Proteomic, genomic and translational approaches identify CRMP1 for a role in schizophrenia and its underlying traits
Open accessAbstract
Schizophrenia is a chronic illness of heterogenous biological origin. We hypothesized that, similar to chronic progressive brain conditions, persistent functional disturbances of neurons would result in disturbed proteostasis in the brains of schizophrenia patients, leading to increased abundance of specific misfolded, insoluble proteins. Identification of such proteins would facilitate the elucidation of molecular processes underlying these devastating conditions. We therefore generated antibodies against pooled insoluble proteome of post-mortem brains from schizophrenia patients in order to identify unique, disease-specific epitopes. We successfully identified such an epitope to be present on collapsin-response mediator protein 1 (CRMP1) in biochemically purified, insoluble brain fractions. A genetic association analysis for the CRMP1 gene in a large Finnish population cohort (n = 4651) corroborated the association of physical and social anhedonia with the CRMP1 locus in a DISC1 (Disrupted-in-schizophrenia 1)-dependent manner. Physical and social anhedonia are heritable traits, present as chronic, negative symptoms of schizophrenia and severe major depression, thus constituting serious vulnerability factors for mental disease. Strikingly, lymphoblastoid cell lines derived from schizophrenia patients mirrored aberrant CRMP1 immunoreactivity by showing an increase of CRMP1 expression, suggesting its potential role as a blood-based diagnostic marker. CRMP1 is a novel candidate protein for schizophrenia traits at the intersection of the reelin and DISC1 pathways that directly and functionally interacts with DISC1. We demonstrate the impact of an interdisciplinary approach where the identification of a disease-associated epitope in post-mortem brains, powered by a genetic association study, is rapidly translated into a potential blood-based diagnostic marker.
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Single nucleotide polymorphisms in genes implicated in neurodevelopment are associated with social anhedonia along the psychosis continuum.
“Similarly, single nucleotide polymorphisms (SNPs) in genes implicated in neurodevelopment have been associated with social anhedonia along the psychosis continuum (155, 156).”
From A transdiagnostic perspective on social anhedonia (2019) · cites this paper as [155]
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- Authors
- Bader, V., Tomppo, L., Trossbach, S. V., Bradshaw, N. J., Prikulis, I., Leliveld, S. R., Lin, C.-Y., Ishizuka, K., Sawa, A., Ramos, A., Rosa, I., García, Á., Requena, J. R., Hipolito, M., Rai, N., Nwulia, E., Henning, U., Ferrea, S., Luckhaus, C., Ekelund, J., Veijola, J., Järvelin, M.-R., Hennah, W., & Korth, C.
- Affiliations
- Heinrich Heine University Düsseldorf (DE)
- University of Helsinki (FI)
- Johns Hopkins University (US)
- Universidade de Santiago de Compostela (ES)
- Howard University (US)
- Oulu University Hospital (FI)
- MRC Centre for Environment and Health (GB)
- Corresponding author
- Korth, Carsten
- ORCID
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-07-13
- Volume
- 21
- Issue
- 20
- Pages
- 4406-4418
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- PMC
- PMC3529585
- OpenAlex
- W2121634929
- Cited by
- 70
- References
- 80
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 2 · 2023: 6 · 2022: 4 · 2021: 7 · 2020: 4 · 2019: 6 · 2018: 5 · 2017: 6 · 2016: 6 · 2015: 6 · 2014: 6 · 2013: 5
- FWCI
- 3.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Human Molecular Genetics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- RUNA. Repositorio Institucional del Sergas (Servicio Gallego de Salud (SERGAS)) (submittedVersion, other-oa)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- Funders
- Stanley Medical Research Institute
- Johns Hopkins University
- Heinrich-Heine-Universität Düsseldorf
- National Institute of Mental Health (R21MH085226, MH084018, MH085226, RC1MH088753, MH 092443, MH‑088753, P20MH084018, R01MH069853, R01MH091460, MH-094268, MH-091460, P50MH094268, MH069853, R01MH092443)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Social Sciences › Arts and Humanities › Philosophy › Mental Health and Psychiatry
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- schizophrenia, CRMP1, DISC1, anhedonia, proteostasis, protein misfolding, postmortem brain, genetic association, lymphoblastoid cell lines, negative symptoms, major depressive disorder
- MeSH terms
- Reelin Protein, Collapsin Response Mediator Protein 1, Adult, Animals, Brain, Humans, Nerve Tissue Proteins, Schizophrenia, Transfection, Cohort Studies, Genetic Predisposition to Disease, Proteome, Genomics, Proteomics, Cell Line, Tumor, Mice
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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