Component

Neurological outcome in molybdenum cofactor deficiency

Neurological outcome in molybdenum cofactor deficiency. Species, exposure and limitations are retained in each linked 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 acts on it

  1. Despite fosdenopterin within ten minutes of birth, the infant developed early seizures and retained motor impairment; seizures resolved and cognition was relatively spared.

    Cyclic pyranopterin monophosphate / cPMP → Neurological outcome in molybdenum cofactor deficiency source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/40429556.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25a9bcc9dc74084f82ec89ca2850ea25ee8ae156c6650d69ccd460d66d02e1d1", "start_char": 0, "end_char": 1369, "text_sha256": "25a9bcc9dc74084f82ec89ca2850ea25ee8ae156c6650d69ccd460d66d02e1d1"}
    experimental_model
    Prenatally diagnosed MoCD-A single case with immediate neonatal fosdenopterin
    exposure
    Delivery at 32 weeks 6 days; drug within 10 minutes of birth
    limitations
    One case. Residual injury suggests prenatal disease, but does not prove efficacy or safety of fetal treatment.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Homo sapiens
    plain_language
    Even rapid replacement may not undo injury that began before birth.
    primary_references
    [mo-p40429556] Early Neonatal Fosdenopterin Treatment for Molybdenum Cofactor Deficiency Type A: New Insights into Its Natural History and Potential Role for Fetal Therapy. (2025). https://pubmed.ncbi.nlm.nih.gov/40429556/ DOI: 10.3390/jcm14103561
    tissue_or_cell_type
    Fetal/neonatal brain and follow-up to 24 months
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1210–1221

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prenatally diagnosed MoCD-A single case with immediate neonatal fosdenopterin · source_derived_draft · unverified_draft

    ### mo-cpmp-early-limit Despite fosdenopterin within ten minutes of birth, the infant developed early seizures and retained motor impairment; seizures resolved and cognition was relatively spared. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Even rapid replacement may not undo injury that began before birth. organism: Homo sapiens tissue_or_cell_type: Fetal/neonatal brain and follow-up to 24 months experimental_model: Prenatally diagnosed MoCD-A single case with immediate neonatal fosdenopterin limitations: One case. Residual injury suggests prenatal disease, but does not prove efficacy or safety of fetal treatment. exposure: Delivery at 32 weeks 6 days; drug within 10 minutes of birth evidence_span: {"source_cache": "artifacts/molybdenum-research/40429556.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25a9bcc9dc74084f82ec89ca2850ea25ee8ae156c6650d69ccd460d66d02e1d1", "start_char": 0, "end_char": 1369, "text_sha256": "25a9bcc9dc74084f82ec89ca2850ea25ee8ae156c6650d69ccd460d66d02e1d1"} [mo-p40429556] Early Neonatal Fosdenopterin Treatment for Molybdenum Cofactor Deficiency Type A: New Insights into Its Natural History and Potential Role for Fetal Therapy. (2025). https://pubmed.ncbi.nlm.nih.gov/40429556/ DOI: 10.3390/jcm14103561
    Complete structured claim and evidence

  2. Memantine protected against symptom manifestation in a tungstate-induced MoCD mouse model.

    Memantine → Neurological outcome in molybdenum cofactor deficiency source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"}
    experimental_model
    Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice
    exposure
    SSC/sulfite exposure; receptor/calcium/calpain inhibition
    limitations
    Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus neurons and mice; chemical reaction assays
    plain_language
    An NMDA blocker helped in this induced mouse model.
    primary_references
    [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    tissue_or_cell_type
    Neuronal receptors, intracellular calcium and inhibitory synapses
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1353–1364

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice · source_derived_draft · unverified_draft

    ### mo-memantine-mouse Memantine protected against symptom manifestation in a tungstate-induced MoCD mouse model. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: An NMDA blocker helped in this induced mouse model. organism: Mus musculus neurons and mice; chemical reaction assays tissue_or_cell_type: Neuronal receptors, intracellular calcium and inhibitory synapses experimental_model: Primary murine neurons, chemical reaction assays and tungstate-induced MoCD mice limitations: Mechanistic model evidence. Mouse drug rescue does not establish human treatment efficacy; sulfite also has SSC-independent toxicity. exposure: SSC/sulfite exposure; receptor/calcium/calpain inhibition evidence_span: {"source_cache": "artifacts/molybdenum-research/29106383.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c", "start_char": 0, "end_char": 1472, "text_sha256": "34a677525363617e386b99e8ada3d049bc6147617c92764ca09caf1cae8efa1c"} [mo-p29106383] S-sulfocysteine/NMDA receptor-dependent signaling underlies neurodegeneration in molybdenum cofactor deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29106383/ DOI: 10.1172/jci89885
    Complete structured claim and evidence

  3. Forty-nine of 58 patients had neonatal-onset symptoms; seizures, feeding difficulties and progressive neurological disability were common.

    Molybdenum cofactor / Moco → Neurological outcome in molybdenum cofactor deficiency source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/35192225.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab9083746ef775c196770d3f4d0208378f1796abf1d7056fe5b23f60421032d4", "start_char": 0, "end_char": 1812, "text_sha256": "ab9083746ef775c196770d3f4d0208378f1796abf1d7056fe5b23f60421032d4"}
    experimental_model
    Retrospective natural history in 58 patients; prospective biomarkers in 21 survivors
    exposure
    MoCD A:41; MoCD B:17
    limitations
    Severe inherited cofactor defects; not a prevalence study of ordinary nutritional deficiency or a validated population screening threshold.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Homo sapiens
    plain_language
    Severe inherited assembly failure has a very different course from a mildly low nutrient intake.
    primary_references
    [mo-p35192225] Molybdenum cofactor deficiency: A natural history. (2022). https://pubmed.ncbi.nlm.nih.gov/35192225/ DOI: 10.1002/jimd.12488
    tissue_or_cell_type
    Neurological course and plasma/urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1171–1182

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective natural history in 58 patients; prospective biomarkers in 21 survivors · source_derived_draft · unverified_draft

    ### mo-mocd-course Forty-nine of 58 patients had neonatal-onset symptoms; seizures, feeding difficulties and progressive neurological disability were common. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe inherited assembly failure has a very different course from a mildly low nutrient intake. organism: Homo sapiens tissue_or_cell_type: Neurological course and plasma/urine experimental_model: Retrospective natural history in 58 patients; prospective biomarkers in 21 survivors limitations: Severe inherited cofactor defects; not a prevalence study of ordinary nutritional deficiency or a validated population screening threshold. exposure: MoCD A:41; MoCD B:17 evidence_span: {"source_cache": "artifacts/molybdenum-research/35192225.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ab9083746ef775c196770d3f4d0208378f1796abf1d7056fe5b23f60421032d4", "start_char": 0, "end_char": 1812, "text_sha256": "ab9083746ef775c196770d3f4d0208378f1796abf1d7056fe5b23f60421032d4"} [mo-p35192225] Molybdenum cofactor deficiency: A natural history. (2022). https://pubmed.ncbi.nlm.nih.gov/35192225/ DOI: 10.1002/jimd.12488
    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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