Component

Acetylcholine

Acetylcholine

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. ChAT catalyzes reversible acetylcholine synthesis from choline and acetyl-CoA.

    Human choline acetyltransferase / CHAT → Acetylcholine source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/11172068.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39", "start_char": 0, "end_char": 1231, "text_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39"}
    experimental_model
    Human CHAT genetics, recombinant expression and enzyme kinetics
    exposure
    Ten recessive variants in five patients; nine mutant proteins assayed
    limitations
    Inherited enzyme defects, not a dietary choline-deficiency model. Acetyl-CoA and choline are distinct substrates.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human CHAT proteins; COS-cell and bacterial expression systems
    plain_language
    The neurotransmitter needs both the choline headgroup and an acetyl group supplied by acetyl-CoA.
    primary_references
    [choline-p11172068] Choline acetyltransferase mutations cause myasthenic syndrome associated with episodic apnea in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11172068/ DOI: 10.1073/pnas.98.4.2017
    tissue_or_cell_type
    Neuromuscular acetylcholine resynthesis

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 412–423

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CHAT genetics, recombinant expression and enzyme kinetics · source_derived_draft · unverified_draft

    ### choline-chat-acetylcholine ChAT catalyzes reversible acetylcholine synthesis from choline and acetyl-CoA. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The neurotransmitter needs both the choline headgroup and an acetyl group supplied by acetyl-CoA. organism: Human CHAT proteins; COS-cell and bacterial expression systems tissue_or_cell_type: Neuromuscular acetylcholine resynthesis experimental_model: Human CHAT genetics, recombinant expression and enzyme kinetics limitations: Inherited enzyme defects, not a dietary choline-deficiency model. Acetyl-CoA and choline are distinct substrates. exposure: Ten recessive variants in five patients; nine mutant proteins assayed evidence_span: {"source_cache": "artifacts/choline-research/11172068.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39", "start_char": 0, "end_char": 1231, "text_sha256": "691b96b9c5c149c554b99d8e1532ffee25084a8970f8deb23f0991dfd6013d39"} [choline-p11172068] Choline acetyltransferase mutations cause myasthenic syndrome associated with episodic apnea in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11172068/ DOI: 10.1073/pnas.98.4.2017
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CHT1 supports reutilization of choline liberated by synaptic acetylcholine hydrolysis, sustaining presynaptic acetylcholine synthesis.

    Human high-affinity choline transporter CHT1 / SLC5A7 → Choline source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/38589607.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3cf951acec5056180aacccf73a96951c54fa40be5446cd778bd90eb23b43fd3a", "start_char": 0, "end_char": 1090, "text_sha256": "3cf951acec5056180aacccf73a96951c54fa40be5446cd778bd90eb23b43fd3a"}
    experimental_model
    Human CHT1 cryo-EM and functional characterization
    exposure
    Choline-bound, inhibitor-bound and apo conformations
    limitations
    Structural transport cycle; no claim of cognitive benefit from increasing intake.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human CHT1 protein
    plain_language
    After acetylcholine is broken down, choline can be taken back up and reused.
    primary_references
    [choline-p38589607] Transport mechanism of presynaptic high-affinity choline uptake by CHT1. (2024). https://pubmed.ncbi.nlm.nih.gov/38589607/ DOI: 10.1038/s41594-024-01259-w
    tissue_or_cell_type
    Presynaptic uptake mechanism and experimental structures

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 334–345

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CHT1 cryo-EM and functional characterization · source_derived_draft · unverified_draft

    ### choline-cht1-recycling CHT1 supports reutilization of choline liberated by synaptic acetylcholine hydrolysis, sustaining presynaptic acetylcholine synthesis. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: After acetylcholine is broken down, choline can be taken back up and reused. organism: Human CHT1 protein tissue_or_cell_type: Presynaptic uptake mechanism and experimental structures experimental_model: Human CHT1 cryo-EM and functional characterization limitations: Structural transport cycle; no claim of cognitive benefit from increasing intake. exposure: Choline-bound, inhibitor-bound and apo conformations evidence_span: {"source_cache": "artifacts/choline-research/38589607.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3cf951acec5056180aacccf73a96951c54fa40be5446cd778bd90eb23b43fd3a", "start_char": 0, "end_char": 1090, "text_sha256": "3cf951acec5056180aacccf73a96951c54fa40be5446cd778bd90eb23b43fd3a"} [choline-p38589607] Transport mechanism of presynaptic high-affinity choline uptake by CHT1. (2024). https://pubmed.ncbi.nlm.nih.gov/38589607/ DOI: 10.1038/s41594-024-01259-w
    Complete structured claim and evidence

  2. VAChT recognizes acetylcholine and packages it into vesicles for subsequent release.

    Human vesicular acetylcholine transporter VAChT / SLC18A3 → Human VAChT-mediated vesicular acetylcholine packaging source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/39806024.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2c63d42f1864e1d9401293ec0c67d659eca8dbb0d571a8d1a328ec04883eb78", "start_char": 0, "end_char": 1047, "text_sha256": "e2c63d42f1864e1d9401293ec0c67d659eca8dbb0d571a8d1a328ec04883eb78"}
    experimental_model
    Human VAChT cryo-EM in apo, substrate-bound and inhibitor-bound states
    exposure
    Acetylcholine and vesamicol ligand binding
    limitations
    Packaging is distinct from synthesis and release. Structures support substrate recognition and protonation coupling, not a clinical effect of choline supplementation.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human VAChT protein
    plain_language
    Making acetylcholine and loading it into a release vesicle are separate steps.
    primary_references
    [choline-p39806024] Binding mechanism and antagonism of the vesicular acetylcholine transporter VAChT. (2025). https://pubmed.ncbi.nlm.nih.gov/39806024/ DOI: 10.1038/s41594-024-01462-9
    tissue_or_cell_type
    Synaptic-vesicle transporter

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 438–449

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human VAChT cryo-EM in apo, substrate-bound and inhibitor-bound states · source_derived_draft · unverified_draft

    ### choline-vacht-packaging VAChT recognizes acetylcholine and packages it into vesicles for subsequent release. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Making acetylcholine and loading it into a release vesicle are separate steps. organism: Human VAChT protein tissue_or_cell_type: Synaptic-vesicle transporter experimental_model: Human VAChT cryo-EM in apo, substrate-bound and inhibitor-bound states limitations: Packaging is distinct from synthesis and release. Structures support substrate recognition and protonation coupling, not a clinical effect of choline supplementation. exposure: Acetylcholine and vesamicol ligand binding evidence_span: {"source_cache": "artifacts/choline-research/39806024.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2c63d42f1864e1d9401293ec0c67d659eca8dbb0d571a8d1a328ec04883eb78", "start_char": 0, "end_char": 1047, "text_sha256": "e2c63d42f1864e1d9401293ec0c67d659eca8dbb0d571a8d1a328ec04883eb78"} [choline-p39806024] Binding mechanism and antagonism of the vesicular acetylcholine transporter VAChT. (2025). https://pubmed.ncbi.nlm.nih.gov/39806024/ DOI: 10.1038/s41594-024-01462-9
    Complete structured claim and evidence

  3. The potassium-induced increment in glucose-derived carbon-14 acetylcholine was 75% lower in deficient rat brain slices.

    Thiamine (vitamin B1) → Brain acetylcholine synthesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Links thiamine-dependent carbon metabolism with synthesis of a choline-containing transmitter; no choline repletion outcome was tested.
    evidence_location
    Abstract
    evidence_span
    declined by 50 and 75%, respectively
    experimental_model
    Symptomatic pyrithiamine-induced thiamine-deficient rats; brain slices assayed with uniformly carbon-14-labeled glucose at rest and during potassium stimulation; seven-day thiamine reversal arm.
    exposure
    Pyrithiamine-induced deficiency followed by potassium stimulation of rat brain slices
    limitations
    This tracer experiment did not test choline deficiency or choline supplementation; synthesis labeling is not transmitter release.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Rattus norvegicus
    plain_language
    Thiamine disruption limited stimulated production of the choline-containing transmitter from glucose-derived carbon.
    primary_references
    [gibson-1984-brain-flux] Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal (1984). https://pubmed.ncbi.nlm.nih.gov/6149477/ DOI: 10.1007/BF00965667
    tissue_or_cell_type
    Brain slices
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1112–1125

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Symptomatic pyrithiamine-induced thiamine-deficient rats; brain slices assayed with uniformly carbon-14-labeled glucose at rest and during potassium stimulation; seven-day thiamine reversal arm. · source_derived_draft · unverified_draft

    ### thiamine-def-stimulated-acetylcholine-synthesis The potassium-induced increment in glucose-derived carbon-14 acetylcholine was 75% lower in deficient rat brain slices. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Thiamine disruption limited stimulated production of the choline-containing transmitter from glucose-derived carbon. organism: Rattus norvegicus tissue_or_cell_type: Brain slices experimental_model: Symptomatic pyrithiamine-induced thiamine-deficient rats; brain slices assayed with uniformly carbon-14-labeled glucose at rest and during potassium stimulation; seven-day thiamine reversal arm. limitations: This tracer experiment did not test choline deficiency or choline supplementation; synthesis labeling is not transmitter release. evidence_location: Abstract evidence_span: declined by 50 and 75%, respectively cross_nutrient: Links thiamine-dependent carbon metabolism with synthesis of a choline-containing transmitter; no choline repletion outcome was tested. exposure: Pyrithiamine-induced deficiency followed by potassium stimulation of rat brain slices [gibson-1984-brain-flux] Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal (1984). https://pubmed.ncbi.nlm.nih.gov/6149477/ DOI: 10.1007/BF00965667
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards