Component

Human GABA transaminase / ABAT

Context-specific entity; species, compartment and exposure are stated on each claim.

3 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 it acts on

  1. Recombinant human ABAT efficiently transaminated beta-alanine.

    Human GABA transaminase / ABAT → Beta-alanine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human enzyme expressed in HEK293T cells.
    limitations
    No clinical effect of changing vitamin B6 intake was established.
    nutrient_topic
    Carnosine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnosine / beta-alanyl-L-histidine
    plain_language
    A competing enzyme can divert the precursor away from peptide synthesis.
    primary_references
    Carnosine and anserine homeostasis in skeletal muscle and heart is controlled by β-alanine transamination. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27062388/ · DOI 10.1113/JP272050

    Carnosine: synthesis, transport, carbonyl chemistry and nutrient interactions (2026-09-19) · lines 124–130

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme expressed in HEK293T cells. · source_derived_draft · unverified_draft

    ## carnosine-transamination-human-abat A competing enzyme can divert the precursor away from peptide synthesis. Recombinant human ABAT efficiently transaminated beta-alanine. Model: Human enzyme expressed in HEK293T cells. Limitations: No clinical effect of changing vitamin B6 intake was established. Evidence access: Primary abstract Carnosine and anserine homeostasis in skeletal muscle and heart is controlled by β-alanine transamination. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27062388/ · DOI 10.1113/JP272050
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Out of 88 patients exposed to vigabatrin in infancy, 28 were able to perform formal visual field testing, mild vigabatrin-attributed visual field defect was found in four patients and severe defect in one, median vigabatrin treatment duration for those with normal visual field was 11 months compared to 19 months for those with the defect, optical coherence tomography showed concomitant attenuated retinal nerve fiber layer in three children, and the overall prevalence after exposure in infancy is lower than the 52% which has been reported after exposure in adulthood while the risk increases with longer treatment duration.

    Vigabatrin → Vigabatrin-attributed visual field defect source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/34716587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887", "start_char": 0, "end_char": 1403, "text_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887"}
    experimental_model
    Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy
    exposure
    Vigabatrin given for infantile spasms, with visual fields and retinal nerve fibre layer measured years later
    limitations
    Only 28 of 88 exposed patients could perform formal visual field testing, which limits the prevalence estimate in both directions.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Human
    plain_language
    The drug that raises brain GABA costs some patients their peripheral vision, and the longer they take it the likelier that is.
    primary_references
    [gb-p34716587] Visual field defects after vigabatrin treatment during infancy: retrospective population-based study. (2022). https://pubmed.ncbi.nlm.nih.gov/34716587/ DOI: 10.1111/dmcn.15099
    tissue_or_cell_type
    Retina

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 170–181

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy · source_derived_draft · unverified_draft

    ### gb-duration-drives-the-field-loss Out of 88 patients exposed to vigabatrin in infancy, 28 were able to perform formal visual field testing, mild vigabatrin-attributed visual field defect was found in four patients and severe defect in one, median vigabatrin treatment duration for those with normal visual field was 11 months compared to 19 months for those with the defect, optical coherence tomography showed concomitant attenuated retinal nerve fiber layer in three children, and the overall prevalence after exposure in infancy is lower than the 52% which has been reported after exposure in adulthood while the risk increases with longer treatment duration. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The drug that raises brain GABA costs some patients their peripheral vision, and the longer they take it the likelier that is. organism: Human tissue_or_cell_type: Retina experimental_model: Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy limitations: Only 28 of 88 exposed patients could perform formal visual field testing, which limits the prevalence estimate in both directions. exposure: Vigabatrin given for infantile spasms, with visual fields and retinal nerve fibre layer measured years later evidence_span: {"source_cache": "artifacts/gaba-research/34716587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887", "start_char": 0, "end_char": 1403, "text_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887"} [gb-p34716587] Visual field defects after vigabatrin treatment during infancy: retrospective population-based study. (2022). https://pubmed.ncbi.nlm.nih.gov/34716587/ DOI: 10.1111/dmcn.15099
    Complete structured claim and evidence

  2. Immune cells synthesize GABA and have the machinery for GABA catabolism, antigen-presenting cells express functional GABA receptors and respond electrophysiologically to GABA, thus the immune system harbors all of the necessary constituents for GABA signaling and GABA itself may function as a paracrine or autocrine factor, increasing GABAergic activity ameliorates ongoing paralysis in experimental autoimmune encephalomyelitis via inhibition of inflammation, and GABAergic agents act directly on antigen-presenting cells decreasing MAPK signals and diminishing subsequent adaptive inflammatory responses to myelin proteins.

    Antigen-presenting cell → Gamma-aminobutyric acid source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/20133656.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd", "start_char": 0, "end_char": 896, "text_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd"}
    experimental_model
    Demonstration of GABA synthesis and catabolism machinery in immune cells with electrophysiology and an autoimmune disease model
    exposure
    Increasing GABAergic activity in established experimental autoimmune encephalomyelitis
    limitations
    The disease effect is on ongoing paralysis rather than prevention. The assignment to antigen-presenting cells rests on direct effects measured on those cells.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Mouse
    plain_language
    The immune system has the whole apparatus to make and break down this transmitter, and uses it on itself.
    primary_references
    [gb-p20133656] Inhibitory role for GABA in autoimmune inflammation. (2010). https://pubmed.ncbi.nlm.nih.gov/20133656/ DOI: 10.1073/pnas.0915139107
    tissue_or_cell_type
    Antigen-presenting cell and central nervous system

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 547–558

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Demonstration of GABA synthesis and catabolism machinery in immune cells with electrophysiology and an autoimmune disease model · source_derived_draft · unverified_draft

    ### gb-immune-cells-make-their-own-gaba Immune cells synthesize GABA and have the machinery for GABA catabolism, antigen-presenting cells express functional GABA receptors and respond electrophysiologically to GABA, thus the immune system harbors all of the necessary constituents for GABA signaling and GABA itself may function as a paracrine or autocrine factor, increasing GABAergic activity ameliorates ongoing paralysis in experimental autoimmune encephalomyelitis via inhibition of inflammation, and GABAergic agents act directly on antigen-presenting cells decreasing MAPK signals and diminishing subsequent adaptive inflammatory responses to myelin proteins. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The immune system has the whole apparatus to make and break down this transmitter, and uses it on itself. organism: Mouse tissue_or_cell_type: Antigen-presenting cell and central nervous system experimental_model: Demonstration of GABA synthesis and catabolism machinery in immune cells with electrophysiology and an autoimmune disease model limitations: The disease effect is on ongoing paralysis rather than prevention. The assignment to antigen-presenting cells rests on direct effects measured on those cells. exposure: Increasing GABAergic activity in established experimental autoimmune encephalomyelitis evidence_span: {"source_cache": "artifacts/gaba-research/20133656.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd", "start_char": 0, "end_char": 896, "text_sha256": "15fc62882eb9a9c1f5daad1bd2845bc99c94f1cf076620badc55b6be390e35fd"} [gb-p20133656] Inhibitory role for GABA in autoimmune inflammation. (2010). https://pubmed.ncbi.nlm.nih.gov/20133656/ DOI: 10.1073/pnas.0915139107
    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