N-methyl-D-aspartic Acid (NMDA) and Cognitive Remediation in Schizophrenia
Public ClinicalTrials.gov record NCT01474395. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.
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Official title
NMDA and Cognitive Remediation in Schizophrenia
Brief summary
Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.
Persistent neurocognitive deficits are a major cause of severe disability and impaired long-term psychosocial outcome in schizophrenia (SZ). In particular, within the auditory system, early deficits such as the behavioral and neurophysiological ability to match tones that vary in pitch correlate with impairments in auditory emotion recognition (affective prosody) and general functioning, suggesting that interventions aimed at remediating sensory-level dysfunction may lead to significant improvement in higher order cognitive/emotion processes. Efforts to ameliorate cognitive deficits in schizophrenia utilize either pharmacological agents or behavioral treatments such as cognitive remediation, which generally focus on higher order processes, and not on the early sensory processing which may be key to functioning. Numerous pharmacological agents have been proposed, but accumulating evidence suggests that dysfunction of the N-methyl-D-aspartic acid (NMDA) receptor may be one of the root causes of schizophrenia, including sensory and cognitive impairments, suggesting that an NMDA based treatment may be efficacious in reversing these deficits. D-Cycloserine, a synthetic partial NMDA agonist has been used in anxiety disorders to augment learning in cognitive remediation. Because of a tendency to act as an NMDA antagonist at higher doses D-cycloserine is not effective in schizophrenia. In contrast, D-serine (DSR), is a full agonist, and is therefore more ideal for enhancing NMDA function and cognitive remediation. While previous use of DSR was limited by safety concerns in rodents,the investigators have shown that it can safely be used at doses of 60 mg/kg and, moreover, demonstrates converging improvement in symptomatic, cognitive and sensory-based measures in schizophrenia. Evidence also suggests that NMDA receptor dysfunction in schizophrenia may be relative, rather than absolute, suggesting that the enhanced practice of a cognitive remediation paradigm might be able to overcome reduced plasticity and treat cognitive dysfunction. This project will be the first to combine the NMDA based and sensory-based cognitive remediation (SBR) approaches, and will utilize not only DSR, but also a tone matching SBR paradigm has been shown to enhance learning in healthy controls, as well as a paradigm designed to augment visual motion detection. This study will pilot these interventions in a double-blind, placebo-controlled, randomized crossover design that will use neurophysiology together with cognitive tests to explore the effects on brain activity and cognitive function in 16 patients with schizophrenia or schizoaffective disorder. The investigators hypothesize that DSR+SBR will lead to improvement. Subjects will have an initial visit to establish baseline performance on cognitive tasks before returning for 3 visits when they will receive blinded study medication \[60 mg/kg of DSR (2 days) or placebo (1 day)\] in a randomized order. The procedures on the treatment days will include the SBR paradigm and pre/post neurophysiological measurements. Primary outcomes are improvements in neurophysiologic and behavioral sensory processing. The main goal is to establish the preliminary efficacy to use in a follow-up multi-dose study utilizing a multiple session SBR R01 application.
Study identification
- NCT ID
- NCT01474395
- Recruitment status
- Not listed
- Study type
- Interventional
- Phase
- Phase 2
- Enrollment
- 16 participants
Conditions and interventions
Conditions
Interventions
- D-serine Drug
- placebo Drug
- Sensory Based remediation paradigm Behavioral
Drug · Behavioral
Eligibility (public fields only)
- Age range
- 18 Years to 64 Years
- Sex
- All
- Healthy volunteers
- Healthy volunteers not accepted
This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.
Study timeline
- Start date
- Feb 29, 2012
- Primary completion
- May 31, 2013
- Completion
- May 31, 2013
- Last update posted
- Oct 24, 2012
2012 – 2013
United States locations
- U.S. sites
- 1
- U.S. states
- 1
- U.S. cities
- 1
| Facility | City | State | ZIP | Site status |
|---|---|---|---|---|
| Nathan Kline Insitute for Psychiatric Research | Orangeburg | New York | 10962 | Recruiting |
Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.
About this trial record page
- What this page shows
- Public field values for ClinicalTrials.gov record NCT01474395, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
- What this page does not do
- No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
- Where the data comes from
- Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
- Last refresh
- Last update posted Oct 24, 2012 · Synced Sep 5, 2026
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Open the official record
The complete protocol, eligibility criteria, and contact information for NCT01474395 live on ClinicalTrials.gov.