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The present study was conducted to examine the rates of symptomatic remission, the level of community functioning; and to assess functional recoveryin a sample of chronic schizophrenia out-patients; to compare recovered versus non-recovered patients according to demographic and clinical variables; and to identify predictive factors for recovery. Results indicate that 48.4% (n=92) patients fulfilled the criteria of symptomatic remission. The level of social functioning according to the mean GAF score of was 60.3 (S.D.=8.7). Considering the four criteria to attain recovery; 48.4% (n=92) patients met the criteria of symptomatic remission, followed by 46.3% (n=88) who met the criteria of vocational functioning, 26.3% (n=50) for peer relationships, and independent living was met by only 23.7% (n=45) of the sample. From these four criteria, a total of 10.5% (n=20) of the patients were considered to attained functional recovery as they met the required criteria. Functioning was higher in recovered patients with a GAF of 72.2 compared to a GAF of 58.8 in non-recovered patients.The logistic regression model included 2 predictors for recovery: 1) increased age of illness onset (>23years old) and, 2) better functioning according to a higher GAF score (>60 points). The results of this study indicate that symptomatic remission and functional recovery can be attainable goals in Mexican patients with schizophrenia.
Schizophrenia (SCZ) is a highly heritable, chronic, severe, disabling neurodevelopmental brain disorder with a heterogeneous genetic and neurobiological background, which is still poorly understood. Because schizophrenia has no distinguishing pathology or diagnostic criteria, it is difficult to relate gene changes to discrete physiological or biochemical changes associated with the disease. SCZ fits the profile of a complex disorder in which multiple genes interact along with environmental influences to produce a range of phenotypes. There is accumulating evidence that both common genetic variants with small effects and rare genetic lesions with large effects determine risk of SCZ. Thousands of common single nucleotide polymorphisms cumulatively could explain high percentage of the underlying genetic risk of SCZ. Therefore, it requires lifelong treatment, even when symptoms have subsided. Treatment with medications and psychosocial therapy help in managing the condition. In this review, we summarize the current understanding of genetic and pathogenesis of SCZ and highlight their potential role as diagnostic agents and therapeutic targets.
Schizophrenia is one of the most intriguing human diseases because it affects the most complex functions emanating from the brain. Bleuler defined the term in 1911 as a psychotic disorder characterized by four primary symptoms: “abnormal associations, autistic behavior and thinking, abnormal affect, and ambivalence” . Developing an animal model that is expected to mimic deficits in such functions is an achievement in itself. However, it is an absolute necessity first because the pathology is devastating for patients and their families and, secondly and consequently, because there is a crucial the need to find more efficient treatments. Until now, many animal models have been developed by the manipulation of a sole factor (pharmacological, genetics, environmental etc.), while some others have tried to manipulate two of three factors. In this review we describe the main rodent models used in scientific research until now, and the new models more recently developed. Most of them can be considered as successful to trigger positive-like symptoms in animals (increased locomotion) and are useful to assess effects of antipsychotics (locomotion decreased to control level). Some of them also induce negative-like symptoms (decreased social interaction and anhedonia) and/or cognitive deficits (altered memory, attention, and sensorimotor gating), conferring an added-value to assess effects of existing psychotics and developing new ones.