Component

Human glycogen synthase kinase 3 beta / GSK3B

Human glycogen synthase kinase 3 beta / GSK3B. Species, exposure and limitations are retained in each linked claim.

5 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. GSK3β mRNA decreased 2.2-fold from baseline in activated T lymphocytes in the combined-treatment group.

    Chromium → Human glycogen synthase kinase 3 beta / GSK3B source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"}
    experimental_model
    Four-arm randomized supplementation study; 120 insulin-resistant adults
    exposure
    Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo
    limitations
    The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Human
    plain_language
    A separate regulator of insulin-related metabolism showed lower gene expression in those immune cells.
    primary_references
    [chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
    tissue_or_cell_type
    Blood measures and activated T lymphocytes

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 588–599

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm randomized supplementation study; 120 insulin-resistant adults · source_derived_draft · unverified_draft

    ### chromium-magnesium-gsk3-transcript GSK3β mRNA decreased 2.2-fold from baseline in activated T lymphocytes in the combined-treatment group. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separate regulator of insulin-related metabolism showed lower gene expression in those immune cells. organism: Human tissue_or_cell_type: Blood measures and activated T lymphocytes experimental_model: Four-arm randomized supplementation study; 120 insulin-resistant adults limitations: The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved. exposure: Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo evidence_span: {"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"} [chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. A 71-person ten-week AD trial found no treatment effect on CSF biomarkers or lymphocyte GSK3 activity.

    Lithium carbonate → Human AD trial CSF tau and lymphocyte GSK3 outcomes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mild AD; six-week titration; serum target 0.5–0.8 mmol/L.
    limitations
    Short duration and different disease stage; neither proves lifelong efficacy nor rules out every regimen.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    A cell mechanism did not translate into measured target effects in this trial.
    primary_references
    Lithium trial in Alzheimer's disease: a randomized, single-blind, placebo-controlled, multicenter 10-week study. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19573486/

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 552–558

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mild AD; six-week titration; serum target 0.5–0.8 mmol/L. · source_derived_draft · unverified_draft

    ## lithium-ad-short-null A cell mechanism did not translate into measured target effects in this trial. A 71-person ten-week AD trial found no treatment effect on CSF biomarkers or lymphocyte GSK3 activity. Model: Mild AD; six-week titration; serum target 0.5–0.8 mmol/L. Limitations: Short duration and different disease stage; neither proves lifelong efficacy nor rules out every regimen. Evidence access: Primary abstract Lithium trial in Alzheimer's disease: a randomized, single-blind, placebo-controlled, multicenter 10-week study. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19573486/
    Complete structured claim and evidence

  2. Lithium increased tau–microtubule binding and microtubule assembly in the NT2N study.

    Lithium ion (Li+) → Human NT2N tau binding to microtubules source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human neuron-like cell culture.
    limitations
    Same paper as the tau-phosphorylation result, not independent replication.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    The altered protein interacted more strongly with the cellular scaffold.
    primary_references
    Lithium reduces tau phosphorylation by inhibition of glycogen synthase kinase-3. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9312151/ · DOI 10.1074/jbc.272.40.25326

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 184–190

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human neuron-like cell culture. · source_derived_draft · unverified_draft

    ## lithium-tau-microtubules The altered protein interacted more strongly with the cellular scaffold. Lithium increased tau–microtubule binding and microtubule assembly in the NT2N study. Model: Human neuron-like cell culture. Limitations: Same paper as the tau-phosphorylation result, not independent replication. Evidence access: Primary abstract Lithium reduces tau phosphorylation by inhibition of glycogen synthase kinase-3. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9312151/ · DOI 10.1074/jbc.272.40.25326
    Complete structured claim and evidence

  3. Lithium reduced tau phosphorylation through reversible GSK3 inhibition in human NT2N neurons.

    Lithium ion (Li+) → Human microtubule-associated protein tau / MAPT source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Cultured human NT2N neurons.
    limitations
    Does not demonstrate dementia prevention in people.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    A signaling enzyme changes chemical marks on a structural protein.
    primary_references
    Lithium reduces tau phosphorylation by inhibition of glycogen synthase kinase-3. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9312151/ · DOI 10.1074/jbc.272.40.25326

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 176–182

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cultured human NT2N neurons. · source_derived_draft · unverified_draft

    ## lithium-tau-phosphorylation A signaling enzyme changes chemical marks on a structural protein. Lithium reduced tau phosphorylation through reversible GSK3 inhibition in human NT2N neurons. Model: Cultured human NT2N neurons. Limitations: Does not demonstrate dementia prevention in people. Evidence access: Primary abstract Lithium reduces tau phosphorylation by inhibition of glycogen synthase kinase-3. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9312151/ · DOI 10.1074/jbc.272.40.25326
    Complete structured claim and evidence

  4. LiCl inhibited GSK3beta and stabilized free beta-catenin in cultured human thyrocytes.

    Lithium ion (Li+) → Human beta-catenin / CTNNB1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Primary and neoplastic human-cell preparations; dose-response assays.
    limitations
    Historical cell-line identities and experimental conditions limit extrapolation.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Thyroid growth signaling can change independently of hormone release.
    primary_references
    Lithium stimulates proliferation in cultured thyrocytes by activating Wnt/beta-catenin signalling. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16322400/ · DOI 10.1530/eje.1.02038

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 408–414

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary and neoplastic human-cell preparations; dose-response assays. · source_derived_draft · unverified_draft

    ## lithium-thyroid-beta-catenin Thyroid growth signaling can change independently of hormone release. LiCl inhibited GSK3beta and stabilized free beta-catenin in cultured human thyrocytes. Model: Primary and neoplastic human-cell preparations; dose-response assays. Limitations: Historical cell-line identities and experimental conditions limit extrapolation. Evidence access: Primary abstract Lithium stimulates proliferation in cultured thyrocytes by activating Wnt/beta-catenin signalling. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16322400/ · DOI 10.1530/eje.1.02038
    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