First in vivo evidence of an NMDA receptor deficit in medication-free schizophrenic patients
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In humans, altered ERK activation causes a variety of developmental disorders which have ASD-like symptoms.
“In humans, altered ERK activation causes a variety of developmental disorders which have ASD-like symptoms, although the pathogenic mechanisms are not precisely understood.”
From Transient blockade of ERK phosphorylation in the critical period causes autistic phenotypes as an adult in mice (2015) · cites this paper as [27]
ASD is common in patients with 22q11.2 deletion syndrome.
“It was reported that ASD is common in patients with 22q11.2 deletion syndrome27.”
From Transient blockade of ERK phosphorylation in the critical period causes autistic phenotypes as an adult in mice (2015) · cites this paper as [27]
An NMDAR SPECT study pointed to lower NMDAR activity in unmedicated patients with schizophrenia, although this finding awaits confirmation with newer, more specific probes.
“An NMDAR single-photon emission computed tomography (SPECT) study pointed to lower NMDAR activity in unmedicated patients with schizophrenia 19 , although this finding awaits confirmation with newer, more specific probes 20 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [19]
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Mice mutant for genes associated with schizophrenia: Common phenotype or distinct endophenotypes?
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Mutant models for genes associated with schizophrenia
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- Authors
- Pilowsky, L. S., Bressan, R. A., Stone, J. M., Erlandsson, K., Mulligan, R. S., Krystal, J. H., & Ell, P. J.
- Affiliations
- King's College London (GB)
- University College London (GB)
- Yale University (US)
- Venue
- Molecular Psychiatry
- Published
- 2005-09-27
- Volume
- 11
- Issue
- 2
- Pages
- 118-119
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- OpenAlex
- W2066489132
- Cited by
- 278
- References
- 6
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 6 · 2023: 8 · 2022: 11 · 2021: 9 · 2020: 11 · 2019: 8 · 2018: 7 · 2017: 14 · 2016: 20 · 2015: 19 · 2014: 16 · 2013: 21 · 2012: 17
- FWCI
- 6.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- National Institutes of Health (5k05aa014906-03)
- National Institute on Alcohol Abuse and Alcoholism (KO5 AA 014906-02)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- NMDA receptor, schizophrenia, medication-free patients, receptor availability, first-episode psychosis, ketamine, brain volume
- MeSH terms
- Analysis of Variance, Clozapine, Guanidines, Hippocampus, Humans, Functional Laterality, Reference Values, Schizophrenia, Tissue Distribution, Antipsychotic Agents, Tomography, Emission-Computed, Single-Photon, Case-Control Studies, Receptors, N-Methyl-D-Aspartate, Genetic Predisposition to Disease
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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