Component

Free D-aspartate in human dorsolateral prefrontal cortex

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

1 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. 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