably. Persistent NMDA activation drives calcium influx beyond the buffering capacity of the cell, triggering cell death. Neuroprotective peptides studied in stroke and traumatic-brain-injury models often act in part by attenuating excitotoxic damage.
FGFR1
Fibroblast growth factor receptor 1 — a receptor tyrosine kinase that drives neurite outgrowth and synapse formation when activated in the CNS.
FGFR1 is the principal CNS receptor for fibroblast growth factor and is also the binding partner of the neural cell adhesion molecule (NCAM). When NCAM engages FGFR1, downstream PI3K-Akt and MAPK signalling drives neurite outgrowth and synapse maturation. FGL peptide is a 15-amino-acid mimetic of the NCAM motif that binds and activates FGFR1; it is the principal research peptide acting through this pathway.
GABA-A receptor
The principal inhibitory neurotransmitter receptor in the brain; the target of benzodiazepines, barbiturates, and many sedatives.
GABA-A receptors are pentameric chloride channels gated by the inhibitory neurotransmitter GABA. Most clinically used anxiolytics — benzodiazepines, Z-drugs — work as positive allosteric modulators of this receptor, producing anxiolysis along with sedation, motor impairment, anterograde amnesia, and dependence liability. Selank's distinguishing feature is that it produces anxiolysis without direct GABA-A binding, and consequently without those side effects.
Hippocampus
The seahorse-shaped medial temporal lobe structure essential to declarative memory formation.
The hippocampus is the brain region most consistently affected by the cognitive peptides on this site, both as a target of measured BDNF/NGF induction and as the substrate of the LTP-based learning effects reported in animal research. Hippocampal volume and function decline with age and are central to the cognitive profile of Alzheimer's disease.
HPA axis
Hypothalamic-pituitary-adrenal axis — the body's principal stress-response system.
The HPA axis is a three-stage hormonal cascade: the hypothalamus releases CRH, which triggers ACTH release from the pituitary, which drives cortisol release from the adrenal cortex. Acute activation is adaptive; chronic activation contributes to anxiety, depression, sleep disruption, and cognitive impairment. Several research peptides — DSIP, Selank, Pinealon — are studied for their capacity to attenuate stress-induced HPA activation, and that mechanism is one route by which a peptide can affect cognition indirectly.
Human Medicines Regulations 2012
The UK statutory framework governing the licensing, supply, and advertising of medicines.
The 2012 Regulations consolidate UK medicines law and implement the relevant EU directives (as retained post-Brexit). Regulation 46 in particular restricts the supply of unlicensed medicines for human use. Research peptides are sold legally as research chemicals because they are not marketed for human consumption; representations to the contrary by a supplier would breach the Regulations.
Intranasal delivery
Administration through the nasal mucosa, the standard route in nootropic peptide research.
Small peptides applied to the nasal mucosa are transported to the central nervous system via the olfactory and trigeminal nerve pathways, bypassing the bloodstream and the blood-brain barrier. The route is favoured for Semax, Selank, and their acetylated analogues because plasma proteases would degrade the peptides too rapidly for systemic administration to be useful. Bioavailability is sub-parenteral but reproducible, and the route avoids first-pass metabolism entirely.
Khavinson bioregulators
A class of short synthetic peptides developed in the Khavinson school of gerontology, hypothesised to act as direct gene-expression regulators.
Vladimir Khavinson and colleagues at the St. Petersburg Institute of Bioregulation and Gerontology have developed and characterised a family of short peptides (two to four amino acids) including Epitalon (pineal), Pinealon (neuroprotective), Vesugen (vascular), and Thymalin (immune). The school's defining hypothesis is that these peptides act as direct DNA-binding regulators of transcription rather than through conventional receptor pharmacology. The mechanism remains under continuing investigation; phenotypic effects are reproducible, the molecular details less so.
LTP (long-term potentiation)
The cellular mechanism by which repeated activity strengthens a synapse — the molecular basis of learning.
Long-term potentiation is a persistent increase in synaptic strength following a brief period of high-frequency activity. First described by Bliss and Lømo in 1973, LTP is the leading candidate mechanism for activity-dependent memory formation. It requires NMDA receptor activation, calcium entry, and a downstream signalling cascade that includes BDNF release and TrkB activation. Drugs and peptides that facilitate LTP in hippocampal slice preparations are commonly studied as cognitive enhancers; this is the assay behind most of the published Dihexa and FGL work.
MHRA
Medicines and Healthcare products Regulatory Agency — the UK medicines authority.
The MHRA is the executive agency of the Department of Health and Social Care responsible for licensing medicines, medical devices, and blood components in the United Kingdom. None of the peptides discussed on this site is MHRA-licensed. The MHRA's position on unlicensed peptides supplied as research chemicals is principally enforced through the Human Medicines Regulations 2012, which restricts supply for human consumption rather than possession for research.
Monoamines
The neurotransmitter family comprising dopamine, noradrenaline, serotonin, and histamine.
The monoamine neurotransmitters underlie much of the brain's regulation of mood, arousal, motivation, and attention. Several of the research peptides discussed on this site modulate monoamine turnover indirectly — Semax affects serotonergic and dopaminergic metabolites; Selank shows similar but distinct patterns — and this is one of the routes through which they affect cognitive performance and mood.
NCAM
Neural cell adhesion molecule — a cell-surface protein critical to synapse formation and neural plasticity.
NCAM is a glycoprotein expressed on the surface of neurons. It mediates cell-to-cell adhesion and, through its interaction with FGFR1, triggers signalling cascades that drive neurite outgrowth and synapse maturation. NCAM is essential to normal brain development and continues to play a role in adult plasticity. The FGL peptide is a synthetic mimetic of NCAM's key functional motif.
Neprilysin
A zinc metallopeptidase (also called neutral endopeptidase) that degrades enkephalins, substance P, and amyloid-beta.
Neprilysin is one of the principal enkephalinases. It is also one of the brain's main amyloid-beta-degrading enzymes, which has made it a target of interest in Alzheimer's research. Selank's anxiolytic mechanism involves inhibition of neprilysin and related peptidases, raising the active life of endogenous enkephalins.
Neurogenesis (adult)
The generation of new neurons from neural stem cells in the adult brain.
Adult neurogenesis is restricted in mammals to a few regions, most prominently the dentate gyrus of the hippocampus. New hippocampal neurons appear to play a role in pattern separation and contextual learning. Adult neurogenesis declines with age and with chronic stress; several research peptides are studied for their capacity to support or restore the process, though direct evidence of clinically meaningful enhancement in humans remains limited.
Neurotrophin
A family of growth factors — BDNF, NGF, NT-3, NT-4 — that support neuron survival, growth, and differentiation.
The neurotrophins are structurally related small proteins that bind Trk family receptors. BDNF and NGF are the two most studied; NT-3 and NT-4/5 round out the family. They share a common framework but have distinct receptor preferences and distinct roles in different neuronal populations. Research peptides that 'induce neurotrophins' generally raise BDNF and NGF specifically.
NGF
Nerve growth factor — a neurotrophin closely related to BDNF, supporting neuronal survival and differentiation.
Nerve growth factor was the first neurotrophin discovered (Rita Levi-Montalcini and Stanley Cohen, Nobel Prize 1986) and remains the prototype of the family. NGF binds TrkA receptors and supports the survival of cholinergic neurons in the basal forebrain — the population most vulnerable to age-related decline in Alzheimer-type pathology. Several peptides studied for cognitive effects raise NGF expression alongside BDNF; the dual induction is more characteristic of the family than either neurotrophin alone.
NMDA receptor
A glutamate receptor essential to long-term potentiation and learning.
The NMDA receptor is a glutamate-gated ion channel that conducts calcium when both glutamate is bound and the postsynaptic membrane is depolarised. This coincidence-detection property makes it central to the induction of long-term potentiation. Several research peptides modulate glutamatergic tone indirectly — Noopept is the most-characterised — and the NMDA receptor is the principal downstream effector through which those modulatory effects become learning-relevant.
Peptidase
An enzyme that cleaves peptide bonds, breaking down peptides and proteins.
Peptidases (also called proteases) hydrolyse the peptide bonds that link amino acids. The two principal classes affecting short therapeutic peptides are aminopeptidases (cleaving from the N-terminus) and carboxypeptidases (cleaving from the C-terminus). Peptides intended for sustained CNS action are commonly modified at one or both termini to block these enzymes, which is exactly what the 'N-acetyl ... amidate' modifications in N-Acetyl Semax and N-Acetyl Selank achieve.
Peptidomimetic
A non-peptide molecule designed to reproduce the biological activity of a peptide while improving stability.
Peptidomimetics retain the key spatial features of a peptide's bioactive conformation while replacing peptide bonds with chemistry more resistant to proteolytic degradation. They are designed for oral bioavailability, longer half-life, and improved blood-brain barrier penetration. Noopept is the canonical small-peptidomimetic cognitive enhancer in the research-peptide adjacent literature.
Prefrontal cortex
The forward region of the frontal lobe, supporting working memory, attention control, and executive function.
The prefrontal cortex is the principal substrate for sustained attention, working memory, and executive control. It is the brain region most often probed by 'focus' and 'attention' endpoints in cognitive research. Several of the peptides on this site — Semax, Noopept — produce measurable prefrontal effects in animal and early-phase human research.
Racetam
A class of synthetic compounds (piracetam, aniracetam, oxiracetam, others) studied for cognitive effects, structurally distinct from peptides.
The racetam family is built around a pyrrolidone core and dates to the 1960s, beginning with piracetam. Mechanistically the racetams act on AMPA receptors, membrane fluidity, and cholinergic transmission. They are pharmacologically distinct from research peptides but occupy a partially overlapping cognitive-enhancement niche in research practice. Noopept is sometimes grouped with the racetams because of its peptidomimetic structure; mechanistically it shares more with the Russian cognitive peptide family.
REM sleep
Rapid eye movement sleep — the stage associated with vivid dreaming and procedural memory consolidation.
REM sleep alternates with non-REM sleep across the night, with REM episodes growing longer toward morning. REM is the principal substrate for procedural and emotional-memory consolidation. Many anxiolytic drugs suppress REM; the fact that Selank does not has been argued as an advantage in research protocols where preserving sleep architecture matters.
Research chemical
A substance sold for laboratory use only, not licensed as a medicine for human use.
The phrase 'research chemical' is a regulatory category, not a chemical one. It denotes a compound that is not a controlled drug, not a licensed medicine, and is supplied strictly for in vitro and preclinical laboratory use. All peptides discussed on this site fall into that category in the United Kingdom. Importation or supply for human consumption is not permitted under the Human Medicines Regulations 2012, even though the substances themselves are not controlled under the Misuse of Drugs Act 1971.
Slow-wave sleep
Stage N3 sleep — the deepest non-REM stage, characterised by delta-wave EEG activity and essential for memory consolidation.
Slow-wave sleep occurs predominantly in the first half of the night and is the dominant substrate for the consolidation of declarative memory. Disruption of slow-wave sleep degrades next-day learning and is implicated in long-term cognitive decline when chronic. Peptides that support slow-wave architecture — DSIP being the prototype — have a plausible indirect cognitive benefit via this mechanism.
Synaptogenesis
The formation of new synaptic connections between neurons.
Synaptogenesis is most active during development but persists at lower rates throughout adult life. Adult synaptogenesis is the cellular basis for ongoing learning and recovery from neural injury. Research peptides that promote synaptogenesis — Dihexa via c-Met, FGL via FGFR1, Cerebrolysin via multiple neurotrophic factor mimics — are candidates for studying age-related cognitive decline and post-injury recovery.
Trk receptors (TrkA, TrkB, TrkC)
The receptor tyrosine kinases that bind neurotrophins and trigger downstream growth and survival signalling.
Trk receptors are the principal high-affinity receptors for the neurotrophin family. TrkA binds NGF, TrkB binds BDNF and NT-4/5, TrkC binds NT-3. Activation triggers PI3K-Akt (survival) and MAPK (differentiation and plasticity) signalling cascades, plus PLCγ-mediated calcium release. The downstream pathways are shared with other receptor tyrosine kinases including c-Met and FGFR1, which is why peptides acting on different upstream receptors can produce overlapping pro-cognitive effects.
Tuftsin
An endogenous tetrapeptide (Thr-Lys-Pro-Arg) with immunomodulatory effects; the parent of Selank.
Tuftsin is a four-amino-acid peptide released by proteolytic cleavage of the Fc region of immunoglobulin G. It activates phagocytic activity in macrophages and neutrophils. Endogenous tuftsin has a vanishingly short half-life; Selank was engineered to extend it by adding a stable proline-glycine-proline C-terminal tail, producing a peptide with anxiolytic activity (via enkephalinase inhibition) alongside the inherited immunomodulatory effects.