Component

Neural progenitor survival and neurogenesis

Neural progenitor survival and neurogenesis. Species, exposure and limitations are retained in each linked claim.

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

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. Myo-inositol supplementation of differentiation medium rescued the reported neuronal-progenitor phenotype in IMPA1-deficient patient-derived cultures.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/inositol-research/32839513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed", "start_char": 0, "end_char": 1711, "text_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed"}
    experimental_model
    Patient-derived iPSC differentiation and rescue
    exposure
    Biallelic IMPA1 defect and myo-inositol-supplemented medium
    limitations
    Cellular rescue is not demonstrated neurological benefit in treated patients; effects were lineage-specific.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Homo sapiens
    plain_language
    Providing the missing downstream molecule helped cells in culture; clinical benefit remains untested here.
    primary_references
    [ino-p32839513] Inositol monophosphatase 1 (IMPA1) mutation in intellectual disability patients impairs neurogenesis but not gliogenesis. (2021). https://pubmed.ncbi.nlm.nih.gov/32839513/ DOI: 10.1038/s41380-020-00862-9
    tissue_or_cell_type
    Hippocampal dentate-gyrus-like neuronal progenitors
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1276–1287

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient-derived iPSC differentiation and rescue · source_derived_draft · unverified_draft

    ### ino-impa1-myo-rescue Myo-inositol supplementation of differentiation medium rescued the reported neuronal-progenitor phenotype in IMPA1-deficient patient-derived cultures. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing the missing downstream molecule helped cells in culture; clinical benefit remains untested here. organism: Homo sapiens tissue_or_cell_type: Hippocampal dentate-gyrus-like neuronal progenitors experimental_model: Patient-derived iPSC differentiation and rescue limitations: Cellular rescue is not demonstrated neurological benefit in treated patients; effects were lineage-specific. exposure: Biallelic IMPA1 defect and myo-inositol-supplemented medium evidence_span: {"source_cache": "artifacts/inositol-research/32839513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed", "start_char": 0, "end_char": 1711, "text_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed"} [ino-p32839513] Inositol monophosphatase 1 (IMPA1) mutation in intellectual disability patients impairs neurogenesis but not gliogenesis. (2021). https://pubmed.ncbi.nlm.nih.gov/32839513/ DOI: 10.1038/s41380-020-00862-9
    Complete structured claim and evidence
  2. IMPA1-deficient patient-derived neuronal progenitors showed impaired proliferation, cell-cycle arrest, apoptosis and reduced neuronal differentiation.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/inositol-research/32839513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed", "start_char": 0, "end_char": 1711, "text_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed"}
    experimental_model
    Patient-derived iPSC differentiation and rescue
    exposure
    Biallelic IMPA1 defect and myo-inositol-supplemented medium
    limitations
    Cellular rescue is not demonstrated neurological benefit in treated patients; effects were lineage-specific.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Homo sapiens
    plain_language
    Failure of the inositol-processing machinery affected developing nerve cells.
    primary_references
    [ino-p32839513] Inositol monophosphatase 1 (IMPA1) mutation in intellectual disability patients impairs neurogenesis but not gliogenesis. (2021). https://pubmed.ncbi.nlm.nih.gov/32839513/ DOI: 10.1038/s41380-020-00862-9
    tissue_or_cell_type
    Hippocampal dentate-gyrus-like neuronal progenitors
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1263–1274

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient-derived iPSC differentiation and rescue · source_derived_draft · unverified_draft

    ### ino-impa1-progenitors IMPA1-deficient patient-derived neuronal progenitors showed impaired proliferation, cell-cycle arrest, apoptosis and reduced neuronal differentiation. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Failure of the inositol-processing machinery affected developing nerve cells. organism: Homo sapiens tissue_or_cell_type: Hippocampal dentate-gyrus-like neuronal progenitors experimental_model: Patient-derived iPSC differentiation and rescue limitations: Cellular rescue is not demonstrated neurological benefit in treated patients; effects were lineage-specific. exposure: Biallelic IMPA1 defect and myo-inositol-supplemented medium evidence_span: {"source_cache": "artifacts/inositol-research/32839513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed", "start_char": 0, "end_char": 1711, "text_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed"} [ino-p32839513] Inositol monophosphatase 1 (IMPA1) mutation in intellectual disability patients impairs neurogenesis but not gliogenesis. (2021). https://pubmed.ncbi.nlm.nih.gov/32839513/ DOI: 10.1038/s41380-020-00862-9
    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