Component

D-Aspartate

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

52 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.

Human evidence only

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

Oral D-aspartate at 20 mM in drinking water for one month and a separate 500 mg/kg intraperitoneal exposure increased extracellular prefrontal D-aspartate in mice.
D-Aspartate → Extracellular D-aspartate in mouse prefrontal cortex source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse microdialysis; chronic oral and separate acute injection conditions.
limitations
Water concentration is not a fixed mg/kg dose; human brain exposure remains unmeasured here.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Both tested routes changed the brain extracellular pool in mice.
primary_references
Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 216–222
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse microdialysis; chronic oral and separate acute injection conditions. · source_derived_draft · unverified_draft
## d-aspartate-brain-exposure Both tested routes changed the brain extracellular pool in mice. Oral D-aspartate at 20 mM in drinking water for one month and a separate 500 mg/kg intraperitoneal exposure increased extracellular prefrontal D-aspartate in mice. Model: Mouse microdialysis; chronic oral and separate acute injection conditions. Limitations: Water concentration is not a fixed mg/kg dose; human brain exposure remains unmeasured here. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidence
One-month 20 mM oral D-aspartate increased extracellular prefrontal glutamate; acute 500 mg/kg injection did not increase striatal glutamate.
D-Aspartate → Extracellular glutamate in mouse prefrontal cortex source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse regional microdialysis.
limitations
Different regions and routes remain explicit; not a claim of globally elevated brain glutamate.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The response depends on which brain region is measured.
primary_references
Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 224–230
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse regional microdialysis. · source_derived_draft · unverified_draft
## d-aspartate-brain-glutamate The response depends on which brain region is measured. One-month 20 mM oral D-aspartate increased extracellular prefrontal glutamate; acute 500 mg/kg injection did not increase striatal glutamate. Model: Mouse regional microdialysis. Limitations: Different regions and routes remain explicit; not a claim of globally elevated brain glutamate. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidence
Porcine DDO showed substrate activation above approximately 0.2 mM D-aspartate; N-methyl-D-aspartate instead produced substrate inhibition.
D-Aspartate → Porcine D-aspartate oxidase / DDO source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified porcine enzyme concentration-response assays.
limitations
Do not extrapolate assay thresholds to dietary dosing.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Different substrates change the enzyme kinetics differently.
primary_references
Functional and structural characterization of D-aspartate oxidase from porcine kidney: non-Michaelis kinetics due to substrate activation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17234685/ · DOI 10.1093/jb/mvm041
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 120–126
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified porcine enzyme concentration-response assays. · source_derived_draft · unverified_draft
## d-aspartate-ddo-substrate-activation Different substrates change the enzyme kinetics differently. Porcine DDO showed substrate activation above approximately 0.2 mM D-aspartate; N-methyl-D-aspartate instead produced substrate inhibition. Model: Purified porcine enzyme concentration-response assays. Limitations: Do not extrapolate assay thresholds to dietary dosing. Evidence access: Primary abstract Functional and structural characterization of D-aspartate oxidase from porcine kidney: non-Michaelis kinetics due to substrate activation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17234685/ · DOI 10.1093/jb/mvm041
Complete structured claim and evidence
In a 24-man resistance-trained trial, 3 g/day for 14 days did not change testosterone; 6 g/day lowered total and calculated free testosterone.
D-Aspartate → Circulating total testosterone concentration source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Eight men per placebo, 3 g and 6 g arm; at least two years of resistance training.
limitations
Small groups and short duration; calculated free testosterone is not a direct free-hormone assay.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
More was not better in this short dose-comparison trial.
primary_references
Three and six grams supplementation of d-aspartic acid in resistance trained men. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25844073/ · DOI 10.1186/s12970-015-0078-7
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 344–350
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Eight men per placebo, 3 g and 6 g arm; at least two years of resistance training. · source_derived_draft · unverified_draft
## d-aspartate-human-dose-trial More was not better in this short dose-comparison trial. In a 24-man resistance-trained trial, 3 g/day for 14 days did not change testosterone; 6 g/day lowered total and calculated free testosterone. Model: Eight men per placebo, 3 g and 6 g arm; at least two years of resistance training. Limitations: Small groups and short duration; calculated free testosterone is not a direct free-hormone assay. Evidence access: Primary full text Three and six grams supplementation of d-aspartic acid in resistance trained men. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25844073/ · DOI 10.1186/s12970-015-0078-7
Complete structured claim and evidence
After 12 days, 23 men taking 3.12 g/day sodium D-aspartate with B6, folate and B12 had a reported 33% mean LH rise from baseline; 20 men received sodium-chloride placebo with the same vitamins.
D-Aspartate → Human circulating luteinizing hormone source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Men aged 27-37; morning serum sampling; DADAVIT formulation.
limitations
Randomization was not clearly described in the accessed methods. Sodium-salt mass is not free-acid mass; no evidence of vitamin synergy from this design.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A small early study reported a hormone change with a matched-vitamin comparison.
primary_references
The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 320–326
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Men aged 27-37; morning serum sampling; DADAVIT formulation. · source_derived_draft · unverified_draft
## d-aspartate-human-early-lh A small early study reported a hormone change with a matched-vitamin comparison. After 12 days, 23 men taking 3.12 g/day sodium D-aspartate with B6, folate and B12 had a reported 33% mean LH rise from baseline; 20 men received sodium-chloride placebo with the same vitamins. Model: Men aged 27-37; morning serum sampling; DADAVIT formulation. Limitations: Randomization was not clearly described in the accessed methods. Sodium-salt mass is not free-acid mass; no evidence of vitamin synergy from this design. Evidence access: Primary full text The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
Complete structured claim and evidence
The same 12-day sodium D-aspartate study reported mean testosterone rising from 4.5 to 6.4 ng/mL; the matched-vitamin placebo group showed no corresponding increase.
D-Aspartate → Circulating total testosterone concentration source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
23 treated and 20 placebo men; 3.12 g/day sodium D-aspartate, B6/folate/B12 in both arms.
limitations
Not a general testosterone-boosting effect; same cohort as the LH claim, not independent evidence.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The early testosterone result belongs to this specific short study.
primary_references
The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 328–334
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 23 treated and 20 placebo men; 3.12 g/day sodium D-aspartate, B6/folate/B12 in both arms. · source_derived_draft · unverified_draft
## d-aspartate-human-early-testosterone The early testosterone result belongs to this specific short study. The same 12-day sodium D-aspartate study reported mean testosterone rising from 4.5 to 6.4 ng/mL; the matched-vitamin placebo group showed no corresponding increase. Model: 23 treated and 20 placebo men; 3.12 g/day sodium D-aspartate, B6/folate/B12 in both arms. Limitations: Not a general testosterone-boosting effect; same cohort as the LH claim, not independent evidence. Evidence access: Primary full text The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
Complete structured claim and evidence
The 6 g/day D-aspartate arm showed a reported 16% estradiol decrease over 12 weeks.
D-Aspartate → Estradiol in the 12-week D-aspartate trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Resistance-trained men; within-group change estimate, 95% confidence interval -27% to -5%.
limitations
This does not prove direct aromatase inhibition or establish a hormone-management treatment.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
One trial measured an estrogen change alongside unchanged testosterone.
primary_references
The effects of d-aspartic acid supplementation in resistance-trained men over a three month training period: A randomised controlled trial. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28841667/ · DOI 10.1371/journal.pone.0182630
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 360–366
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Resistance-trained men; within-group change estimate, 95% confidence interval -27% to -5%. · source_derived_draft · unverified_draft
## d-aspartate-human-estradiol One trial measured an estrogen change alongside unchanged testosterone. The 6 g/day D-aspartate arm showed a reported 16% estradiol decrease over 12 weeks. Model: Resistance-trained men; within-group change estimate, 95% confidence interval -27% to -5%. Limitations: This does not prove direct aromatase inhibition or establish a hormone-management treatment. Evidence access: Primary full text The effects of d-aspartic acid supplementation in resistance-trained men over a three month training period: A randomised controlled trial. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28841667/ · DOI 10.1371/journal.pone.0182630
Complete structured claim and evidence
A 12-week 6 g/day trial in trained men found no testosterone benefit or added strength/hypertrophy benefit over placebo.
D-Aspartate → Circulating total testosterone concentration source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
22 randomized, 19 completed; resistance training four days weekly.
limitations
Overlapping investigators with the 2015 trial; not independent laboratory replication. Hormonal and training endpoints are distinct.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The longer higher-dose trial also failed to show a testosterone advantage.
primary_references
The effects of d-aspartic acid supplementation in resistance-trained men over a three month training period: A randomised controlled trial. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28841667/ · DOI 10.1371/journal.pone.0182630
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 352–358
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 22 randomized, 19 completed; resistance training four days weekly. · source_derived_draft · unverified_draft
## d-aspartate-human-longer-trial The longer higher-dose trial also failed to show a testosterone advantage. A 12-week 6 g/day trial in trained men found no testosterone benefit or added strength/hypertrophy benefit over placebo. Model: 22 randomized, 19 completed; resistance training four days weekly. Limitations: Overlapping investigators with the 2015 trial; not independent laboratory replication. Hormonal and training endpoints are distinct. Evidence access: Primary full text The effects of d-aspartic acid supplementation in resistance-trained men over a three month training period: A randomised controlled trial. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28841667/ · DOI 10.1371/journal.pone.0182630
Complete structured claim and evidence
In resistance-trained men, 3 g/day D-aspartic acid for 28 days did not improve testosterone, strength or body composition relative to placebo.
D-Aspartate → Circulating total testosterone concentration source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Randomized blinded resistance-training trial; four training days per week.
limitations
Different population, formulation and duration from the early sodium-salt study; absence of benefit here is not proof of no effect in every population.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A later trained-population trial did not reproduce a testosterone increase.
primary_references
D-aspartic acid supplementation combined with 28 days of heavy resistance training has no effect on body composition, muscle strength, and serum hormones associated with the hypothalamo-pituitary-gonadal axis in resistance-trained men. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24074738/ · DOI 10.1016/j.nutres.2013.07.010
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 336–342
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized blinded resistance-training trial; four training days per week. · source_derived_draft · unverified_draft
## d-aspartate-human-trained-3g A later trained-population trial did not reproduce a testosterone increase. In resistance-trained men, 3 g/day D-aspartic acid for 28 days did not improve testosterone, strength or body composition relative to placebo. Model: Randomized blinded resistance-training trial; four training days per week. Limitations: Different population, formulation and duration from the early sodium-salt study; absence of benefit here is not proof of no effect in every population. Evidence access: Primary abstract D-aspartic acid supplementation combined with 28 days of heavy resistance training has no effect on body composition, muscle strength, and serum hormones associated with the hypothalamo-pituitary-gonadal axis in resistance-trained men. · 2013 · https://pubmed.ncbi.nlm.nih.gov/24074738/ · DOI 10.1016/j.nutres.2013.07.010
Complete structured claim and evidence
In mouse MA-10 cells, D-aspartate alone did not meaningfully increase measured testosterone; 0.1 or 1 nM D-aspartate augmented the hCG-stimulated immunoassay signal.
D-Aspartate → MA-10 medium testosterone immunoassay endpoint source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse Leydig tumor cell line; medium electrochemiluminescence immunoassay.
limitations
Cell-line and assay-specific endpoint, not human testosterone efficacy.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The response required the hormone context in this cell line.
primary_references
D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26122485/ · DOI 10.1007/s40618-015-0333-4
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 384–390
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse Leydig tumor cell line; medium electrochemiluminescence immunoassay. · source_derived_draft · unverified_draft
## d-aspartate-leydig-hcg-gate The response required the hormone context in this cell line. In mouse MA-10 cells, D-aspartate alone did not meaningfully increase measured testosterone; 0.1 or 1 nM D-aspartate augmented the hCG-stimulated immunoassay signal. Model: Mouse Leydig tumor cell line; medium electrochemiluminescence immunoassay. Limitations: Cell-line and assay-specific endpoint, not human testosterone efficacy. Evidence access: Primary abstract D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26122485/ · DOI 10.1007/s40618-015-0333-4
Complete structured claim and evidence
Adding 0.1 nM D-aspartate to hCG stimulation increased StAR protein in mouse MA-10 cells compared with hCG alone.
D-Aspartate → Mouse steroidogenic acute regulatory protein / Star source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse MA-10 immunoblot assay.
limitations
Protein abundance does not directly measure cholesterol transfer flux or prove complete mediation.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The combination changed a protein involved in steroid production.
primary_references
D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26122485/ · DOI 10.1007/s40618-015-0333-4
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 392–398
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse MA-10 immunoblot assay. · source_derived_draft · unverified_draft
## d-aspartate-leydig-star The combination changed a protein involved in steroid production. Adding 0.1 nM D-aspartate to hCG stimulation increased StAR protein in mouse MA-10 cells compared with hCG alone. Model: Mouse MA-10 immunoblot assay. Limitations: Protein abundance does not directly measure cholesterol transfer flux or prove complete mediation. Evidence access: Primary abstract D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26122485/ · DOI 10.1007/s40618-015-0333-4
Complete structured claim and evidence
D-aspartate attenuated hCG-associated LHR staining redistribution from membrane to cytoplasm without changing total LHR protein.
D-Aspartate → LHCGR membrane-to-cytoplasm redistribution in mouse MA-10 cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse MA-10 immunofluorescence and immunoblot comparison.
limitations
Supports a trafficking hypothesis; not proof of universally delayed receptor internalization in human testes.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Receptor location changed even when total receptor amount did not.
primary_references
D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26122485/ · DOI 10.1007/s40618-015-0333-4
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 400–406
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse MA-10 immunofluorescence and immunoblot comparison. · source_derived_draft · unverified_draft
## d-aspartate-leydig-trafficking Receptor location changed even when total receptor amount did not. D-aspartate attenuated hCG-associated LHR staining redistribution from membrane to cytoplasm without changing total LHR protein. Model: Mouse MA-10 immunofluorescence and immunoblot comparison. Limitations: Supports a trafficking hypothesis; not proof of universally delayed receptor internalization in human testes. Evidence access: Primary abstract D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26122485/ · DOI 10.1007/s40618-015-0333-4
Complete structured claim and evidence
Ddo deletion or oral D-aspartate elevation enhanced hippocampal LTP without improving cognitive flexibility in the reported mouse experiments.
D-Aspartate → Mouse hippocampal long-term potentiation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse genetic and oral-exposure models; slices and behavioral tests.
limitations
LTP is not synonymous with better memory; oral dose not specified in accessed abstract.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A stronger synaptic-plasticity signal did not translate into a general cognitive advantage.
primary_references
Increased levels of d-aspartate in the hippocampus enhance LTP but do not facilitate cognitive flexibility. · 2008 · https://pubmed.ncbi.nlm.nih.gov/17981050/ · DOI 10.1016/j.mcn.2007.09.012
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 240–246
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic and oral-exposure models; slices and behavioral tests. · source_derived_draft · unverified_draft
## d-aspartate-ltp A stronger synaptic-plasticity signal did not translate into a general cognitive advantage. Ddo deletion or oral D-aspartate elevation enhanced hippocampal LTP without improving cognitive flexibility in the reported mouse experiments. Model: Mouse genetic and oral-exposure models; slices and behavioral tests. Limitations: LTP is not synonymous with better memory; oral dose not specified in accessed abstract. Evidence access: Primary abstract Increased levels of d-aspartate in the hippocampus enhance LTP but do not facilitate cognitive flexibility. · 2008 · https://pubmed.ncbi.nlm.nih.gov/17981050/ · DOI 10.1016/j.mcn.2007.09.012
Complete structured claim and evidence
Two or four weeks of 20 mM sodium D-aspartate in drinking water improved sperm quality and fertilizing performance in young/adult B6N mice without increasing sperm concentration.
D-Aspartate → Mouse sperm quality and IVF performance source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Male mice aged 9 or 16 weeks at study end; frozen sperm, IVF and birth outcomes.
limitations
Animal reproductive/cryobanking experiment; does not establish human infertility treatment.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Quality and sperm number were different outcomes.
primary_references
Oral D-Aspartate Treatment Improves Sperm Fertility in Both Young and Adult B6N Mice. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35681815/ · DOI 10.3390/ani12111350
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 408–414
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Male mice aged 9 or 16 weeks at study end; frozen sperm, IVF and birth outcomes. · source_derived_draft · unverified_draft
## d-aspartate-mouse-fertility Quality and sperm number were different outcomes. Two or four weeks of 20 mM sodium D-aspartate in drinking water improved sperm quality and fertilizing performance in young/adult B6N mice without increasing sperm concentration. Model: Male mice aged 9 or 16 weeks at study end; frozen sperm, IVF and birth outcomes. Limitations: Animal reproductive/cryobanking experiment; does not establish human infertility treatment. Evidence access: Primary abstract Oral D-Aspartate Treatment Improves Sperm Fertility in Both Young and Adult B6N Mice. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35681815/ · DOI 10.3390/ani12111350
Complete structured claim and evidence
D-aspartate excited mouse nigral dopamine neurons with NMDA, AMPA and metabotropic receptor-sensitive components.
D-Aspartate → Excitatory responses of mouse substantia-nigra dopamine neurons source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse substantia nigra pars compacta slice electrophysiology.
limitations
Antagonist-sensitive responses do not by themselves prove direct agonism at every receptor; indirect glutamate release can contribute.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Several receptor pathways contribute to the observed electrical response.
primary_references
Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 192–198
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse substantia nigra pars compacta slice electrophysiology. · source_derived_draft · unverified_draft
## d-aspartate-nigral-excitation Several receptor pathways contribute to the observed electrical response. D-aspartate excited mouse nigral dopamine neurons with NMDA, AMPA and metabotropic receptor-sensitive components. Model: Mouse substantia nigra pars compacta slice electrophysiology. Limitations: Antagonist-sensitive responses do not by themselves prove direct agonism at every receptor; indirect glutamate release can contribute. Evidence access: Primary abstract Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
Complete structured claim and evidence
The pineal melatonin reduction was partly attributed to lower norepinephrine-stimulated serotonin N-acetyltransferase activity.
D-Aspartate → Rat aralkylamine N-acetyltransferase / Aanat source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat pineal preparation enzyme-activity measurements.
limitations
Partial mediation; does not establish direct binding of D-aspartate to AANAT.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A step in converting serotonin toward melatonin was less active.
primary_references
D-aspartate modulates melatonin synthesis in rat pinealocytes. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9682837/ · DOI 10.1016/s0304-3940(98)00414-5
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 184–190
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pineal preparation enzyme-activity measurements. · source_derived_draft · unverified_draft
## d-aspartate-pineal-aanat A step in converting serotonin toward melatonin was less active. The pineal melatonin reduction was partly attributed to lower norepinephrine-stimulated serotonin N-acetyltransferase activity. Model: Rat pineal preparation enzyme-activity measurements. Limitations: Partial mediation; does not establish direct binding of D-aspartate to AANAT. Evidence access: Primary abstract D-aspartate modulates melatonin synthesis in rat pinealocytes. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9682837/ · DOI 10.1016/s0304-3940(98)00414-5
Complete structured claim and evidence
D-aspartate at 1 mM increased intracellular calcium in 11 of 13 tested rat pinealocytes; NMDA, AMPA and kainate did not evoke this response in the reported panels.
D-Aspartate → Calcium entry in rat pinealocytes source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Rat pinealocyte Fura-2 imaging with substrate/agonist comparisons.
limitations
Transporter depolarization and voltage-gated calcium entry explain the model; many detailed blocker experiments used L-aspartate.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
This pineal response differs from ordinary neuronal NMDA-receptor activation.
primary_references
Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18945893/ · DOI 10.1523/JNEUROSCI.0894-08.2008
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 160–166
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pinealocyte Fura-2 imaging with substrate/agonist comparisons. · source_derived_draft · unverified_draft
## d-aspartate-pineal-calcium This pineal response differs from ordinary neuronal NMDA-receptor activation. D-aspartate at 1 mM increased intracellular calcium in 11 of 13 tested rat pinealocytes; NMDA, AMPA and kainate did not evoke this response in the reported panels. Model: Rat pinealocyte Fura-2 imaging with substrate/agonist comparisons. Limitations: Transporter depolarization and voltage-gated calcium entry explain the model; many detailed blocker experiments used L-aspartate. Evidence access: Primary full text Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18945893/ · DOI 10.1523/JNEUROSCI.0894-08.2008
Complete structured claim and evidence
D-aspartate elicited inward transporter-associated current in isolated rat pinealocytes; pharmacology favored GLT-1-type transport over ionotropic glutamate receptors.
D-Aspartate → Glutamate-transporter current in rat pinealocytes source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Rat pinealocytes and slices; electrogenic current assays.
limitations
Subtype assignment is pharmacological and supported by prior expression work, not a subtype-knockout demonstration.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Transporting the amino acid can itself change the cell voltage.
primary_references
Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18945893/ · DOI 10.1523/JNEUROSCI.0894-08.2008
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 152–158
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pinealocytes and slices; electrogenic current assays. · source_derived_draft · unverified_draft
## d-aspartate-pineal-current Transporting the amino acid can itself change the cell voltage. D-aspartate elicited inward transporter-associated current in isolated rat pinealocytes; pharmacology favored GLT-1-type transport over ionotropic glutamate receptors. Model: Rat pinealocytes and slices; electrogenic current assays. Limitations: Subtype assignment is pharmacological and supported by prior expression work, not a subtype-knockout demonstration. Evidence access: Primary full text Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18945893/ · DOI 10.1523/JNEUROSCI.0894-08.2008
Complete structured claim and evidence
D-aspartate inhibited norepinephrine-stimulated melatonin production in rat pineal preparations, with approximately 75 micromolar required for half-maximal inhibition.
D-Aspartate → Melatonin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat pineal gland/pinealocyte incubation.
limitations
Not a human sleep trial or a demonstrated interaction with a melatonin supplement.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The compound can reduce stimulated melatonin production in this tissue model.
primary_references
D-aspartate modulates melatonin synthesis in rat pinealocytes. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9682837/ · DOI 10.1016/s0304-3940(98)00414-5
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 176–182
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pineal gland/pinealocyte incubation. · source_derived_draft · unverified_draft
## d-aspartate-pineal-melatonin The compound can reduce stimulated melatonin production in this tissue model. D-aspartate inhibited norepinephrine-stimulated melatonin production in rat pineal preparations, with approximately 75 micromolar required for half-maximal inhibition. Model: Rat pineal gland/pinealocyte incubation. Limitations: Not a human sleep trial or a demonstrated interaction with a melatonin supplement. Evidence access: Primary abstract D-aspartate modulates melatonin synthesis in rat pinealocytes. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9682837/ · DOI 10.1016/s0304-3940(98)00414-5
Complete structured claim and evidence
The study reported D-aspartate-evoked glutamate secretion with blocker sensitivity similar to L-aspartate, supporting calcium-dependent vesicular release downstream of transport.
D-Aspartate → Glutamate exocytosis from rat pinealocytes source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text; supplementary result described in main text
experimental_model
Rat pinealocytes; HPLC and calcium/exocytosis experiments; D-form comparison reported in supplemental results.
limitations
Main figures often use L-aspartate. Direct D-aspartate binding to inhibitory metabotropic receptors was not established.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
An aspartate signal can release another signaling amino acid.
primary_references
Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18945893/ · DOI 10.1523/JNEUROSCI.0894-08.2008
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 168–174
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pinealocytes; HPLC and calcium/exocytosis experiments; D-form comparison reported in supplemental results. · source_derived_draft · unverified_draft
## d-aspartate-pineal-release An aspartate signal can release another signaling amino acid. The study reported D-aspartate-evoked glutamate secretion with blocker sensitivity similar to L-aspartate, supporting calcium-dependent vesicular release downstream of transport. Model: Rat pinealocytes; HPLC and calcium/exocytosis experiments; D-form comparison reported in supplemental results. Limitations: Main figures often use L-aspartate. Direct D-aspartate binding to inhibitory metabotropic receptors was not established. Evidence access: Primary full text; supplementary result described in main text Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18945893/ · DOI 10.1523/JNEUROSCI.0894-08.2008
Complete structured claim and evidence
Rat Leydig cells incubated with 0.1 or 1 mM D-aspartate showed increased measured testosterone and cAMP.
D-Aspartate → Testosterone output in rat Leydig-cell incubation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Isolated rat Leydig cells, 60-minute incubations.
limitations
cAMP involvement is supported by co-change, not an exclusive pathway demonstrated by blocking or rescue.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A second rat experiment located a response in steroid-producing cells.
primary_references
The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 376–382
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated rat Leydig cells, 60-minute incubations. · source_derived_draft · unverified_draft
## d-aspartate-rat-leydig A second rat experiment located a response in steroid-producing cells. Rat Leydig cells incubated with 0.1 or 1 mM D-aspartate showed increased measured testosterone and cAMP. Model: Isolated rat Leydig cells, 60-minute incubations. Limitations: cAMP involvement is supported by co-change, not an exclusive pathway demonstrated by blocking or rescue. Evidence access: Primary full text The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
Complete structured claim and evidence
Rat pituitary incubation with 0.1 or 1 mM D-aspartate increased measured LH and cGMP over 60 minutes.
D-Aspartate → LH content/output in rat pituitary incubation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Isolated rat pituitary; tissue plus medium assays.
limitations
The association does not alone prove cGMP is the exclusive causal mediator; not direct human pituitary evidence.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A rat tissue experiment links the response to a second-messenger change.
primary_references
The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated rat pituitary; tissue plus medium assays. · source_derived_draft · unverified_draft
## d-aspartate-rat-pituitary-lh A rat tissue experiment links the response to a second-messenger change. Rat pituitary incubation with 0.1 or 1 mM D-aspartate increased measured LH and cGMP over 60 minutes. Model: Isolated rat pituitary; tissue plus medium assays. Limitations: The association does not alone prove cGMP is the exclusive causal mediator; not direct human pituitary evidence. Evidence access: Primary full text The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19860889/ · DOI 10.1186/1477-7827-7-120
Complete structured claim and evidence
Intravenous D-aspartate at 0.05 or 0.1 mmol/kg/min for 20 minutes increased circulating growth hormone in wethers.
D-Aspartate → Plasma growth hormone in wethers source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Castrated male sheep; high- and low-dose infusion tests.
limitations
Not an oral human result. Pituitary tissue experiments did not show a statistically significant direct secretion effect, so the route remains unresolved.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
An intravenous animal experiment found an endocrine effect beyond testosterone.
primary_references
D-aspartate stimulates growth hormone secretion in wethers. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39432441/ · DOI 10.1093/jas/skae318
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Castrated male sheep; high- and low-dose infusion tests. · source_derived_draft · unverified_draft
## d-aspartate-sheep-gh An intravenous animal experiment found an endocrine effect beyond testosterone. Intravenous D-aspartate at 0.05 or 0.1 mmol/kg/min for 20 minutes increased circulating growth hormone in wethers. Model: Castrated male sheep; high- and low-dose infusion tests. Limitations: Not an oral human result. Pituitary tissue experiments did not show a statistically significant direct secretion effect, so the route remains unresolved. Evidence access: Primary abstract D-aspartate stimulates growth hormone secretion in wethers. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39432441/ · DOI 10.1093/jas/skae318
Complete structured claim and evidence
Both D-aspartate infusion doses reduced plasma insulin; glucose and circulating catecholamines did not significantly change.
D-Aspartate → Plasma insulin in wethers source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Wethers; 20-minute intravenous infusion at 0.05 or 0.1 mmol/kg/min.
limitations
This does not establish improved insulin sensitivity or a desirable human metabolic outcome.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Hormone concentrations changed without a demonstrated glucose improvement.
primary_references
D-aspartate stimulates growth hormone secretion in wethers. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39432441/ · DOI 10.1093/jas/skae318
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 424–430
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Wethers; 20-minute intravenous infusion at 0.05 or 0.1 mmol/kg/min. · source_derived_draft · unverified_draft
## d-aspartate-sheep-insulin Hormone concentrations changed without a demonstrated glucose improvement. Both D-aspartate infusion doses reduced plasma insulin; glucose and circulating catecholamines did not significantly change. Model: Wethers; 20-minute intravenous infusion at 0.05 or 0.1 mmol/kg/min. Limitations: This does not establish improved insulin sensitivity or a desirable human metabolic outcome. Evidence access: Primary abstract D-aspartate stimulates growth hormone secretion in wethers. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39432441/ · DOI 10.1093/jas/skae318
Complete structured claim and evidence
D-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; NMDA, AMPA/kainate and mGlu5 antagonists attenuated or prevented the effect.
D-Aspartate → Glutamate release from mouse cortical synaptosomes source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA.
limitations
This is evoked release under transporter blockade, not basal release in an intact human brain.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Receptor-sensitive feedback changed release under an uptake-blocked assay condition.
primary_references
Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 232–238
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA. · source_derived_draft · unverified_draft
## d-aspartate-terminal-glutamate Receptor-sensitive feedback changed release under an uptake-blocked assay condition. D-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; NMDA, AMPA/kainate and mGlu5 antagonists attenuated or prevented the effect. Model: Mouse cortical terminals; 15 mM potassium stimulus, 10 micromolar TBOA. Limitations: This is evoked release under transporter blockade, not basal release in an intact human brain. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidence

What acts on it

Purified human DDO-1 oxidized D-aspartate; the reported Km was 2.7 mM and kcat 52.5 per second.
Human D-aspartate oxidase / DDO → D-Aspartate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant human 341-residue DDO-1.
limitations
Assay kinetic constants are not clinical plasma targets; do not assign these activities to the alternatively spliced deletion isoform.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Humans have an enzyme that breaks down D-aspartate.
primary_references
Structural and functional characterization of the human brain D-aspartate oxidase. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9163533/ · DOI 10.1093/oxfordjournals.jbchem.a021655
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 72–78
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human 341-residue DDO-1. · source_derived_draft · unverified_draft
## d-aspartate-human-ddo-activity Humans have an enzyme that breaks down D-aspartate. Purified human DDO-1 oxidized D-aspartate; the reported Km was 2.7 mM and kcat 52.5 per second. Model: Recombinant human 341-residue DDO-1. Limitations: Assay kinetic constants are not clinical plasma targets; do not assign these activities to the alternatively spliced deletion isoform. Evidence access: Primary abstract Structural and functional characterization of the human brain D-aspartate oxidase. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9163533/ · DOI 10.1093/oxfordjournals.jbchem.a021655
Complete structured claim and evidence
Purified mammalian serine racemase catalyzed aspartate racemization in the reported two-base reaction mechanism.
Mammalian serine-racemase assay, species unresolved in accessed abstract → D-Aspartate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant mammalian enzyme; protein species not resolved in the accessed abstract.
limitations
Do not substitute a specific human enzyme identity or infer rates in intact human tissues.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
An enzyme best known for serine can also change aspartate chirality.
primary_references
Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant mammalian enzyme; protein species not resolved in the accessed abstract. · source_derived_draft · unverified_draft
## d-aspartate-srr-racemization An enzyme best known for serine can also change aspartate chirality. Purified mammalian serine racemase catalyzed aspartate racemization in the reported two-base reaction mechanism. Model: Recombinant mammalian enzyme; protein species not resolved in the accessed abstract. Limitations: Do not substitute a specific human enzyme identity or infer rates in intact human tissues. Evidence access: Primary abstract Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
Complete structured claim and evidence

Where it participates (unsigned role)

Persistent D-aspartate elevation after Ddo deletion accompanied increased extracellular glutamate, active caspases, reactive glia and age-dependent brain abnormalities.
Mouse D-aspartate oxidase / Ddo → Age-dependent brain pathology after mouse Ddo deletion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Constitutive Ddo-knockout mice studied across age.
limitations
Genetic lifelong exposure is not equivalent to a short human supplement course.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Long-term loss of clearance had adverse outcomes despite some short-term signaling effects.
primary_references
d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
trigger_kind
machinery_impairment Imported condition classification; unverified.
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 248–254
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Constitutive Ddo-knockout mice studied across age. · source_derived_draft · unverified_draft
## d-aspartate-chronic-loss-aging Long-term loss of clearance had adverse outcomes despite some short-term signaling effects. Persistent D-aspartate elevation after Ddo deletion accompanied increased extracellular glutamate, active caspases, reactive glia and age-dependent brain abnormalities. Model: Constitutive Ddo-knockout mice studied across age. Limitations: Genetic lifelong exposure is not equivalent to a short human supplement course. Evidence access: Primary abstract d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
Complete structured claim and evidence
Aged Ddo-knockout mice showed reduced synaptic GluN1/GluN2B, altered plasticity and greater vulnerability to phencyclidine-related prepulse-inhibition deficits.
Mouse D-aspartate oxidase / Ddo → Synaptic NMDA receptor availability in mouse hippocampus source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Aging Ddo-knockout mouse hippocampus and behavior.
limitations
Different age/region/endpoint from nigral GluN1/GluN2A increases; recorded as context, not a wording correction.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Receptor adaptation can reverse the apparent direction of an earlier signaling effect.
primary_references
d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
trigger_kind
machinery_impairment Imported condition classification; unverified.
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 256–262
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Aging Ddo-knockout mouse hippocampus and behavior. · source_derived_draft · unverified_draft
## d-aspartate-chronic-loss-receptors Receptor adaptation can reverse the apparent direction of an earlier signaling effect. Aged Ddo-knockout mice showed reduced synaptic GluN1/GluN2B, altered plasticity and greater vulnerability to phencyclidine-related prepulse-inhibition deficits. Model: Aging Ddo-knockout mouse hippocampus and behavior. Limitations: Different age/region/endpoint from nigral GluN1/GluN2A increases; recorded as context, not a wording correction. Evidence access: Primary abstract d-Aspartate oxidase influences glutamatergic system homeostasis in mammalian brain. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25771393/ · DOI 10.1016/j.neurobiolaging.2015.02.003
Complete structured claim and evidence
Rat kidney, liver and brain DDO activity became detectable one to four days after birth and reached adult values around four weeks.
Rat D-aspartate oxidase / Ddo → Postnatal DDO activity in rat tissues source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat tissue oxidase assays; activity greatest in kidney in the tested panel.
limitations
No equivalent human developmental timetable or adult dietary requirement is established.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The breakdown system changes during development.
primary_references
D-aspartate oxidase, a peroxisomal enzyme in liver of rat and man. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1991137/ · DOI 10.1016/0304-4165(91)90203-s
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 136–142
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat tissue oxidase assays; activity greatest in kidney in the tested panel. · source_derived_draft · unverified_draft
## d-aspartate-ddo-development The breakdown system changes during development. Rat kidney, liver and brain DDO activity became detectable one to four days after birth and reached adult values around four weeks. Model: Rat tissue oxidase assays; activity greatest in kidney in the tested panel. Limitations: No equivalent human developmental timetable or adult dietary requirement is established. Evidence access: Primary abstract D-aspartate oxidase, a peroxisomal enzyme in liver of rat and man. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1991137/ · DOI 10.1016/0304-4165(91)90203-s
Complete structured claim and evidence
Human D-aspartate oxidase structure and kinetics showed a FAD-containing enzyme with higher FAD affinity than human D-amino-acid oxidase.
FAD → Human D-aspartate oxidase / DDO source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified human DASPO/DDO structural and kinetic comparison with human DAO.
limitations
Does not show that dietary riboflavin limits DDO in vivo or that DAO inhibitors also inhibit DDO.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Two similarly named enzymes handle different D-amino-acid pathways and bind their cofactor differently.
primary_references
Structure and kinetic properties of human d-aspartate oxidase, the enzyme-controlling d-aspartate levels in brain. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31914658/ · DOI 10.1096/fj.201901703R
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 96–102
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human DASPO/DDO structural and kinetic comparison with human DAO. · source_derived_draft · unverified_draft
## d-aspartate-ddo-fad Two similarly named enzymes handle different D-amino-acid pathways and bind their cofactor differently. Human D-aspartate oxidase structure and kinetics showed a FAD-containing enzyme with higher FAD affinity than human D-amino-acid oxidase. Model: Purified human DASPO/DDO structural and kinetic comparison with human DAO. Limitations: Does not show that dietary riboflavin limits DDO in vivo or that DAO inhibitors also inhibit DDO. Evidence access: Primary abstract Structure and kinetic properties of human d-aspartate oxidase, the enzyme-controlling d-aspartate levels in brain. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31914658/ · DOI 10.1096/fj.201901703R
Complete structured claim and evidence
Porcine kidney DDO oxidized D-aspartate to iminoaspartate while reducing enzyme-bound FAD.
Porcine D-aspartate oxidase / DDO → Iminoaspartate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified native and recombinant porcine kidney enzyme.
limitations
Species-specific enzyme evidence; FAD is recycled rather than consumed once per substrate molecule.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The first chemical step removes reducing equivalents from D-aspartate.
primary_references
Functional and structural characterization of D-aspartate oxidase from porcine kidney: non-Michaelis kinetics due to substrate activation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17234685/ · DOI 10.1093/jb/mvm041
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 104–110
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified native and recombinant porcine kidney enzyme. · source_derived_draft · unverified_draft
## d-aspartate-ddo-imino The first chemical step removes reducing equivalents from D-aspartate. Porcine kidney DDO oxidized D-aspartate to iminoaspartate while reducing enzyme-bound FAD. Model: Purified native and recombinant porcine kidney enzyme. Limitations: Species-specific enzyme evidence; FAD is recycled rather than consumed once per substrate molecule. Evidence access: Primary abstract Functional and structural characterization of D-aspartate oxidase from porcine kidney: non-Michaelis kinetics due to substrate activation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17234685/ · DOI 10.1093/jb/mvm041
Complete structured claim and evidence
Ddo deletion increased NMDA-evoked currents and membrane GluN1/GluN2A in mouse nigral dopamine neurons.
Mouse D-aspartate oxidase / Ddo → Mouse NMDA-type receptors, subunits unresolved source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Ddo-knockout mouse substantia-nigra neurons.
limitations
Region-specific knockout response; not a universal change after oral supplementation.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Prolonged higher D-aspartate was accompanied by receptor remodeling.
primary_references
Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
trigger_kind
machinery_impairment Imported condition classification; unverified.
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ddo-knockout mouse substantia-nigra neurons. · source_derived_draft · unverified_draft
## d-aspartate-ddo-loss-nmdar Prolonged higher D-aspartate was accompanied by receptor remodeling. Ddo deletion increased NMDA-evoked currents and membrane GluN1/GluN2A in mouse nigral dopamine neurons. Model: Ddo-knockout mouse substantia-nigra neurons. Limitations: Region-specific knockout response; not a universal change after oral supplementation. Evidence access: Primary abstract Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
Complete structured claim and evidence
Postnatal mouse Ddo promoter demethylation accompanied rising Ddo mRNA; azacitidine treatment increased Ddo transcripts in embryonic cortical neurons.
Mouse Ddo promoter demethylation → Mouse D-aspartate oxidase / Ddo source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse development and cultured embryonic-neuron demethylating-drug experiments.
limitations
Azacitidine has broad effects. This is not evidence that folate intake directly switches DDO on or off.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Gene regulation can change the capacity to clear D-aspartate.
primary_references
Age-Related Changes in D-Aspartate Oxidase Promoter Methylation Control Extracellular D-Aspartate Levels and Prevent Precocious Cell Death during Brain Aging. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26961959/ · DOI 10.1523/JNEUROSCI.3881-15.2016
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse development and cultured embryonic-neuron demethylating-drug experiments. · source_derived_draft · unverified_draft
## d-aspartate-ddo-methylation Gene regulation can change the capacity to clear D-aspartate. Postnatal mouse Ddo promoter demethylation accompanied rising Ddo mRNA; azacitidine treatment increased Ddo transcripts in embryonic cortical neurons. Model: Mouse development and cultured embryonic-neuron demethylating-drug experiments. Limitations: Azacitidine has broad effects. This is not evidence that folate intake directly switches DDO on or off. Evidence access: Primary abstract Age-Related Changes in D-Aspartate Oxidase Promoter Methylation Control Extracellular D-Aspartate Levels and Prevent Precocious Cell Death during Brain Aging. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26961959/ · DOI 10.1523/JNEUROSCI.3881-15.2016
Complete structured claim and evidence
Reoxidation of reduced FAD by oxygen during porcine DDO turnover produced hydrogen peroxide.
Porcine D-aspartate oxidase / DDO → Hydrogen peroxide source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified porcine enzyme oxidative half-reaction.
limitations
This chemistry alone does not demonstrate oxidative injury after human oral supplementation.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Clearing D-aspartate also generates a peroxide-handling requirement.
primary_references
Functional and structural characterization of D-aspartate oxidase from porcine kidney: non-Michaelis kinetics due to substrate activation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17234685/ · DOI 10.1093/jb/mvm041
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified porcine enzyme oxidative half-reaction. · source_derived_draft · unverified_draft
## d-aspartate-ddo-peroxide Clearing D-aspartate also generates a peroxide-handling requirement. Reoxidation of reduced FAD by oxygen during porcine DDO turnover produced hydrogen peroxide. Model: Purified porcine enzyme oxidative half-reaction. Limitations: This chemistry alone does not demonstrate oxidative injury after human oral supplementation. Evidence access: Primary abstract Functional and structural characterization of D-aspartate oxidase from porcine kidney: non-Michaelis kinetics due to substrate activation. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17234685/ · DOI 10.1093/jb/mvm041
Complete structured claim and evidence
Subcellular fractionation localized D-aspartate oxidase activity to peroxisomes in human liver.
Human D-aspartate oxidase / DDO → Human liver peroxisomes source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human liver fractionation; rat liver also studied.
limitations
The study did not find a significant oxidase deficiency in its Zellweger liver samples; peroxisomal disease is not automatically DDO deficiency.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Clearance chemistry is organized within a cellular compartment.
primary_references
D-aspartate oxidase, a peroxisomal enzyme in liver of rat and man. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1991137/ · DOI 10.1016/0304-4165(91)90203-s
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 88–94
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human liver fractionation; rat liver also studied. · source_derived_draft · unverified_draft
## d-aspartate-ddo-peroxisome Clearance chemistry is organized within a cellular compartment. Subcellular fractionation localized D-aspartate oxidase activity to peroxisomes in human liver. Model: Human liver fractionation; rat liver also studied. Limitations: The study did not find a significant oxidase deficiency in its Zellweger liver samples; peroxisomal disease is not automatically DDO deficiency. Evidence access: Primary abstract D-aspartate oxidase, a peroxisomal enzyme in liver of rat and man. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1991137/ · DOI 10.1016/0304-4165(91)90203-s
Complete structured claim and evidence
Purified human, rat and mouse DDO differed in kinetic and inhibitor-binding properties.
Human D-aspartate oxidase / DDO → Mouse D-aspartate oxidase / Ddo source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Comparative recombinant enzyme assays and structural models.
limitations
Rodent efficacy is not a measured human effect.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A compound that changes rodent clearance may act differently on the human enzyme.
primary_references
Characterization of the enzymatic and structural properties of human D-aspartate oxidase and comparison with those of the rat and mouse enzymes. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25747990/ · DOI 10.1248/bpb.b14-00690
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Comparative recombinant enzyme assays and structural models. · source_derived_draft · unverified_draft
## d-aspartate-ddo-species A compound that changes rodent clearance may act differently on the human enzyme. Purified human, rat and mouse DDO differed in kinetic and inhibitor-binding properties. Model: Comparative recombinant enzyme assays and structural models. Limitations: Rodent efficacy is not a measured human effect. Evidence access: Primary abstract Characterization of the enzymatic and structural properties of human D-aspartate oxidase and comparison with those of the rat and mouse enzymes. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25747990/ · DOI 10.1248/bpb.b14-00690
Complete structured claim and evidence
DDO mRNA was higher in the study prefrontal samples from people with schizophrenia than controls.
Schizophrenia diagnosis in postmortem comparisons → Human prefrontal DDO transcript abundance source_derived_draftungraded
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.
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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
A later postmortem study found no significant schizophrenia-related difference in DDO transcription or methylation despite higher DDO activity in dorsolateral prefrontal cortex.
Schizophrenia diagnosis in postmortem comparisons → Human prefrontal DDO transcript abundance source_derived_draftungraded
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.
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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
Human DDO-1 also oxidized N-methyl-D-aspartate, with reported Km 6.8 mM and kcat 37.7 per second.
Human D-aspartate oxidase / DDO → N-Methyl-D-aspartate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified recombinant human DDO-1.
limitations
Does not establish endogenous NMDA synthesis or justify conflating NMDA with D-aspartate.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The enzyme accepts a related chemical that is distinct from the NMDA receptor.
primary_references
Structural and functional characterization of the human brain D-aspartate oxidase. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9163533/ · DOI 10.1093/oxfordjournals.jbchem.a021655
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified recombinant human DDO-1. · source_derived_draft · unverified_draft
## d-aspartate-human-ddo-nmda The enzyme accepts a related chemical that is distinct from the NMDA receptor. Human DDO-1 also oxidized N-methyl-D-aspartate, with reported Km 6.8 mM and kcat 37.7 per second. Model: Purified recombinant human DDO-1. Limitations: Does not establish endogenous NMDA synthesis or justify conflating NMDA with D-aspartate. Evidence access: Primary abstract Structural and functional characterization of the human brain D-aspartate oxidase. · 1997 · https://pubmed.ncbi.nlm.nih.gov/9163533/ · DOI 10.1093/oxfordjournals.jbchem.a021655
Complete structured claim and evidence
An expanded regional methylation/expression analysis found brain-region differences but no significant diagnostic association for DDO expression or methylation.
Schizophrenia diagnosis in postmortem comparisons → Human prefrontal DDO transcript abundance source_derived_draftungraded
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.
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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
Schizophrenia DLPFC samples had approximately 30% lower free D-aspartate and 25% higher DDO activity; the D-aspartate reduction was not detected in hippocampus.
Schizophrenia diagnosis in postmortem comparisons → Free D-aspartate in human dorsolateral prefrontal cortex source_derived_draftungraded
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.
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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
Lowering assay FAD from 100 to 4 micromolar shifted olanzapine IC50 at mouse DDO from about 5.6 to 1.4 micromolar; the human enzyme did not show this potency shift.
FAD → Olanzapine inhibition potency at mouse DDO source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Recombinant mouse versus human DDO assays.
limitations
This is not an observed dietary riboflavin-drug interaction in people.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Cofactor conditions altered the mouse drug-enzyme interaction.
primary_references
Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant mouse versus human DDO assays. · source_derived_draft · unverified_draft
## d-aspartate-olanzapine-fad-species Cofactor conditions altered the mouse drug-enzyme interaction. Lowering assay FAD from 100 to 4 micromolar shifted olanzapine IC50 at mouse DDO from about 5.6 to 1.4 micromolar; the human enzyme did not show this potency shift. Model: Recombinant mouse versus human DDO assays. Limitations: This is not an observed dietary riboflavin-drug interaction in people. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidence
Olanzapine inhibited recombinant human DDO at an IC50 near 23 micromolar under both 4 and 100 micromolar FAD conditions; clozapine did not inhibit the tested enzyme.
Olanzapine → Human D-aspartate oxidase / DDO source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Purified human DDO drug concentration-response assay.
limitations
Biochemical potency is not proof of clinically relevant brain inhibition or a reason to change treatment.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Two drugs differed at a D-aspartate-clearing enzyme.
primary_references
Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human DDO drug concentration-response assay. · source_derived_draft · unverified_draft
## d-aspartate-olanzapine-human-ddo Two drugs differed at a D-aspartate-clearing enzyme. Olanzapine inhibited recombinant human DDO at an IC50 near 23 micromolar under both 4 and 100 micromolar FAD conditions; clozapine did not inhibit the tested enzyme. Model: Purified human DDO drug concentration-response assay. Limitations: Biochemical potency is not proof of clinically relevant brain inhibition or a reason to change treatment. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidence
Four weeks of olanzapine at 5 mg/kg/day intraperitoneally increased prefrontal extracellular D-aspartate and glutamate in wild-type mice; the increments were absent in Ddo-knockout mice.
Olanzapine → Extracellular D-aspartate in mouse prefrontal cortex source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Mouse microdialysis 24 hours after the final injection.
limitations
Knockouts already differ at baseline. This does not prove the pathway mediates clinical antipsychotic efficacy.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Removing the enzyme removed this drug-associated increment in the mouse experiment.
primary_references
Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse microdialysis 24 hours after the final injection. · source_derived_draft · unverified_draft
## d-aspartate-olanzapine-mouse-dependence Removing the enzyme removed this drug-associated increment in the mouse experiment. Four weeks of olanzapine at 5 mg/kg/day intraperitoneally increased prefrontal extracellular D-aspartate and glutamate in wild-type mice; the increments were absent in Ddo-knockout mice. Model: Mouse microdialysis 24 hours after the final injection. Limitations: Knockouts already differ at baseline. This does not prove the pathway mediates clinical antipsychotic efficacy. Evidence access: Primary full text Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28393897/ · DOI 10.1038/srep46288
Complete structured claim and evidence
Srr-knockout mouse forebrain had less D-aspartate without detected differences in DDO activity or L-aspartate concentrations.
Mouse serine racemase / Srr → Mouse regional brain free D-aspartate pool source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse frontal cortex, hippocampus and striatum; cerebellum unaffected.
limitations
Association supported a production hypothesis; it did not independently identify the complete biosynthetic pathway.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
A smaller pool was not explained by higher measured breakdown or lower L-aspartate.
primary_references
Decreased levels of free D-aspartic acid in the forebrain of serine racemase (Srr) knock-out mice. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23439386/ · DOI 10.1016/j.neuint.2013.02.015
trigger_kind
machinery_impairment Imported condition classification; unverified.
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse frontal cortex, hippocampus and striatum; cerebellum unaffected. · source_derived_draft · unverified_draft
## d-aspartate-srr-loss-ddo-control A smaller pool was not explained by higher measured breakdown or lower L-aspartate. Srr-knockout mouse forebrain had less D-aspartate without detected differences in DDO activity or L-aspartate concentrations. Model: Mouse frontal cortex, hippocampus and striatum; cerebellum unaffected. Limitations: Association supported a production hypothesis; it did not independently identify the complete biosynthetic pathway. Evidence access: Primary abstract Decreased levels of free D-aspartic acid in the forebrain of serine racemase (Srr) knock-out mice. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23439386/ · DOI 10.1016/j.neuint.2013.02.015
Complete structured claim and evidence
Mg2+ and ATP increased recombinant serine-racemase serine racemization and pyruvate production by approximately five- to ten-fold in the study assay.
Serine-racemase cofactor assay, construct species unresolved here → Magnesium/ATP stimulation of serine-racemase activity source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant enzyme and cell-extract experiments; construct species not resolved in accessed abstract.
limitations
This is a shared-machinery connection, not a demonstrated magnesium effect on D-aspartate flux.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Mineral and energy cofactors affect this enzyme, but the measured substrate was serine.
primary_references
Cofactors of serine racemase that physiologically stimulate the synthesis of the N-methyl-D-aspartate (NMDA) receptor coagonist D-serine. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12393813/ · DOI 10.1073/pnas.222421299
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant enzyme and cell-extract experiments; construct species not resolved in accessed abstract. · source_derived_draft · unverified_draft
## d-aspartate-srr-mg-atp Mineral and energy cofactors affect this enzyme, but the measured substrate was serine. Mg2+ and ATP increased recombinant serine-racemase serine racemization and pyruvate production by approximately five- to ten-fold in the study assay. Model: Recombinant enzyme and cell-extract experiments; construct species not resolved in accessed abstract. Limitations: This is a shared-machinery connection, not a demonstrated magnesium effect on D-aspartate flux. Evidence access: Primary abstract Cofactors of serine racemase that physiologically stimulate the synthesis of the N-methyl-D-aspartate (NMDA) receptor coagonist D-serine. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12393813/ · DOI 10.1073/pnas.222421299
Complete structured claim and evidence
Srr deletion lowered D-aspartate in mouse frontal cortex and hippocampus, while cerebellum and testes were unchanged.
Mouse serine racemase / Srr → Mouse regional brain free D-aspartate pool source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Srr-knockout mice; regional amino-acid measurements.
limitations
Not dietary deficiency or proof that a supplement repairs the knockout.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Dependence on the same enzyme varies by tissue.
primary_references
Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
trigger_kind
machinery_impairment Imported condition classification; unverified.
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 40–46
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Srr-knockout mice; regional amino-acid measurements. · source_derived_draft · unverified_draft
## d-aspartate-srr-mouse-loss Dependence on the same enzyme varies by tissue. Srr deletion lowered D-aspartate in mouse frontal cortex and hippocampus, while cerebellum and testes were unchanged. Model: Srr-knockout mice; regional amino-acid measurements. Limitations: Not dietary deficiency or proof that a supplement repairs the knockout. Evidence access: Primary abstract Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
Complete structured claim and evidence
SRR overexpression increased intracellular D-aspartate in rat PC12 cells.
Mammalian serine-racemase assay, species unresolved in accessed abstract → D-aspartate pool in rat PC12 cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat PC12 host cells; overexpressed construct species not resolved here.
limitations
Overexpression does not establish that native SRR is the sole source.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Adding more racemase increased the measured D-aspartate pool.
primary_references
Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 24–30
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat PC12 host cells; overexpressed construct species not resolved here. · source_derived_draft · unverified_draft
## d-aspartate-srr-overexpression Adding more racemase increased the measured D-aspartate pool. SRR overexpression increased intracellular D-aspartate in rat PC12 cells. Model: Rat PC12 host cells; overexpressed construct species not resolved here. Limitations: Overexpression does not establish that native SRR is the sole source. Evidence access: Primary abstract Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
Complete structured claim and evidence
Deleting endogenous SRR in rat PC12 cells lowered D-serine but left D-aspartate production unchanged.
Rat serine racemase / Srr → D-aspartate pool in rat PC12 cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat PC12 SRR knockout.
limitations
The alternative synthesis route was not identified.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
The cells retained another way to maintain D-aspartate.
primary_references
Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
trigger_kind
machinery_impairment Imported condition classification; unverified.
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 32–38
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat PC12 SRR knockout. · source_derived_draft · unverified_draft
## d-aspartate-srr-pc12-loss The cells retained another way to maintain D-aspartate. Deleting endogenous SRR in rat PC12 cells lowered D-serine but left D-aspartate production unchanged. Model: Rat PC12 SRR knockout. Limitations: The alternative synthesis route was not identified. Evidence access: Primary abstract Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
Complete structured claim and evidence
The 1.89-angstrom human serine-racemase holoenzyme structure included its bound pyridoxal-phosphate cofactor.
PLP → Human serine racemase / SRR source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified human SRR crystal structure.
limitations
Structural cofactor binding does not establish dietary B6 control of human D-aspartate or an effective supplementation threshold.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Vitamin B6-derived PLP is part of the shared racemase machinery.
primary_references
Conformational flexibility within the small domain of human serine racemase. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32039887/ · DOI 10.1107/S2053230X20001193
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 56–62
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human SRR crystal structure. · source_derived_draft · unverified_draft
## d-aspartate-srr-plp Vitamin B6-derived PLP is part of the shared racemase machinery. The 1.89-angstrom human serine-racemase holoenzyme structure included its bound pyridoxal-phosphate cofactor. Model: Purified human SRR crystal structure. Limitations: Structural cofactor binding does not establish dietary B6 control of human D-aspartate or an effective supplementation threshold. Evidence access: Primary abstract Conformational flexibility within the small domain of human serine racemase. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32039887/ · DOI 10.1107/S2053230X20001193
Complete structured claim and evidence
EAAT inhibition strongly potentiated D-aspartate-evoked, but not L-aspartate-evoked, currents in Ddo-knockout mouse neurons.
EAAT inhibition in mouse nigral neurons → Excitatory responses of mouse substantia-nigra dopamine neurons source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Ddo-knockout mouse nigral neuron transporter-blocker experiments.
limitations
A protective adaptation is an interpretation; human transporter failure and dietary consequences were not tested.
nutrient_topic
D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
plain_language
Uptake can buffer excitation when breakdown is impaired.
primary_references
Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
trigger_kind
machinery_impairment Imported condition classification; unverified.
D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 208–214
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ddo-knockout mouse nigral neuron transporter-blocker experiments. · source_derived_draft · unverified_draft
## d-aspartate-uptake-buffer Uptake can buffer excitation when breakdown is impaired. EAAT inhibition strongly potentiated D-aspartate-evoked, but not L-aspartate-evoked, currents in Ddo-knockout mouse neurons. Model: Ddo-knockout mouse nigral neuron transporter-blocker experiments. Limitations: A protective adaptation is an interpretation; human transporter failure and dietary consequences were not tested. Evidence access: Primary abstract Persistent elevation of D-Aspartate enhances NMDA receptor-mediated responses in mouse substantia nigra pars compacta dopamine neurons. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26707656/ · DOI 10.1016/j.neuropharm.2015.12.013
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

D-Aspartate

How nutrients influence it

Other things that act on it

How nutrients reach it in more than one step

What it does

What it acts on

Oral D-aspartate at 20 mM in drinking water for one month and a separate 500 mg/kg intraperitoneal exposure increased extracellular prefrontal D-aspartate in mice.

One-month 20 mM oral D-aspartate increased extracellular prefrontal glutamate; acute 500 mg/kg injection did not increase striatal glutamate.

Porcine DDO showed substrate activation above approximately 0.2 mM D-aspartate; N-methyl-D-aspartate instead produced substrate inhibition.

In a 24-man resistance-trained trial, 3 g/day for 14 days did not change testosterone; 6 g/day lowered total and calculated free testosterone.

After 12 days, 23 men taking 3.12 g/day sodium D-aspartate with B6, folate and B12 had a reported 33% mean LH rise from baseline; 20 men received sodium-chloride placebo with the same vitamins.

The same 12-day sodium D-aspartate study reported mean testosterone rising from 4.5 to 6.4 ng/mL; the matched-vitamin placebo group showed no corresponding increase.

The 6 g/day D-aspartate arm showed a reported 16% estradiol decrease over 12 weeks.

A 12-week 6 g/day trial in trained men found no testosterone benefit or added strength/hypertrophy benefit over placebo.

In resistance-trained men, 3 g/day D-aspartic acid for 28 days did not improve testosterone, strength or body composition relative to placebo.

In mouse MA-10 cells, D-aspartate alone did not meaningfully increase measured testosterone; 0.1 or 1 nM D-aspartate augmented the hCG-stimulated immunoassay signal.

Adding 0.1 nM D-aspartate to hCG stimulation increased StAR protein in mouse MA-10 cells compared with hCG alone.

D-aspartate attenuated hCG-associated LHR staining redistribution from membrane to cytoplasm without changing total LHR protein.

Ddo deletion or oral D-aspartate elevation enhanced hippocampal LTP without improving cognitive flexibility in the reported mouse experiments.

Two or four weeks of 20 mM sodium D-aspartate in drinking water improved sperm quality and fertilizing performance in young/adult B6N mice without increasing sperm concentration.

D-aspartate excited mouse nigral dopamine neurons with NMDA, AMPA and metabotropic receptor-sensitive components.

The pineal melatonin reduction was partly attributed to lower norepinephrine-stimulated serotonin N-acetyltransferase activity.

D-aspartate at 1 mM increased intracellular calcium in 11 of 13 tested rat pinealocytes; NMDA, AMPA and kainate did not evoke this response in the reported panels.

D-aspartate elicited inward transporter-associated current in isolated rat pinealocytes; pharmacology favored GLT-1-type transport over ionotropic glutamate receptors.

D-aspartate inhibited norepinephrine-stimulated melatonin production in rat pineal preparations, with approximately 75 micromolar required for half-maximal inhibition.

The study reported D-aspartate-evoked glutamate secretion with blocker sensitivity similar to L-aspartate, supporting calcium-dependent vesicular release downstream of transport.

Rat Leydig cells incubated with 0.1 or 1 mM D-aspartate showed increased measured testosterone and cAMP.

Rat pituitary incubation with 0.1 or 1 mM D-aspartate increased measured LH and cGMP over 60 minutes.

Intravenous D-aspartate at 0.05 or 0.1 mmol/kg/min for 20 minutes increased circulating growth hormone in wethers.

Both D-aspartate infusion doses reduced plasma insulin; glucose and circulating catecholamines did not significantly change.

D-aspartate at 10 micromolar enhanced potassium-evoked glutamate release in cortical synaptosomes superfused with TBOA; NMDA, AMPA/kainate and mGlu5 antagonists attenuated or prevented the effect.

What acts on it

Purified human DDO-1 oxidized D-aspartate; the reported Km was 2.7 mM and kcat 52.5 per second.

Purified mammalian serine racemase catalyzed aspartate racemization in the reported two-base reaction mechanism.

Where it participates (unsigned role)

Persistent D-aspartate elevation after Ddo deletion accompanied increased extracellular glutamate, active caspases, reactive glia and age-dependent brain abnormalities.

Aged Ddo-knockout mice showed reduced synaptic GluN1/GluN2B, altered plasticity and greater vulnerability to phencyclidine-related prepulse-inhibition deficits.

Rat kidney, liver and brain DDO activity became detectable one to four days after birth and reached adult values around four weeks.

Human D-aspartate oxidase structure and kinetics showed a FAD-containing enzyme with higher FAD affinity than human D-amino-acid oxidase.

Porcine kidney DDO oxidized D-aspartate to iminoaspartate while reducing enzyme-bound FAD.

Ddo deletion increased NMDA-evoked currents and membrane GluN1/GluN2A in mouse nigral dopamine neurons.

Postnatal mouse Ddo promoter demethylation accompanied rising Ddo mRNA; azacitidine treatment increased Ddo transcripts in embryonic cortical neurons.

Reoxidation of reduced FAD by oxygen during porcine DDO turnover produced hydrogen peroxide.

Subcellular fractionation localized D-aspartate oxidase activity to peroxisomes in human liver.

Purified human, rat and mouse DDO differed in kinetic and inhibitor-binding properties.

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

A later postmortem study found no significant schizophrenia-related difference in DDO transcription or methylation despite higher DDO activity in dorsolateral prefrontal cortex.

Human DDO-1 also oxidized N-methyl-D-aspartate, with reported Km 6.8 mM and kcat 37.7 per second.

An expanded regional methylation/expression analysis found brain-region differences but no significant diagnostic association for DDO expression or methylation.

Schizophrenia DLPFC samples had approximately 30% lower free D-aspartate and 25% higher DDO activity; the D-aspartate reduction was not detected in hippocampus.

Lowering assay FAD from 100 to 4 micromolar shifted olanzapine IC50 at mouse DDO from about 5.6 to 1.4 micromolar; the human enzyme did not show this potency shift.

Olanzapine inhibited recombinant human DDO at an IC50 near 23 micromolar under both 4 and 100 micromolar FAD conditions; clozapine did not inhibit the tested enzyme.

Four weeks of olanzapine at 5 mg/kg/day intraperitoneally increased prefrontal extracellular D-aspartate and glutamate in wild-type mice; the increments were absent in Ddo-knockout mice.

Srr-knockout mouse forebrain had less D-aspartate without detected differences in DDO activity or L-aspartate concentrations.

Mg2+ and ATP increased recombinant serine-racemase serine racemization and pyruvate production by approximately five- to ten-fold in the study assay.

Srr deletion lowered D-aspartate in mouse frontal cortex and hippocampus, while cerebellum and testes were unchanged.

SRR overexpression increased intracellular D-aspartate in rat PC12 cells.

Deleting endogenous SRR in rat PC12 cells lowered D-serine but left D-aspartate production unchanged.

The 1.89-angstrom human serine-racemase holoenzyme structure included its bound pyridoxal-phosphate cofactor.

EAAT inhibition strongly potentiated D-aspartate-evoked, but not L-aspartate-evoked, currents in Ddo-knockout mouse neurons.

The events it takes part in

Situations it appears in

In the sources

Open hypotheses