Component

Mouse cortical lithium availability

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

9 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. Lithium depletion increased amyloid deposition in AD-model mice.

    Mouse cortical lithium availability → Mouse AD-model amyloid burden source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    3xTg and J20 mice on low-lithium diets.
    limitations
    Same study as the other depletion records, not independent replications.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Lower availability worsened an experimentally measured pathology.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 440–446

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 3xTg and J20 mice on low-lithium diets. · source_derived_draft · unverified_draft

    ## lithium-depletion-amyloid Lower availability worsened an experimentally measured pathology. Lithium depletion increased amyloid deposition in AD-model mice. Model: 3xTg and J20 mice on low-lithium diets. Limitations: Same study as the other depletion records, not independent replications. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

  2. Lithium depletion increased GSK3beta expression and activation-associated signals in mouse brain.

    Mouse cortical lithium availability → Mouse glycogen synthase kinase 3 beta / Gsk3b source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse neurons, oligodendrocytes and microglial analyses.
    limitations
    Not a universal linear relation between serum lithium and enzyme activity.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    The enzyme connects availability to downstream responses.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 456–462

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse neurons, oligodendrocytes and microglial analyses. · source_derived_draft · unverified_draft

    ## lithium-depletion-gsk3 The enzyme connects availability to downstream responses. Lithium depletion increased GSK3beta expression and activation-associated signals in mouse brain. Model: Mouse neurons, oligodendrocytes and microglial analyses. Limitations: Not a universal linear relation between serum lithium and enzyme activity. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

  3. Endogenous lithium depletion did not change brain inositol in the reported mouse comparison.

    Mouse cortical lithium availability → Myo-inositol source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse brain comparison with pharmacological IMPase rationale.
    limitations
    A scoped null measurement, not proof that inositol is irrelevant in every lithium setting.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Trace depletion did not reproduce every pharmacological pathway.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 496–502

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse brain comparison with pharmacological IMPase rationale. · source_derived_draft · unverified_draft

    ## lithium-depletion-inositol-null Trace depletion did not reproduce every pharmacological pathway. Endogenous lithium depletion did not change brain inositol in the reported mouse comparison. Model: Mouse brain comparison with pharmacological IMPase rationale. Limitations: A scoped null measurement, not proof that inositol is irrelevant in every lithium setting. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

  4. Microglia from lithium-depleted mice showed impaired amyloid uptake and degradation.

    Mouse cortical lithium availability → Mouse microglial amyloid uptake and degradation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Primary microglia from dietary-depletion experiments.
    limitations
    Cell isolation and model context retained; not a human immune-treatment result.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Brain immune cells became less effective at clearing amyloid.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 464–470

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary microglia from dietary-depletion experiments. · source_derived_draft · unverified_draft

    ## lithium-depletion-microglia Brain immune cells became less effective at clearing amyloid. Microglia from lithium-depleted mice showed impaired amyloid uptake and degradation. Model: Primary microglia from dietary-depletion experiments. Limitations: Cell isolation and model context retained; not a human immune-treatment result. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

  5. Lithium-depleted mice showed loss of oligodendrocytes and myelin-associated signals.

    Mouse cortical lithium availability → Mouse brain myelin integrity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse dietary-depletion, histological and molecular comparisons.
    limitations
    Not a demonstrated human demyelinating disease mechanism or a substitute for established nutrient-deficiency diagnoses.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    The cells and insulation around nerve fibers were affected.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 472–478

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse dietary-depletion, histological and molecular comparisons. · source_derived_draft · unverified_draft

    ## lithium-depletion-myelin The cells and insulation around nerve fibers were affected. Lithium-depleted mice showed loss of oligodendrocytes and myelin-associated signals. Model: Mouse dietary-depletion, histological and molecular comparisons. Limitations: Not a demonstrated human demyelinating disease mechanism or a substitute for established nutrient-deficiency diagnoses. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

  6. Dietary lithium depletion reduced synaptic markers and synapse density in the studied mice.

    Mouse cortical lithium availability → Mouse synaptic integrity in lithium-depletion experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse brain imaging, protein and structural comparisons.
    limitations
    Same experimental program as the other depletion records; requires independent replication.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Connections between nerve cells also changed.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 480–486

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse brain imaging, protein and structural comparisons. · source_derived_draft · unverified_draft

    ## lithium-depletion-synapses Connections between nerve cells also changed. Dietary lithium depletion reduced synaptic markers and synapse density in the studied mice. Model: Mouse brain imaging, protein and structural comparisons. Limitations: Same experimental program as the other depletion records; requires independent replication. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

  7. Lithium depletion increased phosphorylated tau in 3xTg mice.

    Mouse cortical lithium availability → Mouse AD-model tau phosphorylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Dietary-depletion experiment; hippocampal phospho-tau measurements.
    limitations
    Transgenic mouse result; not proof of human causation.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    A second pathological protein response changed.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 448–454

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Dietary-depletion experiment; hippocampal phospho-tau measurements. · source_derived_draft · unverified_draft

    ## lithium-depletion-tau A second pathological protein response changed. Lithium depletion increased phosphorylated tau in 3xTg mice. Model: Dietary-depletion experiment; hippocampal phospho-tau measurements. Limitations: Transgenic mouse result; not proof of human causation. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

What acts on it

  1. Dietary lithium depletion reduced endogenous cortical lithium by about half in the mouse experiments.

    Experimental mouse low-lithium diet → Mouse cortical lithium availability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Wild-type and transgenic AD mouse paradigms; regimen-specific effects.
    limitations
    Animal depletion does not define a human requirement or safe supplement dose.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    The study experimentally lowered the brain pool.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 432–438

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Wild-type and transgenic AD mouse paradigms; regimen-specific effects. · source_derived_draft · unverified_draft

    ## lithium-dietary-depletion The study experimentally lowered the brain pool. Dietary lithium depletion reduced endogenous cortical lithium by about half in the mouse experiments. Model: Wild-type and transgenic AD mouse paradigms; regimen-specific effects. Limitations: Animal depletion does not define a human requirement or safe supplement dose. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. GSK3 inhibition restored amyloid uptake/degradation in microglia from lithium-depleted mice.

    CHIR99021 → Mouse microglial amyloid uptake and degradation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    CHIR99021 and companion PF-04802367 rescue assays.
    limitations
    Inhibitor rescue supports partial mediation, not a single-target explanation.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Blocking the downstream enzyme helped test the proposed chain.
    primary_references
    Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 488–494

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · CHIR99021 and companion PF-04802367 rescue assays. · source_derived_draft · unverified_draft

    ## lithium-gsk3-rescue Blocking the downstream enzyme helped test the proposed chain. GSK3 inhibition restored amyloid uptake/degradation in microglia from lithium-depleted mice. Model: CHIR99021 and companion PF-04802367 rescue assays. Limitations: Inhibitor rescue supports partial mediation, not a single-target explanation. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
    Complete structured claim and evidence

In the sources

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

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