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Artykuły w czasopismach na temat „Schizophrenia – Genetic aspects”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 7 lutego 2022

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1

Morozova, A. Yu, E. A. Zubkov, Ya A. Zorkina, A. M. Reznik, G. P. Kostyuk, and V. P. Chekhonin. "Genetic aspects of schizophrenia." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 117, no. 6 (2017): 126. http://dx.doi.org/10.17116/jnevro201711761126-132.

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Karayiorgou, Maria. "Genetic aspects of schizophrenia." Clinical Neuroscience Research 1, no. 1-2 (January 2001): 158–63. http://dx.doi.org/10.1016/s1566-2772(00)00015-3.

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Böök, Jan A. "Genetic aspects of schizophrenia." Clinical Genetics 19, no. 5 (April 23, 2008): 357. http://dx.doi.org/10.1111/j.1399-0004.1981.tb00726.x.

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Bellivier, F. "Schizophrenia, antipsychotics and diabetes: Genetic aspects." European Psychiatry 20, S4 (December 2005): S335—S339. http://dx.doi.org/10.1016/s0924-9338(05)80187-7.

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AbstractThe relatively high comorbidity of type 2 diabetes and schizophrenia may suggest a shared biological susceptibility to these twoconditions. Family studies have demonstrated an increased risk of diabetes in unaffected relatives of patients with schizophrenia, consistent with a heritable susceptibility trait. Linkage analyses have identified several loci that are associated with schizophrenia and some of these, notably those on chromosomes 2p22.1-p13.2 and 6g21-824.1 have also been observed in linkage studies in type 2 diabetes. In addition, the dopamine D5 receptor on chromosome 5 and t

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Muir, Walter J. "Genetic aspects of the biology of schizophrenia." Current Opinion in Psychiatry 5, no. 1 (February 1992): 2–5. http://dx.doi.org/10.1097/00001504-199202000-00002.

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Trifu, Simona Corina, Anca Vlăduţi, and Antonia Ioana Trifu. "Genetic aspects in schizophrenia. Receptoral theories. Metabolic theories." Romanian Journal of Morphology and Embryology 61, no. 1 (2020): 25–32. http://dx.doi.org/10.47162/rjme.61.1.03.

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Kambarova, D. K., and A. G. Golubev. "Biochemical and genetic aspects of pathogenesis of schizophrenia." Journal of Evolutionary Biochemistry and Physiology 47, no. 5 (October 2011): 407–19. http://dx.doi.org/10.1134/s0022093011050021.

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Galderisi, S., and M. Maj. "Deficit schizophrenia: An overview of clinical, biological and treatment aspects." European Psychiatry 24, no. 8 (December 2009): 493–500. http://dx.doi.org/10.1016/j.eurpsy.2009.03.001.

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AbstractThe concept of deficit schizophrenia is regarded as one of the most promising attempts to reduce heterogeneity within schizophrenia. This paper summarizes the clinical, neurocognitive, brain imaging and electrophysiological correlates of this subtype of schizophrenia. Attempts to identify genetic and non-genetic risk factors are reviewed. Methodological limitations of studies supporting the efficacy of atypical antipsychotics in the treatment of the syndrome are highlighted. Two decades of research on deficit schizophrenia have failed to prove that it represents the extreme end of a se

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Popov, Nikolay T., Vili K. Stoyanova, Nadezhda P. Madzhirova, and Tihomir I. Vachev. "Epigenetic aspects in schizophrenia etiology and pathogenesis." Folia Medica 54, no. 2 (October 1, 2012): 12–16. http://dx.doi.org/10.2478/v10153-011-0082-x.

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ABSTRACT Epidemiological evidence suggests that etiology of schizophrenia may involve both the influence of genetic factors specific for the individual and the impact of the environment. It is quite likely that a crucial role in the disease development is played by molecular mechanisms mediating the interaction between genes and environment. Modern research have shown that epigenetic mechanisms or chemical modifications of deoxyribonucleic acids (DNA) and histone proteins remain unstable throughout life and can be changed by environmental factors. Thus the epigenetic mechanisms outline an attr

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Syvälahti, E. K. G. "Biological Factors in Schizophrenia Structural and Functional Aspects." British Journal of Psychiatry 164, S23 (April 1994): 9–14. http://dx.doi.org/10.1192/s0007125000292672.

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A number of factors have been proposed as being linked to schizophrenia: genetic, psychological, endocrinological, metabolic, environmental, virological, and auto-immunological factors, as well as neurotransmitter systems and structural disorders of the brain. All may act as predisposing, triggering, or functionally modulating factors in what is probably a condition composed of several types of disorder with varying aetiology. Neuroanatomical and neuromorphological data have revealed ventricular enlargement and diminished frontal and temporal lobe volume in some patients. These changes are con

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Roksana, Zakharyan. "Transcription Factors in Schizophrenia: A Current View of Genetic Aspects." Scientific Journal of Genetics and Gene Therapy 2, no. 1 (December 30, 2016): 017–21. http://dx.doi.org/10.17352/sjggt.000010.

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Alda, Martin, Marta Dvořáková, Petr Zvolský, Hana Papežová, and Marie Pošmurová. "Genetic aspects in chronic schizophrenia morbidity risks and contributory factors." Schizophrenia Research 2, no. 4-5 (July 1989): 339–44. http://dx.doi.org/10.1016/0920-9964(89)90025-x.

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Zhilyaeva, T. V., A. V. Sergeeva, A. S. Blagonravova, G. E. Mazo, and A. O. Kibitov. "One-Carbon Metabolism Disorders in Schizophrenia: Genetic and Therapeutic Aspects." Neurochemical Journal 13, no. 2 (April 2019): 113–20. http://dx.doi.org/10.1134/s1819712419020156.

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Davies, Eric J. "Developmental aspects of schizophrenia and related disorders: possible implications for treatment strategies." Advances in Psychiatric Treatment 13, no. 5 (September 2007): 384–91. http://dx.doi.org/10.1192/apt.bp.106.002600.

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Schizophrenia and other schizophrenia-spectrum disorders are neurodevelopmental disorders which may share genetic susceptibility factors and represent differential expressions of an underlying vulnerability. Schizophrenia may have its onset in childhood and can be reliably diagnosed. However, developmental factors modulate disease expression in children. Although the prevalence of schizophrenia in childhood is low, children who develop schizophrenia in adult life may show subtle and non-specific developmental abnormalities, consistent with the neurodevelopmental hypothesis. Studies of the schi

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Malmberg, A., G. Lewis, A. David, and P. Allebeck. "Premorbid adjustment and personality in people with schizophrenia†." British Journal of Psychiatry 172, no. 4 (April 1998): 308–13. http://dx.doi.org/10.1192/bjp.172.4.308.

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BackgroundSchizoid personality and poor social adjustment have been thought of as common antecedents of schizophrenia but the existing literature is inconclusive. We have carried out a large cohort study with improved methodology.MethodThe premorbid personality and adjustment of 50 054 Swedish men were assessed on entry into the army at the age of 18. Individuals who developed schizophrenia or another psychosis after 15-year follow-up were identified. Odds ratios for variables independently associated with the later development of schizophrenia were calculated, adjusting for potential confound

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Tosato, Sarah, and Antonio Lasalvia. "The contribution of epidemiology to defining the most appropriate approach to genetic research on schizophrenia." Epidemiologia e Psichiatria Sociale 18, no. 2 (June 2009): 81–90. http://dx.doi.org/10.1017/s1121189x00000932.

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AbstractPsychosis is thought to have a strong genetic component, but many efforts to discover the underlying putative schizophrenia genes have yielded disappointing results. In fact, no strong associations emerged in the first genome-wide association studies in psychiatry and weakly observed associations were not related to the candidate genes identified in previous studies. These partially successful findings may be explained by the fact that genetic research in psychiatry suffers from confounding issues related to phenotype definition, the considerable degree of phenotypic variability and di

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Weller, M. P. I. "Medical Concepts in Psychopathy and Violence." Medicine, Science and the Law 26, no. 2 (April 1986): 131–43. http://dx.doi.org/10.1177/002580248602600208.

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It is widely assumed that psychopathic behaviour arises from unsatisfactory parenting, but upbringing difficulties are equally apparent in other psychiatric disorders. The poor response to psychological treatments is noteworthy and organic features, of a specific type, have been implicated. The most recent evidence strongly supports earlier findings of a genetic factor. Damage or malfunction of the left temporal lobe of the brain, or of the frontal area, are associated with violent psychopathic behaviour. Dysfunction in these same areas has also been found in schizophrenic patients and there i

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Weiss, Norbert, and Gerald W. Zamponi. "Genetic T-type calcium channelopathies." Journal of Medical Genetics 57, no. 1 (June 19, 2019): 1–10. http://dx.doi.org/10.1136/jmedgenet-2019-106163.

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T-type channels are low-voltage-activated calcium channels that contribute to a variety of cellular and physiological functions, including neuronal excitability, hormone and neurotransmitter release as well as developmental aspects. Several human conditions including epilepsy, autism spectrum disorders, schizophrenia, motor neuron disorders and aldosteronism have been traced to variations in genes encoding T-type channels. In this short review, we present the genetics of T-type channels with an emphasis on structure-function relationships and associated channelopathies.

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Scotti-Muzzi, Estêvão, and Osvaldo Luis Saide. "Schizo-obsessive spectrum disorders: an update." CNS Spectrums 22, no. 3 (September 27, 2016): 258–72. http://dx.doi.org/10.1017/s1092852916000390.

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The presence of obsessive-compulsive symptoms (OCS) and obsessive-compulsive disorders (OCD) in schizophrenia is frequent, and a new clinical entity has been proposed for those who show the dual diagnosis: the schizo-obsessive disorder. This review scrutinizes the literature across the main academic databases, and provides an update on different aspects of schizo-obsessive spectrum disorders, which include schizophrenia, schizotypal personality disorder (SPD) with OCD, OCD with poor insight, schizophrenia with OCS, and schizophrenia with OCD (schizo-obsessive disorder). An epidemiological disc

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Venables, N. C., E. M. Bernat, and S. R. Sponheim. "Genetic and Disorder-Specific Aspects of Resting State EEG Abnormalities in Schizophrenia." Schizophrenia Bulletin 35, no. 4 (April 1, 2008): 826–39. http://dx.doi.org/10.1093/schbul/sbn021.

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Isohanni, Matti, Erika Lauronen, Kristiina Moilanen, Irene Isohanni, Liisa Kemppainen, Hannu Koponen, Jouko Miettunen, et al. "Predictors of schizophrenia." British Journal of Psychiatry 187, S48 (August 2005): s4—s7. http://dx.doi.org/10.1192/bjp.187.48.s4.

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BackgroundSubtle motor, emotional, cognitive and behavioural abnormalities are often present in apparently healthy individuals who later develop schizophrenia, suggesting that some aspects of causation are established before overt psychosis.AimsTo outline the development of schizophrenia.MethodWe drew on evidence from The Northern Finland 1966 Birth Cohort supplemented by selected findings from other relevant literature.ResultsThe main known risk factors in development of schizophrenia are genetic causes, pregnancy and delivery complications, slow neuromotor development, and deviant cognitive

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Mendez, Mario F. "Huntington's Disease: Update and Review of Neuropsychiatric Aspects." International Journal of Psychiatry in Medicine 24, no. 3 (September 1994): 189–208. http://dx.doi.org/10.2190/hu6w-3k7q-nael-xu6k.

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Objective: This article presents a general update on Huntington's disease (HD) and reviews the psychiatric and cognitive features of this disorder. Method: HD is discussed in five sections: an introduction and update, the psychiatric aspects, the cognitive aspects, brain-behavior relationships, and the differential diagnosis and management. Results: Recent advancements in HD include the identification of presymptomatic testing methods and HD gene defect, structural and metabolic neuroimaging findings, and a neuropsychological profile. HD is associated with mood disorders, personality changes,

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Glatt, Stephen J., William S. Stone, Stephen V. Faraone, Larry J. Seidman, and Ming T. Tsuang. "Psychopathology, personality traits and social development of young first-degree relatives of patients with schizophrenia." British Journal of Psychiatry 189, no. 4 (October 2006): 337–45. http://dx.doi.org/10.1192/bjp.bp.105.016998.

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BackgroundEvaluation of individuals at high genetic risk of schizophrenia is a powerful method for identifying precursors of the illness.AimsTo identify aspects of personality, psychopathology and social development that differentiate high-risk and control individuals.MethodAdolescent and young-adult first-degree relatives (n=35) of people with schizophrenia or schizoaffective disorder and a control group (n=55) were compared on 36 measures at baseline of a longitudinal study Measures differentiating high-risk and control participants were related to four genetic loading indices.ResultsHigh-ri

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Radanovic, Marcia, Rafael T. de Sousa, L. Valiengo, Wagner Farid Gattaz, and Orestes Vicente Forlenza. "Formal Thought Disorder and language impairment in schizophrenia." Arquivos de Neuro-Psiquiatria 71, no. 1 (December 18, 2012): 55–60. http://dx.doi.org/10.1590/s0004-282x2012005000015.

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Schizophrenia is a psychiatric illness in which disorders of thought content are a prominent feature. The disruption of normal flow of thought, or “Formal Thought Disorder” (FTD), has been traditionally assessed through the content and form of patients’ speech, and speech abnormalities in schizophrenia were considered as a by-product of the disruption in conceptual structures and associative processes related to psychosis. This view has been changed due to increasing evidence that language per se is impaired in schizophrenia, especially its semantic, discursive, and pragmatic aspects. Schizoph

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Chen, Jiayu, Ruijie Feng, and Ziyuan Ma. "Advance of Etiologies and Treatments on Schizophrenia." E3S Web of Conferences 292 (2021): 03067. http://dx.doi.org/10.1051/e3sconf/202129203067.

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Schizophrenia is a severe psychiatric disorder. Among the globe, almost 70% of people with schizophrenia would experience hallucinations that make them feel insecure and progressively weakened. Etiologies and treatments of this perilous disease, therefore, are supposed to be studied in depth. Although the exact causes are still unknown, scientists highly suggest that this disorder results from the combination of genes and environments. For genetic influences, genes such as NR3C2, Dysbindin-1 (DTNBP1), Neuritin-1 (NRN1), KPNB3, and KPNA3 play insignificant roles in the development of schizophre

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Nenadic, Igor, Rachel A. Yotter, Heinrich Sauer, and Christian Gaser. "Patterns of cortical thinning in different subgroups of schizophrenia." British Journal of Psychiatry 206, no. 6 (June 2015): 479–83. http://dx.doi.org/10.1192/bjp.bp.114.148510.

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BackgroundAlterations of cortical thickness have been shown in imaging studies of schizophrenia but it is unclear to what extent they are related to disease phenotype (including symptom profile) or other aspects such as genetic liability, disease onset and disease progression.AimsTo test the hypothesis that cortical thinning would vary across different subgroups of patients with chronic schizophrenia, delineated according to their symptom profiles.MethodWe compared high-resolution magnetic resonance imaging data of 87 patients with DSM-IV schizophrenia with 108 controls to detect changes in co

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Diamantopoulou, Anastasia, and Joseph A. Gogos. "Neurocognitive and Perceptual Processing in Genetic Mouse Models of Schizophrenia: Emerging Lessons." Neuroscientist 25, no. 6 (January 17, 2019): 597–619. http://dx.doi.org/10.1177/1073858418819435.

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During the past two decades, the number of animal models of psychiatric disorders has grown exponentially. Of these, genetic animal models that are modeled after rare but highly penetrant mutations hold great promise for deciphering critical molecular, synaptic, and neurocircuitry deficits of major psychiatric disorders, such as schizophrenia. Animal models should aim to focus on core aspects rather than capture the entire human disease. In this context, animal models with strong etiological validity, where behavioral and neurophysiological phenotypes and the features of the disease being mode

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Yolken, R. H., and E. F. Torrey. "Viruses, schizophrenia, and bipolar disorder." Clinical Microbiology Reviews 8, no. 1 (January 1995): 131–45. http://dx.doi.org/10.1128/cmr.8.1.131.

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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

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Kircher, T. "Phenomenology and neural correlates of formal thought disorder." European Psychiatry 33, S1 (March 2016): S52. http://dx.doi.org/10.1016/j.eurpsy.2016.01.924.

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Speech and language disorders, such as concretism and formal thought disorder (FTD) are core symptoms of Schizophrenia, but do occur to a similar extent in other diagnoses such as bipolar disorder and major depression. We will review clinical rating scales of FTD and introduce a new, validated scale, the TALD. Further, structural and functional brain imaging data will be reviewed and own novel findings presented, relating speech and language dysfunctions to neural networks, within schizophrenia and across the “functional psychoses”. The impact of genetic variance and NNDA receptor blockage on

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Nomura, Jun, and Toru Takumi. "Animal Models of Psychiatric Disorders That Reflect Human Copy Number Variation." Neural Plasticity 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/589524.

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The development of genetic technologies has led to the identification of several copy number variations (CNVs) in the human genome. Genome rearrangements affect dosage-sensitive gene expression in normal brain development. There is strong evidence associating human psychiatric disorders, especially autism spectrum disorders (ASDs) and schizophrenia to genetic risk factors and accumulated CNV risk loci. Deletions in 1q21, 3q29, 15q13, 17p12, and 22q11, as well as duplications in 16p11, 16p13, and 15q11-13 have been reported as recurrent CNVs in ASD and/or schizophrenia. Chromosome engineering c

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Rybakowski, Janusz K. "Matrix Metalloproteinase-9 (MMP9)—A Mediating Enzyme in Cardiovascular Disease, Cancer, and Neuropsychiatric Disorders." Cardiovascular Psychiatry and Neurology 2009 (August 31, 2009): 1–7. http://dx.doi.org/10.1155/2009/904836.

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Matrix metalloproteinase-9 (MMP9) has been implicated in numerous somatic illnesses, including cardiovascular disorders and cancer. Recently, MMP9 has been shown to be increasingly important in several aspects of central nervous system activity. Furthermore, a pathogenic role for this enzyme has been suggested in such neuropsychiatric disorders as schizophrenia, bipolar illness, and multiple sclerosis. In this paper, the results of biochemical and molecular-genetic studies on MMP9 that have been performed in these pathological conditions will be summarized. Furthermore, I hypothesize that the

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Yen, Po Yu, Muhammad Zaidi, and Syed Naqvi. "188 Challenges in Differentiating Between Obsession and Delusion in Schizophrenic Patients: A Case Report." CNS Spectrums 25, no. 2 (April 2020): 318–19. http://dx.doi.org/10.1017/s1092852920001030.

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Abstract:Schizophrenia is a serious, chronic mental illness that manifests a variety of symptoms: hallucinations, delusion of grandiose, disorganized behaviors, and neurocognitive decline after each episode. Among the patients with schizophrenia, obsessive- compulsive symptoms (OCS) or obsessive- compulsive disorder (OCD) are two relatively common comorbidities (25% and 12.5%, respectively). The appearance of these comorbidities complicates patient management: selecting the suitable pharmacological treatment may be challenging as delusion and obsession have similar presentation in this populat

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Bora, E., A. Fornito, M. Yücel, and C. Pantelis. "The effects of gender on grey matter abnormalities in major psychoses: a comparative voxelwise meta-analysis of schizophrenia and bipolar disorder." Psychological Medicine 42, no. 2 (August 11, 2011): 295–307. http://dx.doi.org/10.1017/s0033291711001450.

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BackgroundRecent evidence from genetic and familial studies revitalized the debate concerning the validity of the distinction between schizophrenia and bipolar disorder. Comparing brain imaging findings is an important avenue to examine similarities and differences and, therefore, the validity of the distinction between these conditions. However, in contrast to bipolar disorder, most patient samples in studies of schizophrenia are predominantly male. This a limiting factor for comparing schizophrenia and bipolar disorder since male gender is associated with more severe neurodevelopmental abnor

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Tin, L. N. W., S. S. Y. Lui, K. K. Y. Ho, K. S. Y. Hung, Y. Wang, H. K. H. Yeung, T. Y. Wong, S. M. Lam, R. C. K. Chan, and E. F. C. Cheung. "High-functioning autism patients share similar but more severe impairments in verbal theory of mind than schizophrenia patients." Psychological Medicine 48, no. 8 (September 18, 2017): 1264–73. http://dx.doi.org/10.1017/s0033291717002690.

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AbstractBackgroundEvidence suggests that autism and schizophrenia share similarities in genetic, neuropsychological and behavioural aspects. Although both disorders are associated with theory of mind (ToM) impairments, a few studies have directly compared ToM between autism patients and schizophrenia patients. This study aimed to investigate to what extent high-functioning autism patients and schizophrenia patients share and differ in ToM performance.MethodsThirty high-functioning autism patients, 30 schizophrenia patients and 30 healthy individuals were recruited. Participants were matched in

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Dimopoulou, Trisevgeni, Frank I. Tarazi, and Evangelia M. Tsapakis. "Clinical and therapeutic role of mentalization in schizophrenia—a review." CNS Spectrums 22, no. 6 (February 21, 2017): 450–62. http://dx.doi.org/10.1017/s1092852916000687.

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Recent empirical findings from clinical and genetic studies suggest that mentalization, a key area of social cognition, is a distinct construct, although it is closely related to the neurocognitive deficits and symptoms of schizophrenia. Mentalization contributes a great deal to impaired social functioning. Current measures often display methodological problems, and many aspects should be taken into account when assessing mentalization. Moreover, advances in cognitive and affective neurosciences have led to the development of more advanced behavioral methods to assess the relationship between

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Réthelyi, János, and Anna-Dalal Sawalhe. "Comorbidity of metabolic syndrome, diabetes and schizophrenia: theoretical and practical considerations." Orvosi Hetilap 152, no. 13 (March 2011): 505–11. http://dx.doi.org/10.1556/oh.2011.29079.

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Schizophrenia is a psychiatric disorder characterized by heterogeneous symptoms, affecting 0.8-1% of the population worldwide. It usually begins in early adulthood and demonstrates a chronic course. In recent years research interest has turned to the increased burden of somatic illness in schizophrenia, with special emphasis on metabolic syndrome and diabetes. In this article I review the theoretical and practical aspects of the comorbidity of schizophrenia with metabolic syndrome and diabetes mellitus. Epidemiological studies demonstrate the occurrence of metabolic syndrome between 22% and 66

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Crespi, Bernard, and Christopher Badcock. "Psychosis and autism as diametrical disorders of the social brain." Behavioral and Brain Sciences 31, no. 3 (June 2008): 241–61. http://dx.doi.org/10.1017/s0140525x08004214.

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AbstractAutistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizoph

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Andrade, Arturo, Ashton Brennecke, Shayna Mallat, Julian Brown, Juan Gomez-Rivadeneira, Natalie Czepiel, and Laura Londrigan. "Genetic Associations between Voltage-Gated Calcium Channels and Psychiatric Disorders." International Journal of Molecular Sciences 20, no. 14 (July 19, 2019): 3537. http://dx.doi.org/10.3390/ijms20143537.

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Psychiatric disorders are mental, behavioral or emotional disorders. These conditions are prevalent, one in four adults suffer from any type of psychiatric disorders world-wide. It has always been observed that psychiatric disorders have a genetic component, however, new methods to sequence full genomes of large cohorts have identified with high precision genetic risk loci for these conditions. Psychiatric disorders include, but are not limited to, bipolar disorder, schizophrenia, autism spectrum disorder, anxiety disorders, major depressive disorder, and attention-deficit and hyperactivity di

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Bertelli, M., L. Salvador-Carulla, R. Keller, and E. Bradley. "Intellectual developmental disorders, autism, and schizophrenia spectrum: New boundaries in the neurodevelopmental perspective." European Psychiatry 41, S1 (April 2017): S467. http://dx.doi.org/10.1016/j.eurpsy.2017.01.525.

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Background and aimRecent evidences of clinical overlap, familial co-aggregation, and shared genetic alterations support a neurodevelopmental deviation to represent a probable common vulnerability factor not only for the psychiatric disorders included in the meta-structure of neurodevelopmental disorders, but also for other major psychiatric disorders, including schizophrenia.The present paper reviews the literature to identify (1) positive and negative implications of the increasing enlargement of the group of neurodevelopmental disorders and (2) most useful clinical aspect for re-defining dia

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Szendi, I., A. Juhász, G. Szekeres, C. Cimmer, G. Csifcsak, A. Z. Kovacs, A. Rimanoczy, G. Galsi, K. Boda, and Z. Janka. "P.3.a.021 Examination of specific genetic aspects of the dopaminergic neurotransmission and neuronal plasticity in neurocognitive subgrouping of schizophrenia." European Neuropsychopharmacology 16 (January 2006): S375—S376. http://dx.doi.org/10.1016/s0924-977x(06)70450-3.

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Wulandari, Patricia. "Biomolecular Aspects of Schizophrenia." Bioscientia Medicina : Journal of Biomedicine and Translational Research 3, no. 2 (May 30, 2019): 38–43. http://dx.doi.org/10.32539/bsm.v3i2.88.

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Abstract Schizophrenia is a common psychiatric disorder, which is characterized by severe distortion of reality; disturbances in thoughts, feelings and behavior; according to DSM V is a disorder form deviations fundamentals and characteristics of thought and perception, and by the innapropriate or blunted affect. The influence of genetics is believed to have a role in psychiatric disorders, especially if the disorder has occurred in young adults or adolescents. The pathophysiology of schizophrenia is closely related to disorders of the biomolecular aspects of the central nervous system.

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Benítez-Burraco, Antonio, Lorena Di Pietro, Marta Barba, and Wanda Lattanzi. "Schizophrenia and Human Self-Domestication: An Evolutionary Linguistics Approach." Brain, Behavior and Evolution 89, no. 3 (2017): 162–84. http://dx.doi.org/10.1159/000468506.

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Schizophrenia (SZ) is a pervasive neurodevelopmental disorder that entails social and cognitive deficits, including marked language problems. Its complex multifactorial etiopathogenesis, including genetic and environmental factors, is still widely uncertain. SZ incidence has always been high and quite stable in human populations, across time and regardless of cultural implications, for unclear reasons. It has been hypothesized that SZ pathophysiology may involve the biological components that changed during the recent human evolutionary history, and led to our distinctive mode of cognition, wh

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Crow, T. J. "Sex Chromosomes and Psychosis." British Journal of Psychiatry 153, no. 5 (November 1988): 675–83. http://dx.doi.org/10.1192/bjp.153.5.675.

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Although the incidence of the recurrent psychoses (bipolar affective illness and schizophrenia) in the two sexes is approximately equal, gender influences a number of aspects of major psychiatric disease: unipolar depressive illness is twice as common in females, onset of schizophrenia is earlier and outcome is worse in males, and pairs of psychotic first-degree relatives are more often than expected of the same sex. In addition, sex chromosomal aneuploidies (e.g. XXY and XXX) are more frequent in patients with psychosis. Some of these findings can be explained if there is a major locus of pre

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Bora, Emre, Burcu Verim, Ozge Akgul, Ayşegül Ildız, Köksal Alptekin, Ayşegül Özerdem, and Berna Binnur Akdede. "S63. CLINICAL AND DEVELOPMENTAL CHARACTERISTICS OF COGNITIVE SUBGROUPS IN A TRANSDIAGNOSTIC SAMPLE OF SCHIZOPHRENIA, SCHIZOAFFECTIVE DISORDER AND BIPOLAR DISORDER." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S57. http://dx.doi.org/10.1093/schbul/sbaa031.129.

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Abstract Background Evidence suggests that neurocognitive dysfunction is a transdiagnostic feature of individuals across continuum between schizophrenia and bipolar disorder. However, there is a significant heterogeneity of neuropsychological and social cognitive abilities in schizophrenia, schizoaffective disorder and bipolar disorder. In recent years, several studies have investigated cognitive subgroups in schizophrenia-bipolar disorder continuum using data-driven methods and found that bipolar disorder includes several subgroups including a severely impaired and a neurocognitively intact c

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BYRNE, M., A. HODGES, E. GRANT, D. C. OWENS, and E. C. JOHNSTONE. "Neuropsychological assessment of young people at high genetic risk for developing schizophrenia compared with controls: preliminary findings of the Edinburgh High Risk Study (EHRS)." Psychological Medicine 29, no. 5 (September 1999): 1161–73. http://dx.doi.org/10.1017/s0033291799001002.

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Background. Finding risk indicators for schizophrenia among groups of individuals at high genetic risk for the disorder, has been the driving force of the high risk paradigm. The current study describes the preliminary results of a neuropsychological assessment battery conducted on the first 50% of subjects from the Edinburgh High Risk Study.Methods. One hundred and four high risk subjects and 33 normal controls, age and sex matched, were given a neuropsychological assessment battery. The areas of function assessed and reported here include intellectual function, executive function, perceptual

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Crespi, Bernard, Silven Read, Amy Ly, and Peter Hurd. "AMBRA1, Autophagy, and the Extreme Male Brain Theory of Autism." Autism Research and Treatment 2019 (October 10, 2019): 1–6. http://dx.doi.org/10.1155/2019/1968580.

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The extreme male brain theory of autism posits that its male bias is mediated by exaggeration of male-biased sex differences in the expression of autism-associated traits found in typical populations. The theory is supported by extensive phenotypic evidence, but no genes have yet been described with properties that fit its predictions. The autophagy-associated gene AMBRA1 represents one of the top genome-wide “hits” in recent GWAS studies of schizophrenia, shows sex-differential expression, and has been linked with autism risk and traits in humans and mice, especially or exclusively among fema

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Simard, Mathieu, Catherine Laprise, and Simon L. Girard. "Impact of Paternal Age at Conception on Human Health." Clinical Chemistry 65, no. 1 (January 1, 2019): 146–52. http://dx.doi.org/10.1373/clinchem.2018.294421.

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Abstract BACKGROUND The effect of maternal age at conception on various aspects of offspring health is well documented and often discussed. We seldom hear about the paternal age effect on offspring health, although the link is now almost as solid as with maternal age. The causes behind this, however, are drastically different between males and females. CONTENT In this review article, we will first examine documented physiological changes linked to paternal age effect. We will start with all morphological aspects of the testis that have been shown to be altered with aging. We will then move on

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Paulet, Manuel, Alin Ciobica, Sabina Cojocaru, Radu Popescu, and Daniel Timofte. "The relevance of motivation in schizophrenia." Archives of Biological Sciences 67, no. 4 (2015): 1425–29. http://dx.doi.org/10.2298/abs140505122p.

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Lately there is a growing interest in the negative symptoms in schizophrenia and their mechanisms of action, with special focus on the motivation process. The lack of motivation is increasingly recognized to be a very important impediment to positive management in schizophrenic pathology. In this mini-review, we described the current understanding of the nature and causes of the specific motivational deficits in schizophrenia in order to find better management strategies for this heterogeneous disorder. All the data and theories presented here clearly demonstrate that amotivation is a fundamen

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Carter, J. W., J. Parnas, A. Urfer-Parnas, J. Watson, and S. A. Mednick. "Intellectual functioning and the long-term course of schizophrenia-spectrum illness." Psychological Medicine 41, no. 6 (September 22, 2010): 1223–37. http://dx.doi.org/10.1017/s0033291710001820.

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BackgroundRecent neurodevelopmental models of schizophrenia, together with substantial evidence of neurocognitive dysfunction among people with schizophrenia, have led to a widespread view that general cognitive deficits are a central aspect of schizophrenic pathology. However, the temporal relationships between intellectual functioning and schizophrenia-spectrum illness remain unclear.MethodLongitudinal data from the Copenhagen High-Risk Project (CHRP) were used to evaluate the importance of intellectual functioning in the prediction of diagnostic and functional outcomes associated with the s

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Biernacka, J. M., K. Sangkuhl, G. Jenkins, R. M. Whaley, P. Barman, A. Batzler, R. B. Altman, et al. "The International SSRI Pharmacogenomics Consortium (ISPC): a genome-wide association study of antidepressant treatment response." Translational Psychiatry 5, no. 4 (April 2015): e553-e553. http://dx.doi.org/10.1038/tp.2015.47.

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Abstract Response to treatment with selective serotonin reuptake inhibitors (SSRIs) varies considerably between patients. The International SSRI Pharmacogenomics Consortium (ISPC) was formed with the primary goal of identifying genetic variation that may contribute to response to SSRI treatment of major depressive disorder. A genome-wide association study of 4-week treatment outcomes, measured using the 17-item Hamilton Rating Scale for Depression (HRSD-17), was performed using data from 865 subjects from seven sites. The primary outcomes were percent change in HRSD-17 score and response, defi

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