Journal
BIOLOGICAL PSYCHIATRY-COGNITIVE NEUROSCIENCE AND NEUROIMAGING
Volume 3, Issue 7, Pages 581-590Publisher
ELSEVIER
DOI: 10.1016/j.bpsc.2018.02.002
Keywords
Biomarker; Cognition; MMN; NMDA; Plasticity; Schizophrenia; Treatment
Categories
Funding
- National Center for Research Resources, National Institutes of Health [UL1 RR024156]
- National Center for Advancing Translational Sciences, National Institutes of Health [UL1 RR024156]
- Dr. Joseph E. and Lillian Pisetsky Young Investigator Award for Clinical Research in Serious Mental Illness
- Brain & Behavior Research Foundation
- National Institute of Mental Health
- Stanley Foundation
- Taisho
- Lundbeck
- Boehringer Ingelheim
- NeuroRX
- Merck
- Lilly
- [MH59803]
- [MH94320]
- [MH068725]
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Cognitive deficits are predictive of long-term social and occupational functional deficits in schizophrenia but are currently without gold-standard treatments. In particular, augmentation of auditory cortical neuroplasticity may represent a rate-limiting first step before addressing higher-order cognitive deficits. We review the rationale for N-methyl-o-aspartate-type glutamate receptor (NMDAR) modulators as treatments for auditory plasticity deficits in schizophrenia, along with potential serum and electroencephalographic target engagement biomarkers for NMDAR function. Several recently published NMDAR-modulating treatment studies are covered, involving D-serine, memantine, and transcranial direct current stimulation. While all three interventions appear to modulate auditory plasticity, direct agonists (D-serine) appear to have the largest and most consistent effects on plasticity, at least acutely. We hypothesize that there may be synergistic effects of combining procognitive NMDAR-modulating approaches with auditory cortical neuroplasticity cognitive training interventions. Future studies should assess biomarkers for target engagement and patient stratification, along with head-to-head studies comparing putative interventions and potential long-term versus acute effects.
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