Cognition, mood & sleep

Where would you like to start?

These three articles answer different questions. All remain under editorial review; grouping them here is not a comparison of treatment effectiveness.

• FGL: why does the exact peptide construct matter? Follow the differences between FGLL, FGLS and the mouse-study material, and what the early human study actually measured.
• GB-115: which patients were studied? Follow the clinical studies, their population limits and the unresolved identity descriptions in the sources.
• Orexin-A: what did the human experiments measure? Follow the smell, sleep, attention and nerve-activity findings, including negative results and uncertainty about delivery into the brain.

A set of neuropeptides is studied for effects on cognition, mood, anxiety, neuroprotection, and sleep. A recurring theme in this area is that the evidence is often regional (much of it from Russian research) or older and inconsistent, and rarely replicated in large international trials.

Semax and Selank are Russian-developed peptides: Semax studied mainly for nootropic/neuroprotective effects (often linked to BDNF), Selank mainly as an anxiolytic. Both are registered as medicines in Russia but not approved by the FDA or EMA, and their evidence base lacks broad independent replication. Cerebrolysin is not a single peptide but a porcine-brain peptide mixture, marketed in many countries for stroke and dementia, though independent Cochrane reviews have not confirmed benefit for stroke. DSIP (delta sleep-inducing peptide) is the weakest-supported of the group: despite its name, its sleep effects are inconsistent and it has no established receptor or mechanism.

FGL is linked here as a research record awaiting editorial review. Its article separates the peptide constructs, early human studies and preclinical findings; inclusion in this hub does not establish a treatment benefit.

Conditions people ask about

Popular videos and high-claim content in this area promise to "reverse," "cure," or dramatically slow conditions like Alzheimer's, Parkinson's, anxiety, and depression with neurotrophic or "mitochondrial" peptides. Those confident promises run well ahead of what can be shown: inclusion on this site does not establish approval for the conditions below, and we found no controlled human evidence for the reversal claims in the literature we can reach. A caveat worth stating plainly up front: not finding a study here does not make a claim false. Much relevant work is simply outside what we can index — paywalled journals, Russian, Chinese and other regional literature, clinical-practitioner experience, conference abstracts, and unpublished or proprietary data — and absence of evidence in the accessible record is not the same as evidence of absence. The notes here are meant to answer common searches honestly, without either overselling or overclaiming to have disproven anything. Every condition below is a matter for a licensed clinician and a proper diagnostic workup — a research peptide is not a substitute for diagnosis or care.

Dementia and Alzheimer's disease

High-claim content frames Alzheimer's and other dementias as "reversible," or at least dramatically slowable, with a neurotrophic-peptide protocol that supposedly regrows brain tissue and restores memory. What we can actually confirm is narrower: no compound on this wiki is an FDA- or EMA-approved treatment for Alzheimer's or any dementia, and we found no controlled human evidence in the accessible literature that any of them reverses cognitive decline — which is a limit of what is indexed and reachable, not a demonstration that no such effect exists. The most-studied one is approved as a neurotrophic agent in some countries but not by the FDA or EMA, and independent Cochrane reviews found no clear benefit for vascular dementia and only very-low-certainty signals in Alzheimer's [Human]. Dementia is a serious diagnosis requiring a licensed clinician and proper workup — a research peptide is not a substitute for diagnosis or care. Compounds discussed in this context: Cerebrolysin, a porcine-brain-derived peptide/amino-acid mixture approved as a neurotrophic agent in several countries but not by the FDA or EMA — the most-studied compound here for dementia, yet Cochrane reviews report no clear benefit for vascular dementia and only very-low-certainty, disputed signals in Alzheimer's, with a probable increase in non-fatal serious adverse events (studied, effectiveness not established) [Human]; Humanin, a mitochondrial-derived peptide first identified in Alzheimer's research for rescuing neurons from cell death in the lab, whose Alzheimer's link — in the record we can access — is at the cell and animal level, with no completed human therapeutic trials that we could locate (preclinical research interest) [In vitro/Animal]; Pinealon, a synthetic Glu-Asp-Arg tripeptide from the Khavinson "bioregulator" school marketed with neuroprotective/nootropic framing, with cognitive and Alzheimer's-model data in vitro and in rodents and older, single-group Russian human reports we could not find independent replication of (a research reagent, not approved anywhere) [Animal/In vitro]; and Cortagen, a synthetic Ala-Glu-Asp-Pro tetrapeptide from the same Khavinson lineage promoted as a brain "bioregulator," with thin, older, almost entirely preclinical evidence in the sources we searched and no published human clinical trial that we could locate (research reagent) [Animal/In vitro].

Newer "mitochondrial protocol" videos frame dementia as reversible by restoring cellular energy and route viewers to a specific set of compounds — worth naming, because they are exactly what people arrive searching for. None is an approved treatment for Alzheimer's or any dementia, and none has controlled human evidence of reversing cognitive decline: 5-Amino-1MQ is a small-molecule NNMT inhibitor (not a peptide) with only diet-induced-obese-mouse data and no human or Alzheimer's study [Animal]; MOTS-c is a mitochondrial-derived peptide studied in cells and mice for metabolism, whose only human testing was a discontinued analog and which does not cross the blood–brain barrier when given peripherally [Animal/In vitro]; NAD+ is a redox coenzyme (not a peptide) with small, inconsistent human pilot data, no established cognitive benefit, and an unapproved/compounded injectable form [Human — limited]; and BPC-157 has only animal gut–brain data [Animal]. The precise "studies" quoted for these (a "34% hippocampal NAD+" rise, a "44% memory" gain) could not be traced to any locatable paper. The one place this class has been tested in people — α7-nicotinic-receptor agonism, the mechanism behind the "nicotine is neuroprotective" claim — actually failed: the lead drug encenicline had its Phase 3 Alzheimer's program halted in 2015 for severe gastrointestinal harm, and a transdermal-nicotine trial in mild cognitive impairment (Newhouse et al., Neurology 2012) was a small, underpowered pilot, not a dementia-reversal result [Human]. A related framing — that "Alzheimer's is type 3 diabetes" and "amyloid is only a symptom" — rests on real but unsettled hypotheses: brain insulin resistance is a genuine, replicated postmortem association (Talbot et al., J Clin Invest 2012) [Human — observational], while "type 3 diabetes" (de la Monte, J Diabetes Sci Technol 2008), the mitochondrial-cascade hypothesis (Swerdlow & Khan, Med Hypotheses 2004), and amyloid-as-antimicrobial-peptide (Soscia/Moir/Tanzi, PLoS One 2010) are all legitimate, citable hypotheses — none proven, and "type 3 diabetes" is not an official diagnosis [Hypothesis]. The approved amyloid antibodies these videos call a "fraud" (lecanemab, donanemab) in fact produce modest but statistically significant slowing of decline (~27% and ~35% in their pivotal trials, NEJM 2023 and JAMA 2023) with real ARIA risk and rare deaths — a disclosed, regulator-reviewed trade-off, not a reversal and not a scam [Human].

Parkinson's disease

Popular videos suggest Parkinson's motor decline can be halted or reversed with "mitochondrial" and neurotrophic peptides that supposedly protect or regenerate dopamine neurons. No compound on this wiki is an approved treatment for Parkinson's disease, and we found no controlled human evidence in the accessible literature that any of them slows, halts, or reverses it — an absence in what we can reach rather than a proven absence of effect. Community discussion leans on general neuroprotection and mitochondrial rationales rather than Parkinson's-specific human trials, and among the mitochondrial candidates that have been formally tested, several missed their primary endpoints [Human]. Parkinson's is a serious neurological diagnosis that requires a licensed clinician — a research peptide is not a substitute for specialist care. Compounds discussed in this context: Cerebrolysin, marketed as a neurotrophic agent and studied in various neurological settings but with disputed evidence and no FDA/EMA approval, and no robust controlled human evidence we could locate that it changes the course of Parkinson's specifically (discussed, not established) [Human]; SS-31, a mitochondria-targeting tetrapeptide (elamipretide) that stabilizes cristae by binding cardiolipin, with an extensive but mixed human trial record and its only approval (2025 FDA accelerated approval) for the ultra-rare Barth syndrome, not Parkinson's — any Parkinson's use rests on investigational/preclinical rationale only [Human/Animal]; and Methylene Blue, a small-molecule redox dye (not a peptide) approved only for methemoglobinemia, whose "mitochondrial" neuroprotective appeal is, in the literature we can access, largely in vitro and animal with no controlled human evidence in Parkinson's that we could find, and which is a potent MAOI with real serotonin-syndrome risk (off-label and unproven for this) [In vitro/Animal].

Anxiety and "brain fog"

The community markets certain nootropic/anxiolytic peptides as a clean, non-pharmaceutical way to erase anxiety and clear "brain fog" within days, framed as an upgrade over prescription anti-anxiety medication. No compound on this wiki is FDA- or EMA-approved for an anxiety disorder, and "brain fog" is not a medical diagnosis but a symptom of many underlying conditions. The peptides discussed here rest, in the sources we can reach, largely on small, mostly Russian studies or on mechanism/animal work rather than large replicated Western trials — so from where we sit their anxiolytic effect in humans is best described as investigational and not established, which is a statement about the reachable evidence rather than a verdict that they do nothing. Persistent anxiety or cognitive complaints should be assessed by a licensed clinician to find the real cause — a research peptide is not a substitute for diagnosis or evidence-based treatment. Compounds discussed in this context: Selank, a synthetic tuftsin-analog heptapeptide registered as an anxiolytic in Russia but not FDA/EMA approved, whose anti-anxiety evidence rests, in what we can access, largely on small Russian studies and GABAergic/monoaminergic mechanism work without large replicated Western trials (studied, not established) [Human/Animal]; Semax, a Russian-registered ACTH(4-10) analog used as a nootropic/neuroprotective nasal medicine and not FDA/EMA approved, with cognition and attention claims relevant to "brain fog" coming mostly from Russian research linked to BDNF signaling that we could not find independently replicated (discussed, not established outside Russia) [Human/Animal]; BPC-157, a synthetic gastric-derived peptide with anxiolytic-like and neuroprotective effects reported, in the record we searched, only in animal "gut-brain axis" models, with no controlled human evidence for anxiety or brain fog located and no approval anywhere (preclinical rationale) [Animal]; and DSIP, delta sleep-inducing peptide sometimes cited for stress and the HPA axis, whose reported effects are inconsistent, which has no identified receptor, and whose accessible human data are sparse and dated with no controlled human evidence for anxiety that we could find (a research chemical, not a treatment) [Human/Animal].

Depression

High-claim content presents certain peptides as fast-acting, side-effect-free antidepressants that raise BDNF and "reset" mood without the downsides of SSRIs. No compound on this wiki is FDA- or EMA-approved for major depression, and we found no controlled human evidence in the accessible literature that any of them treats a depressive disorder — the antidepressant-like claims we can trace lead to animal models and BDNF-signaling mechanisms, or to small studies we could not find replicated, rather than to large randomized human antidepressant trials. That is a limit of the record we can reach, not proof of no effect. Depression is a serious, sometimes life-threatening condition that requires a licensed clinician; if you are struggling, seek professional help — a research peptide is not a substitute for diagnosis or treatment. Compounds discussed in this context: Semax, a Russian-registered ACTH(4-10) analog studied for neuroprotection and cognition and often discussed around BDNF, whose mood/antidepressant framing rests on mechanism and small Russian research rather than replicated human antidepressant trials in what we can access, and which is not FDA/EMA approved [Human/Animal]; Selank, a tuftsin-analog anxiolytic peptide registered in Russia and discussed for mood via monoaminergic and enkephalin-related mechanisms, but with small-study and animal-level evidence in the reachable record and no approved antidepressant indication (investigational at best) [Human/Animal]; BPC-157, reported to have antidepressant-like effects only in rodent forced-swim-type and gut-brain-axis models in the studies we found, with no located controlled human evidence for depression and no approval anywhere (preclinical signal) [Animal]; and Oxytocin, an approved obstetric hormone (Pitocin/Syntocinon) whose famous mood, bonding, and social-anxiety claims come from a separate body of mostly intranasal research that is mixed and often does not replicate — it is NOT an approved treatment for depression, and the depression-specific human evidence we can access is inconsistent (investigational for mood) [Human].

Understand the signals behind the claims

Use BDNF, NGF and CNTF to distinguish endogenous proteins from interventions studied in people. Follow the orexin system and HGF–MET for receptor relationships. The new records remain under review; each states what was studied and which identity or outcome remains uncertain.

Compare the evidence for GK-2, GSB-106 and GSB-214