Schizophrenia as the price that Homo sapiens pays for language: a resolution of the central paradox in the origin of the species

Crow, T J

doi:10.1016/s0165-0173(99)00029-6

Cited by 327 publications

(236 citation statements)

References 88 publications

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“…88 The speciation of humans seems to have occurred by an X-Y translocation roughly 3 Myr ago that gave rise to the Homo sapiens-specific region of Xq21.3 and Yp11.2 homology. 89 Taking into account the above observations and possibilities, several investigators have tried to find possible linkage loci and susceptibility genes for schizophrenia within the Xq21.3/Yp11.2 region of homology. 10 The results of these studies show a somewhat weak association that probably has an epigenetic background rather than arising from sequence-based variations.…”

Section: Chromosome Xmentioning

confidence: 99%

The myelin-pathogenesis puzzle in schizophrenia: a literature review

2007

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Schizophrenia is a serious and disabling mental disorder with symptoms such as auditory hallucinations, disordered thinking and delusions, avolition, anhedonia, blunted affect and apathy. In this review article we seek to present the current scientific findings from linkage studies and susceptible genes and the pathophysiology of white matter in schizophrenia. The article has been reviewed in two parts. The first part deals with the linkage studies and susceptible genes in schizophrenia in order to have a clear-cut picture of the involvement of chromosomes and their genes in schizophrenia. The genetic linkage results seem to be replicated in some cases but in others are not. From these results, we cannot draw a fine map to a single locus or gene, leading to the conclusion that schizophrenia is not caused by a single factor/gene. In the second part of the article we present the oligodendrocyte-related genes that are associated with schizophrenia, as we hypothesize a potential role of oligodendrocyte-related genes in the pathology of the disorder.

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Section: Chromosome Xmentioning

confidence: 99%

The myelin-pathogenesis puzzle in schizophrenia: a literature review

2007

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“…Concurring genetic and epigenetic factors might alter specifically one hemisphere, because they target specific functional domains that are lateralized in the human brain. [152][153][154][155] This would be reflected in the altered callosal connectivity to and from the affected hemisphere. The possibility that the left hemisphere may be anatomically and electrophysiologically more affected than the right hemisphere fits with a number of anatomical findings, in particular, the greater enlargement of the left than the right lateral ventricles.…”

Section: Developmental-pathogenic Scenariosmentioning

confidence: 99%

“…151 Interestingly, some of the key anatomical findings supporting the notion of hypoconnectivity in S derive from studies of the left hemisphere. 44,63,68,69 A specific linkage between left hemisphere and S is also explicit in proposals relating the phylogenetic origins of language and S. [152][153][154] Unfortunately, the genes responsible for lateralization are undefined, and their number and modalities of phenotypic expression are matters of debate. 156 Thus, the genetic hypotheses on S, although relevant and stimulating, are insufficiently specified in neurobiological terms to account for the structural changes that might underlie the psychosis, its pathophysiology and symptomatology.…”

Section: Developmental-pathogenic Scenariosmentioning

confidence: 99%

Schizophrenia, neurodevelopment and corpus callosum

2003

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The Zeitgeist favors an interpretation of schizophrenia as a condition of abnormal connectivity of cortical neurons, particularly in the prefrontal and temporal cortex. The available evidence points to reduced connectivity, a possible consequence of excessive synaptic pruning in development. A decreased thalamic input to the cerebral cortex appears likely, and developmental studies predict that this decrease should entail a secondary loss of both longand short-range cortico-cortical connections, including connections between the hemispheres. Indeed, morphological, electrophysiological and neuropsychological studies over the last two decades suggest that the callosal connections are altered in schizophrenics. However, the alterations are subtle and sometimes inconsistent across studies, and need to be investigated further with new methodologies.

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“…19 Furthermore, an X-Y homologous locus for a cerebral asymmetry gene within the non-recombining portion of the Y chromosome has been postulated on the basis of the deficits associated with sex chromosome aneuploidies. 20 Most of the Y chromosome is made up of a long nonrecombining region of ෂ60 megabases. 21 Polymorphic markers on the non-recombining region can determine Y chromosome lineages (or haplogroups) which are monophyletic groups of Y chromosomes defined by shared allelic states at slowly mutating binary markers.…”

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confidence: 99%

Y chromosome haplogroups in autistic subjects

et al. 2002

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The male to female ratio in autism is 4:1 in the global autistic population, but increases to 23:1 in autistic subjects without physical or brain abnormalities. 1 Despite this well-recognised gender difference, male predisposition to autistic disorder remains unexplained and the role of sex chromosomes is still debated. Numerical and structural abnormalities of the sex chromosomes are among the most frequently reported chromosomal disorders associated with autism. However, genome scans have failed to detect linkage on the X chromosome 2-4 and this approach cannot study the non-recombining region of the Y chromosome. In this study, we searched for a specific Y chromosome effect in autistic subjects. Using informative Y-polymorphic markers, the Y chromosome haplotypes of 111 autistic subjects from France, Sweden and Norway were defined and compared with relevant control populations. No significant difference in Y-haplotype distribution between the affected and control groups was observed. Although this study cannot exclude the presence of a Y susceptibility gene, our results are not suggestive of a Y chromosome effect in autism.

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Schizophrenia as the price that Homo sapiens pays for language: a resolution of the central paradox in the origin of the species

Cited by 327 publications

References 88 publications

The myelin-pathogenesis puzzle in schizophrenia: a literature review

The myelin-pathogenesis puzzle in schizophrenia: a literature review

Schizophrenia, neurodevelopment and corpus callosum

Y chromosome haplogroups in autistic subjects

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