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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
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 evidenceA 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 evidenceAn 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 evidenceSchizophrenia 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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.