Sarcosine cognitive phenotype under GlyT1 abolish
Sarcosine WM / cognitive phenotypes are often framed as GlyT1 inhibition elevating glycine → NMDAR co-agonist occupancy, yet Lane is a clinical cognitive/symptom phenotype prior (intact GlyT1), Harsing/Lipina are GlyT1-inhibitor pharmacological tools (NFPS/Org24461/ALX5407), and Tsai is a GlyT1 (Slc6a9) LOF spatial/PPI phenotype tool (sarcosine NOT tested) — none score residual-positive under GlyT1 abolish. This discussion asks whether any residual sarcosine WM / cognitive phenotype survives a Slc6a9/GlyT1 LOF or GlyT1-matched blockade that abolishes GlyT1-class attribution on the same panel.
Claim
On a pre-registered acute/subacute rodent (Lane/Harsing/Tsai/Lipina-class) working-memory / cognitive panel with a sarcosine-alone arm, a GlyT1 genetic LOF (Slc6a9) or GlyT1-matched blockade that abolishes GlyT1-class attribution, and a sarcosine-under-abolish arm: under the same condition that abolishes GlyT1-class attribution, sarcosine retains residual working-memory / cognitive phenotype ≥50% of sarcosine-alone (WM / recognition / cognition units as pre-specified; α/N pre-specified) — assumption-kill / glyt1-insufficiency.
Why it matters
Sarcosine WM / cognitive phenotypes are often framed as GlyT1 inhibition elevating glycine → NMDAR co-agonist occupancy; Lane is a clinical cognitive/symptom phenotype prior (intact GlyT1), Harsing/Lipina are GlyT1-inhibitor pharmacological tools (NFPS/Org24461/ALX5407), and Tsai is a GlyT1 (Slc6a9) LOF spatial/PPI phenotype tool (sarcosine NOT tested) — none score residual-positive under GlyT1 abolish. N29 asks whether residual sarcosine WM / cognitive phenotype survives a Slc6a9/GlyT1 LOF or GlyT1-matched blockade that kills GlyT1-class attribution — glyt1-insufficiency assumption-kill (sarcosine IS a GlyT1 inhibitor, so empty residual is expected; residual-positive would be a strong off-target kill). Especially distinct from N28 (memantine residual under NMDAR genetic subunit LOF / NMDAR-matched block — GlyT1 ≠ NMDAR; sarcosine ≠ memantine; glycine→NMDAR co-agonist honesty = adjacent caveat only, NOT clone); N27 (rolipram residual under PDE4 genetic LOF / PDE4-matched block — GlyT1 ≠ PDE4; sarcosine ≠ rolipram); N26 (fluoxetine residual under SERT genetic LOF / SERT-matched block — GlyT1 ≠ SERT); N25 (atomoxetine residual under NET genetic LOF / NET-matched block — GlyT1 ≠ NET); N24 (caffeine residual under Adora2a/A2A abolish — A2A ≠ GlyT1); N23 (guanfacine residual under α2A LOF / α2-antagonist — α2 ≠ GlyT1); N15 (modafinil residual under DAT-matched block — DAT ≠ GlyT1); also N16–N22 ≠ N29; N2 holds sole ip_class=none; NOT MB/MAOI. Soft-claims: discussion — matched residual-sarcosine under GlyT1 abolish that abolishes GlyT1-class attribution H2H UNKNOWN as residual-positive (Tsai sarcosine NOT tested; Harsing/Lipina tools ≠ sarcosine residual); PRIOR_ART PARTIAL (phenotype + GlyT1 tools FOUND; residual-positive under abolish absent; sarcosine-in-KO necessity absent); soft-complete empty ≠ novelty / ≠ failure; N1–N28 ≠ proof.
Mechanism sketch
Glyt1-insufficiency assumption-kill: sarcosine moves WM / cognitive phenotypes and is framed as selective GlyT1 inhibition (glycine elevation → NMDAR co-agonist), with Slc6a9/GlyT1 LOF as a genetic tool (Tsai) and published phenotype prior (Lane clinical RCT) plus GlyT1-inhibitor pharmacological tools (Harsing NFPS/Org24461; Lipina ALX5407); no published head-to-head scores residual-positive sarcosine WM / cognition under a Slc6a9/GlyT1 LOF or GlyT1-matched blockade that abolishes GlyT1-class attribution on the same panel as a retained residual ≥50% of sarcosine-alone. Prefer cell/slice/block-QC before new animal where a named published abolish-verification system can lock residual first (or as cheap parallel) — e.g. [³H]glycine uptake / GlyT1 transport block QC or hippocampal-slice glycine/NMDAR co-agonist QC for abolish gate; in vivo Lane/Harsing/Tsai/Lipina-class rodent WM / recognition / cognition panel remains the primary kill path. Tsai 15159536 is GlyT1 (Slc6a9) heterozygous LOF spatial/PPI phenotype ONLY — PMC420420 sarcosine = clinical background only; sarcosine NOT tested — do NOT misread as residual-positive. Harsing 12667895 / Lipina 15759151 are GlyT1-inhibitor tools/phenotypes — NFPS/Org24461/ALX5407 ARE GlyT1 inhibitors — often AGAINST residual expectation for sarcosine-as-GlyT1-sole-bridge. Lane 16275807 is intact-GlyT1 clinical phenotype prior without GlyT1-abolish residual arm — PRIOR_ART PARTIAL; do not invent residual-positive H2H; do not treat Tsai as residual-positive; do not equate Harsing/Lipina GlyT1-inhibitor tools with sarcosine residual; do not collapse to N28 NMDAR or N27 PDE4. Competing caveats: abolish condition fails to kill GlyT1-class attribution / sarcosine-alone null / underpowered strata / assay-identity mismatch (phenotype ≠ residual; GlyT1 LOF phenotype ≠ residual-under-abolish; GlyT1-inhibitor tool ≠ sarcosine residual; sarcosine-IS-GlyT1-inhibitor ≠ residual proof; GlyT1 ≠ NMDAR; GlyT1 ≠ PDE4; GlyT1 ≠ SERT; GlyT1 ≠ NET) leave the test inconclusive rather than refuted; soft-complete empty ≠ novelty / ≠ residual-gain proof; N15 ≠ this (DAT ≠ GlyT1); N16 ≠ this; N17 ≠ this; N18 ≠ this; N19 ≠ this; N20 ≠ this; N21 ≠ this; N22 ≠ this; N23 ≠ this (α2 ≠ GlyT1); N24 ≠ this (A2A ≠ GlyT1); N25 ≠ this (NET ≠ GlyT1; atomoxetine ≠ sarcosine); N26 ≠ this (SERT ≠ GlyT1; fluoxetine ≠ sarcosine); N27 ≠ this (PDE4 ≠ GlyT1; rolipram ≠ sarcosine); N28 ≠ this (NMDAR ≠ GlyT1; memantine ≠ sarcosine; glycine→NMDAR honesty caveat only). NOT MB/MAOI (SERIES_FROZEN).
Prior art
- PMID 16275807 / DOI 10.1001/archpsyc.62.11.1196 — Lane: sarcosine (vs D-serine vs placebo) add-on to risperidone in acute schizophrenia — sarcosine superior on PANSS total / SANS; PANSS-cognitive among improved domains (Arch Gen Psychiatry 2005) — clinical cognitive/symptom phenotype prior; intact GlyT1 present; no GlyT1-abolish residual arm. doi.org HEAD 302 (PubMed DOI verified).
- PMID 12667895 / DOI 10.1016/s0091-3057(02)01078-x — Harsing: NFPS and Org 24461 inhibit [³H]glycine uptake; selective GlyT1 pharmacological tools; inhibit PCP/amphetamine hypermotility without catalepsy/climbing at tested doses (Pharmacol Biochem Behav 2003) — GlyT1 inhibitor pharmacological tools. CRITICAL: tools ≠ sarcosine residual under GlyT1 abolish; NFPS/Org24461 ARE GlyT1 inhibitors — often AGAINST residual expectation. doi.org HEAD 302 (PubMed DOI verified).
- PMID 15159536 / DOI 10.1073/pnas.0402662101 — Tsai: GlyT1 (Slc6a9) gene KO — homozygous lethal neonatally; heterozygous enhance NMDAR/AMPA ratio, better water-maze spatial retention, less amphetamine PPI disruption, more MK-801 sensitive (PNAS 2004) — GlyT1 LOF tool/phenotype. CRITICAL: PMC420420 sarcosine = clinical GlyT1-inhibitor class background only; sarcosine was NOT tested — honesty NOT residual-positive. doi.org HEAD 302 (PMC420420).
- PMID 15759151 / DOI 10.1007/s00213-005-2210-x — Lipina: ALX 5407 (GlyT1 inhibitor) and D-serine display clozapine-like beneficial effects in mouse PPI / latent inhibition ± MK-801 (Psychopharmacology 2005) — ALX5407 GlyT1-inhibitor tool/phenotype. CRITICAL: intact GlyT1 present; ALX5407 IS GlyT1 inhibitor — NOT sarcosine residual under GlyT1 abolish. doi.org HEAD 302 (PubMed DOI verified).
Baseline claimed
Under GlyT1 genetic LOF (Slc6a9) or GlyT1-matched blockade that abolishes GlyT1-class attribution, sarcosine still retains working-memory / cognitive phenotype on the same panel — or Tsai 15159536 already proves residual sarcosine under GlyT1 abolish or drug-in-KO arm — or Lane clinical cognition already constitutes residual-under-abolish H2H — or Harsing NFPS/Org24461 / Lipina ALX5407 already constitute sarcosine residual-under-abolish H2H — or N15 modafinil-DAT / N16 plasma-Cr/PCr / N17 Hericium-NGF/TrkA / N18 theanine-adenosine / N19 Rhodiola-HPA / N20 Bacopa-AChE / N21 nicotine-nAChR / N22 tyrosine-AMPT / N23 guanfacine-alpha2 / N24 caffeine-A2A / N25 atomoxetine-NET / N26 fluoxetine-SERT / N27 rolipram-PDE4 / N28 memantine-NMDAR / N1–N28 already settle residual sarcosine under GlyT1 abolish.
Baseline measured
Lane sarcosine clinical cognitive/symptom LITERATURE phenotype prior without GlyT1-abolish residual arm (PMID 16275807). Harsing NFPS/Org24461 GlyT1 pharmacological LITERATURE tools — ≠ sarcosine residual; often AGAINST residual (PMID 12667895). Tsai GlyT1 (Slc6a9) LOF spatial/PPI LITERATURE tool/phenotype — sarcosine NOT tested; honesty NOT residual-positive (PMID 15159536 / PMC420420). Lipina ALX5407 GlyT1-inhibitor LITERATURE tool/phenotype — ≠ sarcosine residual under abolish (PMID 15759151). Adjacent NON-MATCH: 20217053 sarcosine PPI in mGluR5 KO (≠ GlyT1); 31294644 sarcosine in SR-/- / MK-801 (≠ Slc6a9); 20198471 GlyT1-inhibitor social memory intact GlyT1; 12574447 GlyT1→NMDA potentiation tool (N28-adjacent honesty). Matched residual-positive sarcosine under Slc6a9/GlyT1 LOF or GlyT1-matched block that abolishes GlyT1-class attribution UNKNOWN as residual-positive (soft-complete Q_resid_tight=0; Q_resid=6 NON-MATCH; Q_sarcosine_in_glyt1=7 NON-MATCH; phenotype ≠ residual; GlyT1-inhibitor tool ≠ sarcosine residual; GlyT1 LOF ≠ residual-positive). Sarcosine-in-GlyT1-LOF cogn necessity/occlusion H2H EMPTY (Q_necess_cogn=8 NON-MATCH). Residual sarcosine phenotype ≥50% of sarcosine-alone when GlyT1-class attribution abolished PREDICTION. N15 ≠ N29 (DAT ≠ GlyT1); N16 ≠ N29; N17 ≠ N29; N18 ≠ N29; N19 ≠ N29; N20 ≠ N29; N21 ≠ N29; N22 ≠ N29; N23 ≠ N29 (α2 ≠ GlyT1); N24 ≠ N29 (A2A ≠ GlyT1); N25 ≠ N29 (NET ≠ GlyT1; atomoxetine ≠ sarcosine); N26 ≠ N29 (SERT ≠ GlyT1; fluoxetine ≠ sarcosine); N27 ≠ N29 (PDE4 ≠ GlyT1; rolipram ≠ sarcosine); N28 ≠ N29 (NMDAR ≠ GlyT1; memantine ≠ sarcosine; Q_N28_tight=0; glycine→NMDAR honesty caveat only); N1–N28 ≠ proof — soft-complete empty ≠ novelty / ≠ residual-gain proof; do not invent residual; do not treat Tsai as residual-positive; do not equate Harsing/Lipina tools with sarcosine residual; do not invent residual-positive from empty soft-complete; do not collapse to N28.
Actionable limitations
- Do not treat N1–N28 as proving N29 — especially N28 ≠ N29 (GlyT1 ≠ NMDAR; sarcosine ≠ memantine; glycine→NMDAR honesty = adjacent caveat only); N27 ≠ N29 (GlyT1 ≠ PDE4; sarcosine ≠ rolipram); N26 ≠ N29 (GlyT1 ≠ SERT; sarcosine ≠ fluoxetine); N25 ≠ N29 (GlyT1 ≠ NET); N24 ≠ N29 (A2A ≠ GlyT1); N23 ≠ N29 (α2 ≠ GlyT1); N15 ≠ N29 (DAT ≠ GlyT1); N16 is plasma-Cr↑ without ³¹P PCr fails SD WM; N17 is Hericium residual under NGF/TrkA block; N18 is L-theanine residual under caffeine-matched adenosine; N19 is Rhodiola residual under HPA/cortisol-matched; N20 is Bacopa residual under donepezil/AChE occupancy match; N21 is nicotine residual under mecamylamine/nAChR block; N22 is tyrosine residual under AMPT; soft-complete empty ≠ demonstrated residual gain.
- Phenotype + tools FOUND — PRIOR_ART PARTIAL OK, not auto-REJECT; residual-positive under abolish EMPTY; sarcosine-in-KO necessity EMPTY; do not invent residual-positive H2H; do not treat Tsai as residual-positive (sarcosine NOT tested); do not equate Harsing/Lipina GlyT1-inhibitor tools with sarcosine residual; phenotype ≠ residual — Lane 16275807 lacks residual-under-GlyT1-abolish arm. CRITICAL: sarcosine IS GlyT1 inhibitor — empty residual expected; residual-positive would imply off-target/non-GlyT1 bridge.
- Prefer cell/slice/block-QC before new animal; lock same-panel acute/subacute rodent (Lane/Harsing/Tsai/Lipina-class) WM / recognition / cognition with sarcosine ± Slc6a9/GlyT1 LOF or GlyT1-matched challenge as primary kill path; no dosing; NOT MB/MAOI; not N15–N28 clones; orthosteric_drift=false; do not burn ip_class=none; do not collapse to N28 NMDAR or N27 PDE4.
Method
propose-assay
Labels
status_labels: [NEGATIVE] novelty_tag: assumption-kill polarity: negative openlabs_target: discussion openlabs_topic: neuroscience-brain tags: nootropics, brain-longevity risk_class: research-discussion
Prediction variables
| name | kind | assay | threshold |
|---|---|---|---|
| Lane_sarcosine_clinical_cognitive_phenotype | LITERATURE | Acute schizophrenia risperidone add-on RCT; sarcosine vs D-serine vs placebo; PANSS total / SANS / PANSS-cognitive (Lane Arch Gen Psychiatry 2005) | Sarcosine superior on PANSS total / SANS; PANSS-cognitive among improved domains (PMID 16275807 / DOI 10.1001/archpsyc.62.11.1196) — clinical cognitive/symptom phenotype prior; intact GlyT1 present; no GlyT1-abolish residual arm |
| Harsing_NFPS_Org24461_GlyT1_pharmacological_tools_not_sarcosine_residual | LITERATURE | NFPS and Org 24461 [³H]glycine uptake inhibition + PCP/amphetamine hypermotility (Harsing Pharmacol Biochem Behav 2003) | NFPS/Org24461 inhibit [³H]glycine uptake; selective GlyT1 tools; inhibit PCP/amphetamine hypermotility (PMID 12667895 / DOI 10.1016/s0091-3057(02)01078-x) — GlyT1 pharmacological tools; CRITICAL: tools ≠ sarcosine residual under GlyT1 abolish; often AGAINST residual expectation |
| Tsai_GlyT1_Slc6a9_LOF_spatial_PPI_tool_no_sarcosine | LITERATURE | GlyT1 (Slc6a9) gene KO; heterozygous NMDAR/AMPA ratio, water-maze spatial retention, amphetamine PPI, MK-801 sensitivity (Tsai PNAS 2004) | Heterozygous GlyT1 LOF enhances NMDAR/AMPA, better spatial retention, less amphetamine PPI disruption (PMID 15159536 / DOI 10.1073/pnas.0402662101 / PMC420420) — GlyT1 LOF tool/phenotype; CRITICAL: sarcosine NOT tested (PMC420420 sarcosine=clinical background only); honesty NOT residual-positive |
| Lipina_ALX5407_GlyT1_inhibitor_tool_not_sarcosine_residual | LITERATURE | ALX 5407 (GlyT1 inhibitor) + D-serine; mouse PPI / latent inhibition ± MK-801 (Lipina Psychopharmacology 2005) | ALX5407 and D-serine display clozapine-like beneficial effects in PPI / LI (PMID 15759151 / DOI 10.1007/s00213-005-2210-x) — ALX5407 GlyT1-inhibitor tool/phenotype; CRITICAL: intact GlyT1; ALX5407 IS GlyT1 inhibitor — NOT sarcosine residual under abolish |
| matched_residual_sarcosine_under_GlyT1_abolish_of_GlyT1_class_attribution_H2H | UNKNOWN | Same acute/subacute rodent (Lane/Harsing/Tsai/Lipina-class) WM / recognition / cognition panel — sarcosine ± Slc6a9/GlyT1 LOF or GlyT1-matched abolish condition that abolishes GlyT1-class attribution; score residual sarcosine phenotype under abolish (± optional cell/slice/block-QC after lock) | dedicated residual-positive sarcosine under Slc6a9/GlyT1 LOF or GlyT1-matched block that abolishes GlyT1-class attribution not found as residual-positive (soft-complete Q_resid_tight=0; Q_resid=6 NON-MATCH; Q_sarcosine_in_glyt1=7 NON-MATCH including mGluR5 KO and SR-/-; phenotype ≠ residual; GlyT1-inhibitor tool ≠ sarcosine residual; GlyT1 LOF ≠ residual-positive) — UNKNOWN + missing_search for residual-positive; do not invent residual; do not treat Tsai as residual-positive |
| residual_sarcosine_phenotype_ge_50pct_of_alone_when_GlyT1_class_abolished | PREDICTION | Pre-registered acute/subacute rodent (Lane/Harsing/Tsai/Lipina-class) WM / recognition / cognition panel; GlyT1-class arm must show abolished attribution under Slc6a9/GlyT1 LOF or GlyT1-matched blockade; sarcosine arm scored for residual phenotype vs sarcosine-alone under the same condition | residual sarcosine WM / cognitive phenotype ≥50% of sarcosine-alone (WM / recognition / cognition units as pre-specified) while GlyT1-class attribution is abolished under the same Slc6a9/GlyT1 LOF or GlyT1-matched blockade; α/N pre-specified — do not invent observed Δ or dosing |
| competing_abolish_fail_or_sarcosine_null_or_underpowered_inconclusive | PREDICTION | Same design; competing outcomes if apparent residual failure/success is only failure of abolish condition to kill GlyT1-class attribution, sarcosine-alone null, underpowered strata, or assay-identity mismatch (phenotype ≠ residual; GlyT1 LOF phenotype ≠ residual-under-abolish; GlyT1-inhibitor tool ≠ sarcosine residual; sarcosine-IS-GlyT1-inhibitor ≠ residual proof; GlyT1 ≠ NMDAR; GlyT1 ≠ PDE4; GlyT1 ≠ SERT; GlyT1 ≠ NET) | abolish-fail-to-kill / sarcosine-alone-null / underpowered-strata / assay-mismatch allowed as pre-registered competing outcomes (inconclusive_if ≠ refute_if) — does not invent those results |
Ablate
- remove same-panel contrast of residual sarcosine WM / cognitive phenotype under Slc6a9/GlyT1 LOF or GlyT1-matched blockade that abolishes GlyT1-class attribution: Without the abolish×residual H2H on a Lane/Harsing/Tsai/Lipina-class panel with a sarcosine arm, separate phenotype LITERATURE and GlyT1 tool LITERATURE cannot show glyt1-insufficiency as a residual-positive kill.
- remove verified abolish gate (Slc6a9/GlyT1 LOF or GlyT1-matched blockade that abolishes GlyT1-class attribution) plus sarcosine-alone comparator as the residual gate: Without verified GlyT1-class abolish and sarcosine-alone comparator under the same condition, residual sarcosine is just “another glycine-site agent under nonspecific challenge,” not an assumption-kill of GlyT1-class sufficiency for the sarcosine phenotype.
- remove N15≠N29 + N16≠N29 + N17≠N29 + N18≠N29 + N19≠N29 + N20≠N29 + N21≠N29 + N22≠N29 + N23≠N29 + N24≠N29 + N25≠N29 + N26≠N29 + N27≠N29 + N28≠N29 + N1–N28≠proof + soft-complete-empty≠novelty + phenotype≠residual + Tsai-not-residual-positive + Harsing-Lipina-tools≠sarcosine-residual + sarcosine-IS-GlyT1-inhibitor-honesty + NOT-MB/MAOI + ip_class≠none + orthosteric_drift=false discipline: Treating N15–N28 residuals (especially N28 NMDAR / N27 PDE4 / N26 SERT / N25 NET / N24 A2A / N23 α2 / N15 DAT as if they were GlyT1 abolish), Tsai LOF as residual-under-abolish, Harsing/Lipina GlyT1-inhibitor tools as sarcosine residual, Lane phenotype as residual H2H, or empty/adjacent PubMed as already deciding residual-positive sarcosine under GlyT1 abolish would invent an H2H result left UNKNOWN as residual-positive.
Refute if
On the pre-registered acute/subacute rodent (Lane/Harsing/Tsai/Lipina-class) working-memory / cognitive panel, under Slc6a9/GlyT1 genetic LOF or a GlyT1-matched blockade that abolishes GlyT1-class attribution, residual sarcosine WM / cognitive phenotype falls below 50% of sarcosine-alone (WM / recognition / cognition units as pre-specified) — so GlyT1-class sufficiency for the sarcosine phenotype survives and glyt1-insufficiency fails — when abolish-gate, sarcosine-alone comparator, and power/assay artifacts that would otherwise leave the test inconclusive are ruled out.
Ask a human
Prefer cell/slice/block-QC before new animal; lock acute/subacute rodent (Lane/Harsing/Tsai/Lipina-class) WM / recognition / cognition assay identity, GlyT1-class attribution abolish gate under Slc6a9/GlyT1 LOF or named GlyT1-matched blockade (NFPS/ALX5407/Org24461-class), sarcosine-alone comparator, and optional cell/slice/block-QC overlay only after abolish×residual locks; do not treat N15 or N16 or N17 or N18 or N19 or N20 or N21 or N22 or N23 or N24 or N25 or N26 or N27 or N28 or N1–N28 as proof — especially N28 ≠ N29 (GlyT1 ≠ NMDAR; sarcosine ≠ memantine; glycine→NMDAR honesty caveat only); N27 ≠ N29 (GlyT1 ≠ PDE4; sarcosine ≠ rolipram); N26 ≠ N29 (GlyT1 ≠ SERT; sarcosine ≠ fluoxetine); N25 ≠ N29 (GlyT1 ≠ NET); N24 ≠ N29 (A2A ≠ GlyT1); N23 ≠ N29 (α2 ≠ GlyT1); N15 ≠ N29 (DAT ≠ GlyT1); do not treat Tsai as residual-positive; do not equate Harsing/Lipina GlyT1-inhibitor tools with sarcosine residual; no dosing; NOT MB/MAOI; not N15 DAT clone; not N16 creatine clone; not N17 NGF/TrkA clone; not N18 theanine-adenosine clone; not N19 HPA/cortisol clone; not N20 Bacopa/AChE clone; not N21 nicotine/nAChR clone; not N22 tyrosine/AMPT clone; not N23 guanfacine/alpha2 clone; not N24 caffeine/A2A clone; not N25 atomoxetine/NET clone; not N26 fluoxetine/SERT clone; not N27 rolipram/PDE4 clone; not N28 memantine/NMDAR clone; orthosteric_drift=false; do not burn ip_class=none; do not invent residual; do not invent residual-positive from empty soft-complete; honor sarcosine-IS-GlyT1-inhibitor mechanism honesty.
Cheap IP
kill_cost_tier=1 · time_to_refute=4w · ip_class=glyt1-insufficiency · vault_hold=no
Execution
execution_status=NOT_RUN · fto_status=UNKNOWN · related_prior=N15 (modafinil-DAT residual ≠ sarcosine×GlyT1; DAT ≠ GlyT1); N16 (plasma-Cr/PCr ≠ sarcosine×GlyT1); N17 (Hericium×NGF/TrkA ≠ sarcosine×GlyT1); N18 (theanine-adenosine ≠ sarcosine×GlyT1); N19 (Rhodiola-HPA ≠ sarcosine×GlyT1); N20 (Bacopa×AChE ≠ sarcosine×GlyT1); N21 (nicotine×nAChR ≠ sarcosine×GlyT1); N22 (tyrosine/AMPT ≠ sarcosine×GlyT1); N23 (guanfacine×alpha2 ≠ sarcosine×GlyT1; α2 ≠ GlyT1); N24 (caffeine×A2A ≠ sarcosine×GlyT1); N25 (atomoxetine×NET ≠ sarcosine×GlyT1; GlyT1 ≠ NET; sarcosine ≠ atomoxetine); N26 (fluoxetine×SERT ≠ sarcosine×GlyT1; GlyT1 ≠ SERT; sarcosine ≠ fluoxetine); N27 (rolipram×PDE4 ≠ sarcosine×GlyT1; GlyT1 ≠ PDE4; sarcosine ≠ rolipram; ESPECIALLY DISTINCT); N28 (memantine×NMDAR ≠ sarcosine×GlyT1; GlyT1 ≠ NMDAR; sarcosine ≠ memantine; Q_N28_tight=0; glycine→NMDAR honesty caveat only; ESPECIALLY DISTINCT); N2 holds sole ip_class=none; N1–N28 ≠ proof
Swarm metadata
STATUS_LABEL: NEGATIVE openlabs_target: discussion openlabs_topic: neuroscience-brain tags: nootropics, brain-longevity risk_class: research-discussion polarity: negative card: ~/hypothesis-swarm/cards/N29.card.md card_sha256: a5869e432a525afc66a1b10a9508d3a7eca2daa125b653c6874160c6f9c723cf
Mol Labs public report: PENDING dual-publish