The DOI matches its Crossref record.
Temporal Lobe Asymmetries as the Key to the Etiology of Schizophrenia
Open accessAbstract
With evidence that determinants of psychosis are present early and influence brain development, and in the absence of a significant environmental contribution, schizophrenia may be regarded as a genetic encephalopathy. Morphological abnormalities are particularly apparent in the temporal lobe and on the left side of the brain, and in a number of studies significant diagnosis x side interactions have been detected. Such interactions suggest an intimate relationship between the disease process and the mechanisms that determine asymmetrical brain development. These mechanisms presumably relate to the human capacity for speech and communication, and they may have played a critical role in the evolution of the human brain. A candidate locus for an asymmetry determinant and the psychosis gene within the exchange region of the sex chromosomes is proposed. Some sex differences in schizophrenia (e.g., with respect to age of onset and brain structure) may relate to subtle differences in the rate of asymmetry development in the two sexes.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cited by
A review of MRI findings in schizophrenia
Shenton, M. E., Dickey, C. C., Frumin, M., & McCarley, R. W. (2001) · Schizophrenia Research · doi:10.1016/s0920-9964(01)00163-3 · Cited by 2,346
The neuropathology of schizophrenia
Harrison, P. J. (1999) · Brain · doi:10.1093/brain/122.4.593 · Cited by 1,677
Neuropsychological deficits in neuroleptic naive patients with first-episode schizophrenia
Saykin, A. J. (1994) · Archives of General Psychiatry · doi:10.1001/archpsyc.1994.03950020048005 · Cited by 1,086
The reduced neuropil hypothesis: a circuit based model of schizophrenia
Selemon, L. D., & Goldman-Rakic, P. S. (1999) · Biological Psychiatry · doi:10.1016/s0006-3223(98)00281-9 · Cited by 909
Harrison, P. (2004) · Psychopharmacology · doi:10.1007/s00213-003-1761-y · Cited by 693
Lipska, B. K., Jaskiw, G. E., & Weinberger, D. R. (1993) · Neuropsychopharmacology · doi:10.1038/npp.1993.44 · Cited by 697
Pantelis, C. (2005) · Schizophrenia Bulletin · doi:10.1093/schbul/sbi034 · Cited by 573
Hypomethylation of MB-COMT promoter is a major risk factor for schizophrenia and bipolar disorder
Abdolmaleky, H. M., Cheng, K.-H., Faraone, S. V., Wilcox, M., Glatt, S. J., Gao, F., Smith, C. L., Shafa, R., Aeali, B., Carnevale, J., et al. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl253 · Cited by 462
Elliott, R., Sahakian, B. J., Herrod, J. J., Robbins, T. W., & Paykel, E. S. (1997) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.63.1.74 · Cited by 285
Yucel, M., Stuart, G. W., Maruff, P., Velakoulis, D., Crowe, S. F., Savage, G., & Pantelis, C. (2001) · Cerebral Cortex · doi:10.1093/cercor/11.1.17 · Cited by 222
Chidhood precursors of psychiosis as clues to its evolutionary orgins
Crow, T. J., Done, D. J., & Sacker, A. (1995) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/bf02190732 · Cited by 204
Self-citationMapping Cortical Thickness in Children with 22q11.2 Deletions
Bearden, C. E., van Erp, T. G. M., Dutton, R. A., Tran, H., Zimmermann, L., Sun, D., Geaga, J. A., Simon, T. J., Glahn, D. C., Cannon, T. D., et al. (2007) · Cerebral Cortex · doi:10.1093/cercor/bhl097 · Cited by 92
Association between schizophrenia and genetic variation in DCC: a case–control study
Grant, A., Fathalli, F., Rouleau, G., Joober, R., & Flores, C. (2012) · Schizophrenia Research · doi:10.1016/j.schres.2012.02.023 · Cited by 53
Neuropathology of Schizophrenia
Harrison, P. J., Lewis, D. A., & Kleinman, J. E. (2010) · Schizophrenia · doi:10.1002/9781444327298.ch18 · Cited by 26
Metadata
- Authors
- Crow, T. J.
- Venue
- Schizophrenia Bulletin
- Publisher
- Oxford University Press (OUP)
- Published
- 1990-01-01
- Volume
- 16
- Issue
- 3
- Pages
- 433-443
- ISSN
- 0586-7614 (ISSN-L)
- 1745-1701
- OpenAlex
- W2159004633
- Cited by
- 395
- References
- 0
- FWCI
- 8.23
- Type
- journal article
- Language
- en
- Open access
- bronze
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 ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.