Symptoms, signs, and diagnosis of schizophrenia

Andreasen, N.C.

doi:10.1016/s0140-6736(95)91325-4

Cited by 271 publications

(180 citation statements)

References 31 publications

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“…Moreover, the phenotypic manifestations of schizophrenia are numerous and variable, and may include delusions, disordered thought, hallucinations, negative symptoms, and cognitive and functional impairment. 1 In addition, many distinct epilepsy syndromes do exist, which are defined by seizure characteristics, location and age of onset. These factors have complicated the identification of genes and their products that serve as vulnerability factors for these disorders.…”

Section: Introductionmentioning

confidence: 99%

CNTNAP2 gene dosage variation is associated with schizophrenia and epilepsy

et al. 2007

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A homozygous mutation of the CNTNAP2 gene has been associated with a syndrome of focal epilepsy, mental retardation, language regression and other neuropsychiatric problems in children of the Old Order Amish community. Here we report genomic rearrangements resulting in haploinsufficiency of the CNTNAP2 gene in association with epilepsy and schizophrenia. Genomic deletions of varying sizes affecting the CNTNAP2 gene were identified in three nonrelated Caucasian patients. In contrast, we did not observe any dosage variation for this gene in 512 healthy controls. Moreover, this genomic region has not been identified as showing large-scale copy number variation. Our data thus confirm an association of CNTNAP2 to epilepsy outside the Old Order Amish population and suggest that dosage alteration of this gene may lead to a complex phenotype of schizophrenia, epilepsy and cognitive impairment.

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Section: Introductionmentioning

confidence: 99%

CNTNAP2 gene dosage variation is associated with schizophrenia and epilepsy

et al. 2007

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“…Brain areas that are strongly influenced by genes in healthy subjects may allow a more powerful search for candidate genes that are predominantly expressed in these brain regions. This in turn facilitates the interpretation of morphological changes found in neuropsychiatric disorders with an origin in puberty or early adolescence, such as schizophrenia [Andreasen, 1995] and anxiety or mood disorders [Kessler et al, 2005]. Also, puberty is a period during which a child's environment changes from parentdependent to more self-or peer-dependent [Steinberg, 2005].…”

Section: Introductionmentioning

confidence: 96%

Heritability of regional and global brain structure at the onset of puberty: A magnetic resonance imaging study in 9‐year‐old twin pairs

Peper

Schnack

Brouwer

et al. 2009

Human Brain Mapping

163

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Puberty represents the phase of sexual maturity, signaling the change from childhood into adulthood. During childhood and adolescence, prominent changes take place in the brain. Recently, variation in frontal, temporal, and parietal areas was found to be under varying genetic control between 5 and 19 years of age. However, at the onset of puberty, the extent to which variation in brain structures is influenced by genetic factors (heritability) is not known. Moreover, whether a direct link between human pubertal development and brain structure exists has not been studied. Here, we studied the heritability of brain structures at 9 years of age in 107 monozygotic and dizygotic twin pairs (N 5 210 individuals) using volumetric MRI and voxel-based morphometry. Children showing the first signs of secondary sexual characteristics (N 5 47 individuals) were compared with children without these signs, based on Tanner-stages. High heritabilities of intracranial, total brain, cerebellum, and gray and white matter volumes (up to 91%) were found. Regionally, the posterior fronto-occipital, corpus callosum, and superior longitudinal fascicles (up to 93%), and the amygdala, superior frontal and middle temporal cortices (up to 83%) were significantly heritable. The onset of secondary sexual characteristics of puberty was associated with decreased frontal and parietal gray matter densities. Thus, in 9-year-old children, global brain volumes, white matter density in fronto-occipital and superior longitudinal fascicles, and gray matter density of (pre-)frontal and temporal areas are highly heritable. Pubertal development may be directly involved in the decreases in gray matter areas that accompany the transition of our brains from childhood into adulthood.

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“…It is clinically characterized by disturbed thought processes, delusions, hallucinations, and/or reduced social skills. 1 A number of studies indicate a genetic component contributing to schizophrenia, but the mode of inheritance does not follow a simple Mendelian pattern. In spite of the failure to identify a schizophrenia gene of major import in multiply affected families, more than one data set from genome-wide scans provides convincing evidence that 8p22-p21 may harbor candidate genes which may confer susceptibility to schizophrenia to an individual.…”

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confidence: 99%