Component

Brain total creatine concentration

Brain total creatine concentration. Species, exposure and limitations are retained in each linked claim.

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. The AGAT-deficient sisters had low urinary guanidinoacetate, absent AGAT activity and brain creatine depletion.

    Human glycine amidinotransferase AGAT / GATM → Brain total creatine concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/creatine-research/11555793.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3", "start_char": 0, "end_char": 1044, "text_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3"}
    experimental_model
    Biochemical and genetic investigation with oral replacement observations
    exposure
    Inherited AGAT deficiency and oral creatine substitution
    limitations
    Rare synthesis disorder; treatment response is not equivalent to a diagnosis of dietary creatine deficiency.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Two human sisters
    plain_language
    A broken first synthesis step can leave both precursor and brain creatine low.
    primary_references
    [creatine-p11555793] Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11555793/ DOI: 10.1086/323765
    tissue_or_cell_type
    Urine, brain magnetic-resonance spectroscopy and AGAT assays
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 841–852

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical and genetic investigation with oral replacement observations · source_derived_draft · unverified_draft

    ### creatine-agat-brain-deficiency The AGAT-deficient sisters had low urinary guanidinoacetate, absent AGAT activity and brain creatine depletion. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A broken first synthesis step can leave both precursor and brain creatine low. organism: Two human sisters tissue_or_cell_type: Urine, brain magnetic-resonance spectroscopy and AGAT assays experimental_model: Biochemical and genetic investigation with oral replacement observations limitations: Rare synthesis disorder; treatment response is not equivalent to a diagnosis of dietary creatine deficiency. exposure: Inherited AGAT deficiency and oral creatine substitution evidence_span: {"source_cache": "artifacts/creatine-research/11555793.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3", "start_char": 0, "end_char": 1044, "text_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3"} [creatine-p11555793] Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11555793/ DOI: 10.1086/323765
    Complete structured claim and evidence

  2. Oral creatine substitution reversed the brain creatine depletion in the reported AGAT-deficient patients.

    Creatine → Brain total creatine concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/creatine-research/11555793.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3", "start_char": 0, "end_char": 1044, "text_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3"}
    experimental_model
    Biochemical and genetic investigation with oral replacement observations
    exposure
    Inherited AGAT deficiency and oral creatine substitution
    limitations
    Rare synthesis disorder; treatment response is not equivalent to a diagnosis of dietary creatine deficiency.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Two human sisters
    plain_language
    Replacing the finished molecule could bypass this synthesis defect.
    primary_references
    [creatine-p11555793] Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11555793/ DOI: 10.1086/323765
    tissue_or_cell_type
    Urine, brain magnetic-resonance spectroscopy and AGAT assays
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 854–865

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical and genetic investigation with oral replacement observations · source_derived_draft · unverified_draft

    ### creatine-agat-creatine-replacement Oral creatine substitution reversed the brain creatine depletion in the reported AGAT-deficient patients. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing the finished molecule could bypass this synthesis defect. organism: Two human sisters tissue_or_cell_type: Urine, brain magnetic-resonance spectroscopy and AGAT assays experimental_model: Biochemical and genetic investigation with oral replacement observations limitations: Rare synthesis disorder; treatment response is not equivalent to a diagnosis of dietary creatine deficiency. exposure: Inherited AGAT deficiency and oral creatine substitution evidence_span: {"source_cache": "artifacts/creatine-research/11555793.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3", "start_char": 0, "end_char": 1044, "text_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3"} [creatine-p11555793] Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11555793/ DOI: 10.1086/323765
    Complete structured claim and evidence

  3. Mean brain total creatine increased 8.7%, with regional and individual variability, after four weeks of supplementation; changes were reversible on follow-up.

    Creatine monohydrate → Brain total creatine concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/creatine-research/10484486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "91190f8691b1728904ae6d8a46b65c2c731b75fe9fe876d964e18facc61c7c9d", "start_char": 0, "end_char": 1490, "text_sha256": "91190f8691b1728904ae6d8a46b65c2c731b75fe9fe876d964e18facc61c7c9d"}
    experimental_model
    Before/after quantitative proton MRS with washout
    exposure
    20 g/day creatine monohydrate for four weeks
    limitations
    Small non-placebo-controlled study; total creatine includes the creatine/phosphocreatine signal and is not a direct cognition endpoint.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Six healthy human volunteers
    plain_language
    Brain stores rose modestly and unevenly, rather than matching the much larger changes sometimes seen in muscle.
    primary_references
    [creatine-p10484486] Increase of total creatine in human brain after oral supplementation of creatine-monohydrate. (1999). https://pubmed.ncbi.nlm.nih.gov/10484486/ DOI: 10.1152/ajpregu.1999.277.3.r698
    tissue_or_cell_type
    Multiple brain regions

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 1023–1034

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Before/after quantitative proton MRS with washout · source_derived_draft · unverified_draft

    ### creatine-brain-loading Mean brain total creatine increased 8.7%, with regional and individual variability, after four weeks of supplementation; changes were reversible on follow-up. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Brain stores rose modestly and unevenly, rather than matching the much larger changes sometimes seen in muscle. organism: Six healthy human volunteers tissue_or_cell_type: Multiple brain regions experimental_model: Before/after quantitative proton MRS with washout limitations: Small non-placebo-controlled study; total creatine includes the creatine/phosphocreatine signal and is not a direct cognition endpoint. exposure: 20 g/day creatine monohydrate for four weeks evidence_span: {"source_cache": "artifacts/creatine-research/10484486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "91190f8691b1728904ae6d8a46b65c2c731b75fe9fe876d964e18facc61c7c9d", "start_char": 0, "end_char": 1490, "text_sha256": "91190f8691b1728904ae6d8a46b65c2c731b75fe9fe876d964e18facc61c7c9d"} [creatine-p10484486] Increase of total creatine in human brain after oral supplementation of creatine-monohydrate. (1999). https://pubmed.ncbi.nlm.nih.gov/10484486/ DOI: 10.1152/ajpregu.1999.277.3.r698
    Complete structured claim and evidence

  4. The SLC6A8-deficient male had absent brain creatine on spectroscopy and defective fibroblast creatine uptake despite high plasma and urinary creatine and normal guanidinoacetate.

    Human creatine transporter CRT / SLC6A8 → Brain total creatine concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/creatine-research/11326334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9", "start_char": 0, "end_char": 739, "text_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9"}
    experimental_model
    Human family genetics and fibroblast transport assay
    exposure
    SLC6A8 loss-of-function variant
    limitations
    Single family; circulating creatine cannot substitute for cellular transport. No treatment failure claim is inferred from this abstract.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Human male patient and relatives
    plain_language
    A high blood or urine value did not mean creatine reached the brain.
    primary_references
    [creatine-p11326334] X-linked creatine-transporter gene (SLC6A8) defect: a new creatine-deficiency syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11326334/ DOI: 10.1086/320595
    tissue_or_cell_type
    Brain spectroscopy, plasma, urine and fibroblasts
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 906–917

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and fibroblast transport assay · source_derived_draft · unverified_draft

    ### creatine-transporter-brain-loss The SLC6A8-deficient male had absent brain creatine on spectroscopy and defective fibroblast creatine uptake despite high plasma and urinary creatine and normal guanidinoacetate. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A high blood or urine value did not mean creatine reached the brain. organism: Human male patient and relatives tissue_or_cell_type: Brain spectroscopy, plasma, urine and fibroblasts experimental_model: Human family genetics and fibroblast transport assay limitations: Single family; circulating creatine cannot substitute for cellular transport. No treatment failure claim is inferred from this abstract. exposure: SLC6A8 loss-of-function variant evidence_span: {"source_cache": "artifacts/creatine-research/11326334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9", "start_char": 0, "end_char": 739, "text_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9"} [creatine-p11326334] X-linked creatine-transporter gene (SLC6A8) defect: a new creatine-deficiency syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11326334/ DOI: 10.1086/320595
    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.

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