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(searched for: doi:10.1192/bjp.140.6.600)
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, V. B. Searles Quick
Published: 15 January 2018
Journal: Human genetics
Human genetics, Volume 137, pp 1-13; https://doi.org/10.1007/s00439-017-1865-9

Abstract:
Evolution often deals in genomic trade-offs: changes in the genome that are beneficial overall persist even though they also produce disease in a subset of individuals. Here, we explore the possibility that such trade-offs have occurred as part of the evolution of the human brain. Specifically, we provide support for the possibility that the same key genes that have been major contributors to the rapid evolutionary expansion of the human brain and its exceptional cognitive capacity also, in different combinations, are significant contributors to autism and schizophrenia. Furthermore, the model proposes that one of the primary genes behind this trade-off may not technically be “a gene” or “genes” but rather are the highly duplicated sequences that encode the Olduvai protein domain family (formerly called DUF1220). This is not an entirely new idea. Others have proposed that the same genes involved in schizophrenia were also critical to the rapid expansion of the human brain, a view that has been expressed as “the same ‘genes’ that drive us mad have made us human”. What is new is that a “gene”, or more precisely a protein domain family, has been found that may satisfy these requirements.
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, Vidyulata Kamath, Monica E. Calkins, Warrick J. Brewer, , , Larry J. Seidman, Dolores Malaspina, Kimberley P. Good, Lili C. Kopala, et al.
Published: 14 May 2012
Schizophrenia research, Volume 139, pp 260-261; https://doi.org/10.1016/j.schres.2012.04.016

Chia-Chang Chien, Chi-Hung Lin, Yong-Yuan Chang, For-Wey Lung
The World Journal of Biological Psychiatry, Volume 11, pp 409-416; https://doi.org/10.3109/15622970903304459

Abstract:
To explore the involvement of variable number tandem repeat (VNTR) polymorphisms in the monoamine oxidase A (MAOA) promoter and exon 3 of the dopamine D4 receptor (DRD4) gene in heroin addiction modulate the vulnerability of individuals to heroin addiction. Eight hundred and ninety-four male heroin addicts without other psychiatric disorders, were recruited as subjects. Another community 180 males were selected randomly as controls. The geno-distribution of the DRD4 exon 3 VNTR polymorphism in controls was in Hardy-Weinberg equilibrium (HWEchi(2)=0.925), but the distribution in heroin addicts was not (HWEchi(2)=28.35). The long-repeat alleles of the DRD4 exon 3 VNTR polymorphism were found more frequently in the heroin addicts (P=0.019). However, the long-repeat alleles of the MAOA promoter VNTR polymorphism were not (P=0.828). No interaction between these two VNTR polymorphisms was found by using multiple logistic regression analysis (P=0.261). The long-repeat allelic variants (>4-repeats) and 2-repeat allele of the DRD4 exon 3 VNTR polymorphism might be risk alleles for individual vulnerability to heroin addiction in Chinese men, but the MAOA promoter VNTR polymorphism does not mean that the partial dominant inherited mode might involved in the genetics of heroin dependence.
Olafur Jensson, Astridur Palsdottir, Leifur Thorsteinsson, Alfred Arnason
Published: 28 June 2008
Clinical Genetics, Volume 36, pp 368-377; https://doi.org/10.1111/j.1399-0004.1989.tb03215.x

Abstract:
Firstly, we review investigations of hereditary cystatin C amyloid angiopathy, which is caused by a mutation in the cystatin C gene. Symptoms of brain haemorrhages, which lead to death in young adults, are the hallmark of this disorder. The mutation can now be detected by the RFLP method using Alu I restriction enzyme and cystatin C cDNA probe. Secondly, we give an overview of other clinical genetic studies in Iceland with emphasis on activities initiated or sponsored by the Genetical Committee of the University of Iceland. The list of references covers most publications on genetic studies of Icelanders.
, Nathan Chen, Bih-Ching Shu
Psychiatric genetics, Volume 16, pp 139-143; https://doi.org/10.1097/01.ypg.0000199446.54420.ff

Abstract:
The dopamine D4 receptor (DRD4) is a candidate gene for increasing genetic susceptibility to schizophrenia. A recent study found that a -521C>T promoter base pair change affects transcriptional regulation of the DRD4 gene. The present study was designed to investigate the role of both the -521C>T single nucleotide polymorphism and the DRD4 variable number tandem repeat (VNTR) polymorphism. A case-control study of 630 Chinese schizophrenic patients and 428 Chinese controls was conducted to test for allelic association with schizophrenia. The number of DRD4 VNTR fragments was associated with schizophrenia. Long DRD4 VNTR fragments as opposed to short fragments were commoner in schizophrenia. No evidence was found for allelic association between the -521C>T DRD4 polymorphism and schizophrenia. This study provides preliminary and unconfirmed evidence for the involvement of the DRD4 repeat VNTR in the pathogenesis of schizophrenia.
F.-W. Lung, Y.-C. Yen, L.-J. Chou, C.-J. Hong, C.-K. Wu
Published: 1 January 2005
Acta Psychiatrica Scandinavica, Volume 111, pp 38-43; https://doi.org/10.1111/j.1600-0447.2004.00394.x

Abstract:
This study aimed to determine the impact of the present of apolipoprotein epsilon (Apoepsilon) 2 on the relationship between Apoepsilon4 and Alzheimer's disease (AD). We examined ApoE genotypes in 428 Taiwanese patients with AD and 807 controls; all participants were older than 65 years. The allele frequency of Apoepsilon4 was greater in AD patients than controls, but significantly lower than in Caucasians. The presence of an epsilon2 allele alone was not associated with lower risk for AD, but the presence of an epsilon2 allele was associated with an epsilon4 allele frequency similar to that of controls. The low allele frequency of epsilon4 in persons with an epsilon2 allele suggests that this may be part of the protective effect of epsilon2 against AD.
, Helinä Häkkänen
The Journal of Forensic Psychiatry & Psychology, Volume 15, pp 451-474; https://doi.org/10.1080/1478994042000226750

Abstract:
Background characteristics of homicide offenders in relation to their diagnoses were investigated. Forensic psychiatric examination statements of 183 Finnish homicide offenders belonging to five different diagnostic categories were content-analysed for 90 dichotomous offender background variables. In several aspects alcoholics resembled offenders with no diagnosis, in that these offenders had less problematic backgrounds compared to other groups. Offenders with schizophrenia were relatively well-adjusted in childhood, however, in adolescence and adulthood, social isolation, withdrawal and other difficulties attributable to the illness of these offenders became evident. Offenders with personality disorder or drug addiction had experienced multiple difficulties in their early environments: both family and individual problems, such as parental alcohol abuse and school problems, were typical. The results suggest that offenders with different disorders differ in their background variables. These results emphasize the importance of early interventions for problem families and children at risk of antisocial behaviour and may also benefit development of effective treatments for violent offenders as well as investigations of homicide. Some methodological problems in forensic psychiatric examination based research are considered.
, , Bih-Ching Shu
Published: 25 September 2001
Schizophrenia research, Volume 57, pp 239-245; https://doi.org/10.1016/s0920-9964(01)00313-9

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Jun Wei, C.N. Ramchand, Anne E. Clark, Gwynneth P. Hemmings
Published: 31 March 1996
Schizophrenia research, Volume 19, pp 27-32; https://doi.org/10.1016/0920-9964(95)00044-5

Abstract:
The concentrations of serum homovanillic acid (HVA), norepinephrine (NE), tyrosine (Tyr), phenylalanine (Phe) and tryptophan (Trp), and the activities of serum dopamine-beta-hydroxylase (DBH), platelet monoamine oxidase (MAO), and erythrocyte catechol-O-methyl transferase (COMT) were measured in 68 healthy parents who had schizophrenic offspring. The results show a significant correlation between the parents of schizophrenic patients in serum HVA (r=0.38, n=34, p<0.05), NE (r=0.40, n=33, p<0.02), Phe (r=0.44, n=34, p<0.0l), Tyr (r=0.43, n = 34, p <0.02) and DBH activity (r=0.51, n = 30, p <0.005), but do not show a significant correlation in erythrocyte COMT (r=0.01, n=27), platelet MAO (r=0.04, n=23) or serum Trp (r=0.10, n=34). There were no significant correlations in these measurements between randomly matched parents. The present study suggests that both parental sides of schizophrenic patients are likely to have similar alleles associated with the catecholamine pathway, and their ill offspring may possess a double dose of the schizophrenogenic alleles.
Jon Brynjolfsson, Hannes Petursson, Hugh Gurling, Robin Sherrington
Published: 1 January 1990
Nordisk Psykiatrisk Tidsskrift, Volume 44, pp 499-505; https://doi.org/10.3109/08039489009096604

Abstract:
Brvnjólfsson J, Pétursson H, Gurling H, Sherrington R. Diagnostic issues in the study of schizophrenia genetics. As a result of a series of collaborative studies, we have reported preliminary evidence of linkage between a locus on chromosome 5 and schizophrenia in Icelandic and British families. The purpose of this article is to describe the part of our work carried out in Iceland, in particular the population background, as well as the methods of selection, diagnostic assessment, interview schedules, and clinical aspects. The project group chose to study high-density pedigrees with schizophrenia in at least three generations. Extensive pedigree tracing work aimed at selecting families without manic depression (bipolar disorder) and in which there was only one possible source for a schizophrenia allele segregating into the kindred. Diagnosis included schizophrenia, schizophreniform disorder, unspecified functional psychosis, schizoid personality disorder with and without schizotypal features, and other psychiatric disorders. Most of the schizophrenic cases were deemed chronic or subchronic. One third of the schizophrenia subtypes were undifferentiated, and almost a half were of the paranoid type. Other aspects of the results are discussed, as are implications for further work.
Robin Sherrington, Jon Brynjolfsson, Hannes Petursson, Mark Potter, Keith Dudleston, Brian Barraclough, John Wasmuth, Mark Dobbs, Hugh Gurling
Published: 1 November 1988
Journal: Nature
Nature, Volume 336, pp 164-167; https://doi.org/10.1038/336164a0

Abstract:
Schizophrenia is a common disorder with a life time prevalence of approximately 1 per cent. The illness often develops in young adults, who were previously normal, and is characterized by a constellation of symptoms including hallucinations and delusions (psychotic symptoms) and symptoms such as severely inappropriate emotional responses, a disorder of thinking and concentration, erratic behaviour as well as social and occupational deterioration. A considerable proportion of the variance in the liability to develop schizophrenia may be genetic, but segregation analysis, to establish a mode of transmission, has not produced a consistent result. One of these studies was carried out in Iceland and made use of the large family size and extensive geneaological information present in that country. Here we demonstrate genetic linkage of two DNA polymorphisms on the long arm of human chromosome 5 to schizophrenia in seven British and Icelandic families with multiple affected members. The results indicate the existence of a gene locus with a dominant schizophrenia-susceptibility allele. Inheritance of the allele in the families studied suggests that it may also predispose to psychiatric conditions such as schizophrenia spectrum disorders and a variety of other disorders. This report provides the first strong evidence for the involvement of a single gene in the causation of schizophrenia.
Steven Taylor, Elizabeth Hinton
Published: 1 December 1987
Psychological Reports, Volume 61, pp 875-878; https://doi.org/10.2466/pr0.1987.61.3.875

Abstract:
The present article considers the recent increase in community-based support systems for psychiatric patients. Although these systems appear to offer some short-term benefits, the long-term consequences have received little attention. Here, the case is examined for such systems actually facilitating the reproductive rates and hence general incidence of genetically transmitted disorders such as schizophrenia.
Pierre Etienne, Michel Baudry
Published: 31 August 1987
Neurobiology of Aging, Volume 8, pp 362-366; https://doi.org/10.1016/0197-4580(87)90081-9

Abstract:
(1) The functional and structural reorganization of dendritic spines by calcium activated proteases is postulated to play a causal role in the production of the phenomenology of brain aging and in particular in the development of pathology and degeneration. Excitatory neurotransmission appears to be essential for the development of irreversible synaptic changes. (2) One of the genes modified in schizophrenia is postulated to be directly or indirectly linked to the control of excitatory neurotransmission; possibly the normal switching on of the expression of the adult form of the NMDA receptor is altered, resulting in an inappropriate functioning of this receptor. This genetic characteristic might explain the apparent resistance of schizophrenic brains to aging.
Jon L. Karlsson
Published: 1 March 1984
Journal: Hereditas
Hereditas, Volume 100, pp 83-86; https://doi.org/10.1111/j.1601-5223.1984.tb00108.x

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M McGue, I I Gottesman, D C Rao
Published: 1 November 1983
American journal of human genetics, Volume 35, pp 1161-78

Abstract:
Family studies of schizophrenia have reported elevated rates of both definite and definite-plus-probable schizophrenia among the relatives of definite schizophrenics. These elevated rates imply a strong association between the two forms of diagnosis and suggest some form of familial transmission. Here we have used recently developed maximum likelihood methods to investigate this association and characterize the nature of the familial transmission. Results indicated that although the two forms of diagnosis were strongly related, they could not be considered alternative manifestations of a single liability distribution. Heritability estimates for either form of diagnosis were comparable (h2 = .668 +/- .052 and c2 = .191 +/- .038 for definite while h2 = .628 +/- .073 and c2 = .236 +/- .106 for definite-plus-probable), although cultural transmission (i.e., c2) was statistically significant only for definite-plus-probable. For either form of diagnosis, residual twin resemblance was statistically significant and could not be explained in terms of the effects of genetic dominance. These results are comparable to those of an earlier analysis based upon a similar data set. Finally, the statistical correction used to adjust for between-study heterogeneity in morbidity risk figures did not noticeably alter the parameter estimates.
Jon L. Karlsson
Published: 1 September 1983
Journal: Hereditas
Hereditas, Volume 99, pp 69-72; https://doi.org/10.1111/j.1601-5223.1983.tb00733.x

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