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, Alice Charach
Published: 21 April 2009
European child & adolescent psychiatry, Volume 18, pp 587-595; https://doi.org/10.1007/s00787-009-0018-7

Abstract:
The objective of this study was to examine the predictors associated with adherence to atypical antipsychotic medication following discharge from hospital for children and adolescents with first-episode psychosis. Sixty-five children and adolescents, age 15.35 ± 2.08 years, 59% boys, who had participated in a longitudinal cohort study examining relapse following first hospitalization for episode of psychosis were included in this study. All those studied were discharged on one of three atypical antipsychotics, risperidone, quetiapine, or olanzapine between January 1999 and October 2003. Time 1 data were collected retrospectively from medical charts using a standardized questionnaire; time 2 data were obtained using questionnaire mailed to participants’ parents a minimum of 2 years post-discharge, mean 3.9 ± 1.3 years. Variables examined as predictors of adherence fell into broad categories of biological, social and treatment variables. Discharge on concurrent pharmacologic agent for affective symptoms in addition to atypical antipsychotic, OR = 10.5 [95% confidence interval (CI) = 2.06–53.19] was a strong predictor of medication adherence in adolescents. The results indicated that children and adolescents discharged from their first hospitalization following a psychotic episode may be more likely to stay on prescribed antipsychotic medication if they are prescribed concurrent medication for affective symptoms.
T.J. Crow, J.S. Close, H.-S. Kim, M.T. Ross
Published: 15 November 2007
The publisher has not yet granted permission to display this abstract.
, S. Leicester, , , G.E. Berger, S.M. Francey, H.P. Yuen, P.D. McGorry
Published: 31 May 2006
Schizophrenia research, Volume 84, pp 67-76; https://doi.org/10.1016/j.schres.2006.02.018

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, Tao Li
Published: 7 November 2003
European journal of pharmacology, Volume 480, pp 177-184; https://doi.org/10.1016/j.ejphar.2003.08.105

Abstract:
The major targets of current drugs used in mental health, such as neurotransmitter receptors and transporters, are based on serendipitous findings from several decades ago, and there is currently a severe drought of new drug targets. There is a pressing need for novel drugs, and much hope has been placed on the use of molecular genetics to help define them. However, despite evidence for a genetic basis to schizophrenia stretching back for over a century, and a heritability of about 80%, the identification of susceptibility genes has been an uphill struggle. Candidate gene studies, which have generally focussed on obvious candidates from the dopamine and serotonin systems, as well as genes involved in brain development, have not generally been successful, although meta-analysis indicates that the dopamine D3 receptor gene (DRD3) and the serotonin receptor gene type 2A (HTR2A) may have a very small influence on risk. Linkage analysis has provided robust evidence of genetic loci, for example, on chromosomes 8p, 13q and 22q, and also implies shared genetic aetiology with bipolar disorder. The identification of these loci together with advances in genetic technology, especially the characterisation of polymorphisms, the understanding of haplotypes and the development of statistical methods, has lead to the identification of several plausible susceptibility genes, including neuregulin 1, proline dehydrogenase and dysbindin. Interestingly, these genes point more towards a role for the glutamate pathway rather than the dopamine pathway in schizophrenia. We have attempted to replicate some of these findings in schizophrenic patients from SW China, and we find significant association with a novel neuregulin 1 haplotype, with proline dehydrogenase polymorphisms, but not with catechol-O-methyltransferase (COMT). The replication of neuregulin 1 association on chromosome 8p by several investigators is the most convincing to date, and the presence of a syndrome similar to dementia praecox of 8p linked families, and the lack of linkage of bipolar disorder to this region is a testament to the ideas of Kraepelin more than 100 years ago.
D. V. Jeste, L. A. McAdams, , D. Braff, T. L. Jernigan, , , L. L. Symonds, A. Bailey, R. K. Heaton
Published: 1 August 1998
Acta Psychiatrica Scandinavica, Volume 98, pp 156-164; https://doi.org/10.1111/j.1600-0447.1998.tb10058.x

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Rajiv P. Sharma, Sheila M. Dowd, John M. Davis, Philip G. Janicak
Published: 5 July 1996
Schizophrenia research, Volume 20, pp 295-300; https://doi.org/10.1016/0920-9964(96)00005-9

Abstract:
The authors examine the relationship between the age of illness onset and the ability to tolerate a medication-free period in a sample of acutely ill schizophrenic patients. Patients were admitted to an inpatient research unit for the treatment of acute and recurrent psychiatric symptoms. Prior medications were discontinued upon admission to the unit for purposes of clinical research and behavioral assessment uncontaminated by medication side effects. The age of illness onset was significantly and positively correlated with the duration of hospital washout. Furthermore, age of illness onset was significantly correlated with the BPRS total score and the BPRS hostility/suspiciousness factor measured at the end of washout. Our results suggest that early onset schizophrenics deteriorate more rapidly in an acute episode than do their later age of onset counterparts.
Padraig Wright, Pak C. Sham, Catherine M. Gilvarry, , , Tonmoy Sharma,
Published: 1 July 1996
Schizophrenia research, Volume 20, pp 261-267; https://doi.org/10.1016/0920-9964(96)82950-1

Abstract:
Autoimmune diseases aggregate in individuals and within pedigrees, and it has been postulated that autoimmune mechanisms may account for a proportion of schizophrenia. Structured questionnaires were used to interview the mothers of 121 DSM-III-R schizophrenic patients and the mothers of 116 controls in order to determine the prevalence of schizophrenia and of autoimmune diseases in their pedigrees. Patients with a schizophrenic first degree relative were significantly more likely to also have a parent or sibling with an autoimmune disease (60% vs. 20%, OR=6.1, 95% CI=2.3−16.5, p=0.0003). A significant excess of insulin dependent diabetes mellitus (IDDM) was present in the parents and siblings of schizophrenic patients (OR=9.65, 95% CI=1.3−429.2, p=0.009). These findings suggest that autoimmune mechanisms may play a role in the aetiology of schizophrenia, particularly familial schizophrenia. Associations have been established between autoimmune diseases and the HLA encoding genes of the major histocompatibility complex on chromosome six, and it may be that some of the genetic liability to schizophrenia involves these genes.
Joy L. Welham, Michael R. Pemberton,
Published: 31 May 1996
Schizophrenia research, Volume 20, pp 125-132; https://doi.org/10.1016/0920-9964(95)00087-9

Abstract:
Epidemiological studies often use age-of-first-admission from psychiatric case registers to estimate age-of-onset in schizophrenia. Retrospective, interview-based methods have shown that there is a delay between onset of symptoms and eventual contact with psychiatric services, and that this delay can vary both among individuals and at different ages. This delay or lag can confound the interpretation of first admission data such as age-of-onset. To evaluate the potential impact of this factor, we constructed a flexible mathematical model which integrates age-at-first-admission with estimates of this lag, which were derived from interview-based studies and clinical judgement. We applied this model to age-of-first-admission data for 4218 patients with ICD8/9 schizophrenia drawn from a state-wide psychiatric register. Both the raw age-of-first-admission distribution curve and the transformed data ('estimated age-of-onset') reinforce previous findings that (a) there is a wide range of age-of-onset and (b) the shapes of the curves differ between the sexes. Inspection of the mathematically derived distribution supports the proposition that (a) transformation for a lag effect produces a lower onset age and (b) including a variable length of lag produces a change in shape of the distribution. We propose that the mathematical transformation of age-of-first-admission data may have heuristic value, but requires further empirical data on which to base the assumptions of the model.
Catherine M. Gilvarry, Pak C. Sham, , , Padraig Wright, , , Brian K. Toone,
Published: 31 March 1996
Schizophrenia research, Volume 19, pp 33-40; https://doi.org/10.1016/0920-9964(95)00045-3

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T.J Crow
Published: 31 December 1995
European Neuropsychopharmacology, Volume 5, pp 59-63; https://doi.org/10.1016/0924-977x(95)00032-k

Abstract:
The incidence and typical symptoms of schizophrenia are similar in diverse human populations; it is likely that the same is true for manic-depressive illnesses. Relative constancy of incidence over time and place (referred to as the ‘anthropo-parity principle') and absence of evidence for environmental causation suggest that these disorders are genetic in origin and in some way characteristic of the human condition. Continued high prevalence in the face of a fertility disadvantage requires explanation—why do the genes persist and what is their function? It is proposed that the origins of psychosis are closely linked to the evolution of the human brain. The capacity for language evolved by the process of hemispheric specialisation, a gene for asymmetry (the ‘right shift factor’ or cerebral dominance gene) playing a critical role. This gene, it is suggested, is represented in homologous form on the X and Y chromosomes and has been subject to sexual selection. Such a locus could explain sex differences in cerebral asymmetry, and in age of onset and outcome of psychosis.
Margot Albus, Wolfgang Maier
Published: 31 December 1995
Schizophrenia research, Volume 18, pp 51-57; https://doi.org/10.1016/0920-9964(95)00038-0

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T. J. Crow
Archives of General Psychiatry, Volume 52, pp 1011-1014; https://doi.org/10.1001/archpsyc.1995.03950240029006

Abstract:
Olney and Farber1present a "unified hypothesis" based onN-methyl-D-aspartate (NMDA) receptor hypofunction, which they claim accounts for "major clinical and pathophysiological aspects of schizophrenia." Although, as I shall show, there are elements of interest in thishypothesis, it is flawed in that it depends on an erroneous account of etiology, predicts neurological symptoms that are not present in schizophrenia, and is inconsistent with the known epidemiological characteristics of the disease. A comparison of this hypothesis with previous hypotheses of the same type ("neurohumoral" theories) and with two other classes of hypotheses of pathogenesis ("focal damage" and "connectionist" theories) in their ability to explain known drug effects, phenomenological characteristics, brain changes, and epidemiological characteristics, reveals constraints on the type of theory that we may entertain and a pattern of strengths and weaknesses that points the way to a more incisive theory. See also pages 998, 1008, 1015, and 1019 THE
T. J. Crow, D. J. Done,
European archives of psychiatry and clinical neuroscience, Volume 245, pp 61-69; https://doi.org/10.1007/bf02190732

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R H Yolken, E F Torrey
Published: 1 January 1995
Clinical Microbiology Reviews, Volume 8, pp 131-45

Abstract:
The hypothesis that viruses or other infectious agents may cause schizophrenia or bipolar disorder dates to the 19th century but has recently been revived. It could explain many clinical, genetic, and epidemiologic aspects of these diseases, including the winter-spring birth seasonality, regional differences, urban birth, household crowding, having an older sibling, and prenatal exposure to influenza as risk factors. It could also explain observed immunological changes such as abnormalities of lymphocytes, proteins, autoantibodies, and cytokines. However, direct studies of viral infections in individuals with these psychiatric diseases have been predominantly negative. Most studies have examined antibodies in blood or cerebrospinal fluid, and relatively few studies have been done on viral antigens, genomes, cytopathic effect on cell culture, and animal transmission experiments. Viral research on schizophrenia and bipolar disorder is thus comparable to viral research on multiple sclerosis and Parkinson's disease: an attractive hypothesis with scattered interesting findings but no clear proof. The application of molecular biological techniques may allow the identification of novel infectious agents and the associations of these novel agents with serious mental diseases.
Nick Bass, Lynn E. DeLisi, Angela Boccio, Gail Shields, Carla Morganti,
Archives of General Psychiatry, Volume 51, pp 334-335; https://doi.org/10.1001/archpsyc.1994.03950040078012

Abstract:
The age of onset of schizophrenia chatacteristically peaks in early adulthood, although spanning at least four decades of life among unrelated individuals, and on average, it peaks a few years earlier in males than females.1,2 It also has been previously shown that the age of onset, rather than the time of onset, is highly correlated among affected sibling pairs, thus suggesting a genetic determination of the age of on set. There recently have been reports of a curious lack of gender differences in the age of onset when only schizophrenic individuals with a positive family history of schizophrenia (ie, multiplex families) are examined.4-6 However, L. S. Penrose, in a large cohort of familial mental illness, previously observed that the age of onset for males was lower than for females (mean difference, 3.7 years), with a wider scatter in male ages at first admission than in female and a
Timothy J. Crow, Lynn E. DeLisi, Raymond Lofthouse, Mark Poulter, Thomas Lehner, Nicholas Bass, Tarulata Shah, Catherine Walsh, Angela Boccio-Smith, Gail Shields, et al.
Published: 1 February 1994
The British Journal of Psychiatry, Volume 164, pp 159-164; https://doi.org/10.1192/bjp.164.2.159

Abstract:
We investigated linkage between schizophrenia and the loci DXYS14, DXYS17, and MIC2 within the pseudoautosomal region in 85 families with two or more siblings suffering from schizophrenia or schizoaffective disorder. A maximum lod score of 2.44 was reached at MIC2, with a dominant model of inheritance at a recombination fraction of 0.367 in females and 0.046 in males (a F: M sex ratio > 1, i.e. opposite to that expected with a pseudoautosomal locus). Evidence consistent with linkage (P = 0.01) was also obtained with a sibling pair analysis at the MIC2 locus. These data do not support (although they do not definitively exclude) a locus within the pseudoautosomal region; they are consistent with the presence of a gene that predisposes to schizophrenia in the sex-specific regions of the X and Y chromosomes.
T.J. Crow
Published: 4 September 1993
Journal: The Lancet
The Lancet, Volume 342, pp 594-598; https://doi.org/10.1016/0140-6736(93)91415-i

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Gertrude Rubinstein
Published: 31 August 1993
Schizophrenia research, Volume 10, pp 95-102; https://doi.org/10.1016/0920-9964(93)90043-i

Abstract:
Two factors which seem to have a significant role in schizophrenia are infection and temperature. Evidence is presented that the schizophrenic population may be part of a sub-population which has preferential resistance to epidemic infection. This characteristic alone may not be responsible for vulnerability to schizophrenia. Part at least of the genetic predisposition to schizophrenia may lie in an abnormal response to hormonal disturbances in the intrauterine environment which may result from prenatal viral infection; this abnormal response may cause neurodevelopmental damage. Then in effect the vulnerability of some to schizophrenia will be the cost of population survival in epidemics. Dopamine is involved in central thermoregulation, and may be involved in response to infection. In two inbred mouse strains, one virus-resistant and the other virus-susceptible, there is also a difference in core body temperature response to dopamine. Because of the connection of dopamine sensitivity, temperature and resistance to infection the paired mouse strains are suggested as an animal model for studies relevant to schizophrenia.
P. C. Sham, N. Takei, G. Murray, R. M. Murray, E. O'callaghan
Published: 1 October 1992
The British Journal of Psychiatry, Volume 161, pp 571-572; https://doi.org/10.1192/s0007125000129927

T. J. Crow, D. J. Done
Published: 1 September 1992
The British Journal of Psychiatry, Volume 161, pp 390-393; https://doi.org/10.1192/bjp.161.3.390

Abstract:
Claims have been made that maternal infection with influenza during pregnancy is a cause of schizophrenia in the child. These assertions are based upon some apparently significant associations between the timing of influenza epidemics in the general population and birth rates of people who later suffered from schizophrenia. Such associations have not been present in studies of the 1919 and 1957 epidemics, with sample sizes larger than those on which the claims were made. More decisively, in an investigation of the subsequent psychiatric admissions of people born a few months after the 1957 epidemic, it was found that the children of 945 mothers who actually suffered from influenza during the second trimester of pregnancy were at no greater risk of developing schizophrenia than children of mothers who were not infected. In contrast to the predictions of the influenza hypothesis of 26.5 extra cases by broad diagnostic criteria and 15.8 cases by narrow criteria, the numbers observed in children of mothers exposed to influenza in the second trimester were 3 and 1 cases respectively, close to the expected rate. It is concluded that prenatal influenza and schizophrenia are unrelated.
John Knight, Allison Knight, Gabor Ungvari
The British Journal of Psychiatry, Volume 160, pp 533-540; https://doi.org/10.1192/bjp.160.4.533

Abstract:
Applications of molecular genetic techniques to schizophrenia have shown great initial promise but have then proved disappointing. In order to maximise chances of elucidating the genetic mechanism underlying schizophrenia, diverse strategies and diverse perspectives must be adopted. Most studies begin with the premise that, although schizophrenia may be a heterogeneous collection of diseases, some subtypes will be primarily single-gene disorders. We are concerned that this single-gene hypothesis may be incorrect. Schizophrenia research may benefit from application of knowledge from other disciplines and from other diseases which, in terms of epidemiology and apparent genetic mechanisms, bear some resemblance to schizophrenia.
Robert L. Hendren, Janet Hodde-Vargas
Published: 1 January 1992
The publisher has not yet granted permission to display this abstract.
Mark A. Coggiano, Robert C. Alexander, Darrell G. Kirch, Richard Jed Wyatt, Henrietta Kulaga
Published: 31 October 1991
Schizophrenia research, Volume 5, pp 243-247; https://doi.org/10.1016/0920-9964(91)90082-3

Abstract:
Retroviral infection has been proposed as an etiologic factor in schizophrenia. In an effort to unmask a latent retrovirus, short term cultures of peripheral lynphocytes from 15 schizophrenic subjects and nine normal controls were exposed to ionizing radiation and co-cultured with indicator cells. Reverse transcriptase activity, a marker of retroviral infection, could not be detected in any of the cultures. Our findings are further evidence against a role for retroviral infection in the etiology of schizophrenia.
T. J. Crow
The British Journal of Psychiatry, Volume 158, pp 611-614; https://doi.org/10.1192/bjp.158.5.611

Abstract:
The major psychoses remain an enigma. Affective and schizophrenic psychoses are apparently present (probably at about the same lifetime prevalence of approximately 2%) in all human societies. Yet their aetiology is obscure. While a genetic contribution is acknowledged by most authorities, few accept that genes are a sufficient explanation of causation because: onset is in adult life; psychosis – particularly schizophrenia – is associated with a substantial fertility disadvantage; and most cases lack a family history of illness. But genetic determination has to be considered because onset is determined by chronological age rather than environmental insult (Crow & Done, 1986), adoption away from a family with schizophrenia does not reduce risk of illness, and no plausible environmental precipitant of psychosis has been identified. The fact that psychosis occurs across widely differing climatic, industrial, and social environments without obvious variations in incidence suggests that the disease is relatively independent of the external milieu. The suggestion that birth injury is relevant has been tested in a prospective study (the National Child Development Study) and found wanting (Done et al, 1991).
Timothy J. Crow
Published: 1 January 1991
The publisher has not yet granted permission to display this abstract.
T. J. Crow
Published: 1 May 1990
Acta Psychiatrica Scandinavica, Volume 81, pp 401-408; https://doi.org/10.1111/j.1600-0447.1990.tb05471.x

Abstract:
The recurrent psychoses, rather than, as Kraepelin supposed, constituting 2 major entities, manic depressive illness and schizophrenia, as separate diseases, may be distributed along a continuum that extends from unipolar depressive illness through bipolar and schizoaffective psychosis to schizophrenia with increasing severities of defect state. It is proposed that this continuum rests on a genetic base, variations in the form of the gene accounting for variations in form of psychosis. The simplest interpretation of the continuum is that such variation relates to changes at a single genetic locus. Evidence from a postmortem study of brain structure in schizophrenia suggests that this is the gene that determines the development of asymmetries in the human brain, i.e., the cerebral dominance gene or right shift factor of Annett; a possible genomic location is in the pseudoautosomal region of the sex chromosomes.
Lynn E. DeLisi, Michael Lovett, John A. Talbott, Anthony Kales
Published: 1 January 1990
The publisher has not yet granted permission to display this abstract.
Costas N. Stefanis, John A. Talbott
Published: 1 January 1990
The publisher has not yet granted permission to display this abstract.
Kenneth S. Kendler, Charles J. MacLean, D. C. Rao
Published: 1 January 1990
Genetic epidemiology, Volume 7, pp 409-417; https://doi.org/10.1002/gepi.1370070603

The publisher has not yet granted permission to display this abstract.
Timothy J. Crow, Lynn E. DeLisi, Eve C. Johnstone
The British Journal of Psychiatry, Volume 155, pp 92-97; https://doi.org/10.1192/bjp.155.1.92

Abstract:
The hypothesis that the gene for schizophrenia is located in the pseudoautosomal region of the sex chromosomes predicts that same-sex concordance will occur in paternally rather than maternally derived pairs. In 120 families that included at least one sibling pair with schizophrenia, affected members were significantly more likely to be of the same sex when there was a history of illness on the paternal than on the maternal side, the difference remaining significant when parent of origin was assessed by three different methods. The finding is as predicted by the pseudoautosomal hypothesis: therefore a search for the gene should be focused on this small (three megabase) region of the genome. The ratio of same to mixed sex pairs in paternally-derived cases (approximately 3:1) suggests the gene is located in the centromeric one-third of the pseudoautosomal region.
Hugh Freeman
The British Journal of Psychiatry, Volume 155, pp 90-99; https://doi.org/10.1192/s0007125000296050

Abstract:
Attention was first drawn to the importance of this topic by Schneider (1957) when he proposed that some of his first-rank symptoms could be grouped together under the concept of ‘permeability’ of the barrier between the individual and his/her environment — the ‘loss of ego boundaries’. Similarly, in a recent series of papers (Strauss et al, 1987), the essence of schizophrenia was conceptualised in the processes of interaction between biology, behaviour, and environment. The two main syndromes — acute and chronic — can each be precipitated or made worse by environmental factors, and although most patients with the negative syndrome appear to show some irreducible impairment, poverty of the social environment has been found to worsen their condition, while on the other hand, a moderate degree of social stimulation promotes relative improvement (Wing, 1987).
David J. King, Stephen J. Cooper
Published: 2 January 1989
The British Journal of Psychiatry, Volume 154, pp 1-7; https://doi.org/10.1192/bjp.154.1.1

Abstract:
Are viruses the cause of mental illness, or does stress or mental disorder produce impaired immunity, with increased susceptibility to infection? These two separate but not unrelated questions have been debated periodically and there has been much renewed interest recently, with increased sophistication in immunology and widespread topical concern about immunodeficiency. The neuropsychiatry of the acquired immunodeficiency syndrome (AIDS) (Snider et al, 1983; Carne & Adler, 1986; Wortis, 1986; Burton, 1987; Fenton, 1987) and the validity of a ‘post-viral fatigue syndrome’ as a clinical entity (Behan, 1983; Southern & Oldstone, 1986; Dawson, 1987; David et al, 1988) are not discussed here, but have been dealt with in the editorials and reviews cited.
T. J. Crow
The British Journal of Psychiatry, Volume 152, pp 431-432; https://doi.org/10.1192/bjp.152.3.432

Lynn E. DeLisi, Lynn R. Goldin, Elliot S. Gershon
Published: 31 December 1987
Journal of psychiatric research, Volume 21, pp 507-513; https://doi.org/10.1016/0022-3956(87)90099-9

Abstract:
Although a familial component to schizophrenia has been established through several familial, twin and adoption studies, an inherited biological factor has yet to be established. Efforts to define clinical familial subtypes of schizophrenia have generally been unsuccessful, although recent data from our study population of pairs of siblings with schizophrenia suggests that schizophrenia with recurrent episodes of major depression may define one such group.
T.J. Crow
Published: 31 December 1987
Journal of psychiatric research, Volume 21, pp 479-485; https://doi.org/10.1016/0022-3956(87)90096-3

Abstract:
According to the retrovirus-transposon hypothesis, psychosis is due to the expression of a pathogenic sequence (a "virogene") integrated in the genome and either inherited from an affected or predisposed parent or acquired in the course of reproduction by a genetic rearrangement (e.g. a transposition or the generation of a tandem repeat). The psychoses are viewed as a continuum extending from unipolar through bipolar and schizo-affective disorder to schizophrenia with increasing severity of defect, movement along this continuum occurring by such genetic rearrangements. The locus at which these changes take place is envisaged as related to the genetic determinants of cerebral lateralisation (the "cerebral dominance gene") the interaction between potential pathogen and growth factor gene having possible growth enhancing effects. Such beneficial effects may have ensured the survival of this "hot-spot" in the genome.
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