Component

Schizophrenia diagnosis in postmortem comparisons

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

4 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 it acts on

  1. DDO mRNA was higher in the study prefrontal samples from people with schizophrenia than controls.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human postmortem prefrontal cortex; 10 schizophrenia and 11 control samples.
    limitations
    Observational, small cohort; transcript abundance is not enzyme activity and does not establish causation.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    One brain-sample study found more transcript for the clearing enzyme.
    primary_references
    A role for D-aspartate oxidase in schizophrenia and in schizophrenia-related symptoms induced by phencyclidine in mice. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25689573/ · DOI 10.1038/tp.2015.2
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 288–294

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human postmortem prefrontal cortex; 10 schizophrenia and 11 control samples. · source_derived_draft · unverified_draft

    ## d-aspartate-ddo-transcript-increase One brain-sample study found more transcript for the clearing enzyme. DDO mRNA was higher in the study prefrontal samples from people with schizophrenia than controls. Model: Human postmortem prefrontal cortex; 10 schizophrenia and 11 control samples. Limitations: Observational, small cohort; transcript abundance is not enzyme activity and does not establish causation. Evidence access: Primary full text A role for D-aspartate oxidase in schizophrenia and in schizophrenia-related symptoms induced by phencyclidine in mice. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25689573/ · DOI 10.1038/tp.2015.2
    Complete structured claim and evidence
  2. A later postmortem study found no significant schizophrenia-related difference in DDO transcription or methylation despite higher DDO activity in dorsolateral prefrontal cortex.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human DLPFC and hippocampal tissue comparison.
    limitations
    A null test does not prove equality; cohort and tissue handling can differ.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Enzyme activity changed without a detected transcript change.
    primary_references
    Decreased free d-aspartate levels are linked to enhanced d-aspartate oxidase activity in the dorsolateral prefrontal cortex of schizophrenia patients. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28560262/ · DOI 10.1038/s41537-017-0015-7
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 296–302

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human DLPFC and hippocampal tissue comparison. · source_derived_draft · unverified_draft

    ## d-aspartate-ddo-transcript-null Enzyme activity changed without a detected transcript change. A later postmortem study found no significant schizophrenia-related difference in DDO transcription or methylation despite higher DDO activity in dorsolateral prefrontal cortex. Model: Human DLPFC and hippocampal tissue comparison. Limitations: A null test does not prove equality; cohort and tissue handling can differ. Evidence access: Primary full text Decreased free d-aspartate levels are linked to enhanced d-aspartate oxidase activity in the dorsolateral prefrontal cortex of schizophrenia patients. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28560262/ · DOI 10.1038/s41537-017-0015-7
    Complete structured claim and evidence
  3. An expanded regional methylation/expression analysis found brain-region differences but no significant diagnostic association for DDO expression or methylation.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human postmortem DLPFC, hippocampus and cerebellum; epiallele analysis.
    limitations
    Overlaps the earlier research group and reuses previously reported regional methylation data; not an independent replication of every measurement.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Regional identity mattered more than diagnosis in this analysis.
    primary_references
    DNA methylation landscape of the genes regulating D-serine and D-aspartate metabolism in post-mortem brain from controls and subjects with schizophrenia. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29976992/ · DOI 10.1038/s41598-018-28332-x
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 312–318

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human postmortem DLPFC, hippocampus and cerebellum; epiallele analysis. · source_derived_draft · unverified_draft

    ## d-aspartate-human-epialleles Regional identity mattered more than diagnosis in this analysis. An expanded regional methylation/expression analysis found brain-region differences but no significant diagnostic association for DDO expression or methylation. Model: Human postmortem DLPFC, hippocampus and cerebellum; epiallele analysis. Limitations: Overlaps the earlier research group and reuses previously reported regional methylation data; not an independent replication of every measurement. Evidence access: Primary full text DNA methylation landscape of the genes regulating D-serine and D-aspartate metabolism in post-mortem brain from controls and subjects with schizophrenia. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29976992/ · DOI 10.1038/s41598-018-28332-x
    Complete structured claim and evidence
  4. Schizophrenia DLPFC samples had approximately 30% lower free D-aspartate and 25% higher DDO activity; the D-aspartate reduction was not detected in hippocampus.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human postmortem case-control study.
    limitations
    Not a dietary deficiency diagnosis, proof of disease cause, or a supplementation trial.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    The measured difference was local to a brain region.
    primary_references
    Decreased free d-aspartate levels are linked to enhanced d-aspartate oxidase activity in the dorsolateral prefrontal cortex of schizophrenia patients. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28560262/ · DOI 10.1038/s41537-017-0015-7
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 304–310

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human postmortem case-control study. · source_derived_draft · unverified_draft

    ## d-aspartate-human-low-dasp The measured difference was local to a brain region. Schizophrenia DLPFC samples had approximately 30% lower free D-aspartate and 25% higher DDO activity; the D-aspartate reduction was not detected in hippocampus. Model: Human postmortem case-control study. Limitations: Not a dietary deficiency diagnosis, proof of disease cause, or a supplementation trial. Evidence access: Primary full text Decreased free d-aspartate levels are linked to enhanced d-aspartate oxidase activity in the dorsolateral prefrontal cortex of schizophrenia patients. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28560262/ · DOI 10.1038/s41537-017-0015-7
    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