Revista Brasileira de Psiquiatria ISSN print 1516-4446
ISSN on-line 1809-452X
JCR IF 2017: 2.093
Fully open access
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Current issue Supl.2, Volume 34 - Aug/Sep/Oct/2012


 

EDITORIALS
1 - The relevance of neuroscience research networks for Brazilian Science
Flávio Kapczinski; Marco Aurélio Romano-Silva
Pages: s119 - s120

Descriptors:


2 - Advancing neuroscience applications to psychiatric and neurological disorders: more than ever, an interdisciplinary task
Geraldo Busatto Filho; Luiz Roberto Giorgetti de Britto; João Pereira Leite
Pages: s121 - s124

Descriptors:


ARTICLES
3 - New molecular targets for PET and SPECT imaging in neurodegenerative diseases
Marcel Benadiba; Gert Luurtsema; Lauro Wichert-Ana; Carlos Alberto Buchpigel; Geraldo Busatto Filho
Pages: s125 - s148
Abstract

The pathophysiology of neurodegenerative diseases (ND) such as Alzheimer's disease (AD) and Parkinson's disease (PD) has not yet been completely elucidated. However, in the past few years, there have been great knowledge advances about intra-and extracellular proteins that may display impaired function or expression in AD, PD and other ND, such as amyloid beta (Aβ), α-synuclein, tau protein and neuroinflammatory markers. Recent developments in the imaging techniques of positron emission tomography (PET) and single photon emission computed tomography (SPECT) now allow the non-invasive tracking of such molecular targets of known relevance to ND in vivo. This article summarizes recent findings of PET and SPECT studies using these novel methods, and discusses their potential role in the field of drug development for ND as well as future clinical applications in regard to differential diagnosis of ND and monitoring of disease progression.

Descriptors: Positron emission tomography; Single photon emission tomography; Neurodegenerative diseases; Neuroinflammation; Brain lipid metabolism.


4 - Nitric oxide plasma/serum levels in patients with schizophrenia: A systematic review and meta-analysis
João Paulo Maia-de-Oliveira; Clarissa Trzesniak; Irismar R. Oliveira; Matthew J. Kempton; Tatiana M. N. de Rezende Sandro Iego; Glen B. Baker; Serdar M. Dursun João Paulo Machado-de-Sousa; Jaime E. C. Hallak
Pages: s149 - s162
Abstract

For the last 40 years, schizophrenia has been considered to be the result primarily of a dysfunction in brain dopaminergic pathways. In this review, it is described and discussed findings concerning nitric oxide-mediated neurotransmission in schizophrenia. Studies were searched in PubMed, SciELO, and LILACS using the terms schizophrenia and nitric oxide plasma levels or nitric oxide serum levels, with no time limit. The reference lists of selected articles were also hand-searched for additional articles. From 15 potential reports, 10 were eligible to be included in the review and meta-analysis. These studies included a total of 505 patients with schizophrenia and 339 healthy volunteers. No significant difference was found between patients and healthy controls regarding total nitrite plasma/serum levels (effect size g = 0.285, 95%CI = -0.205 to 0.774, p = 0.254). However, when studies with patients under antipsychotic treatment were examined separately, there was a significant difference between patients and healthy volunteers (effect size g = 0.663, 95%CI = 0.365 to 0.961, p < 0.001), showing that patients under treatment have higher levels of plasma/serum nitric oxide than controls. These results suggest that antipsychotics increase nitric oxide plasma/serum levels and that the nitrergic pathway would be a fertile target for the development of new treatments for patients with schizophrenia.

Descriptors: Nitric Oxide; Schizophrenia; Psychosis; Plasma levels; Serum levels; Meta-analysis; Systematic review.


5 - The endocannabinoid system and its role in schizophrenia: a systematic review of the literature
Rodrigo Ferretjans; Fabrício A. Moreira; Antônio L. Teixeira; João V. Salgado
Pages: S163 - S193
Abstract

OBJECTIVE: Schizophrenia is a psychiatric disorder whose mechanisms have remained only partially elucidated. The current proposals regarding its biological basis, such as the dopaminergic hypothesis, do not fully explain the diversity of its symptoms, indicating that other processes may be involved. This paper aims to review evidence supporting the involvement of the endocannabinoid system (ECS), a neurotransmitter group that is the target of Cannabis sativa compounds, in this disorder.
METHODS: A systematic review of original papers, published in English, indexed in PubMed up to April, 2012.
RESULTS: Most studies employed genetics and histological, neuroimaging or neurochemical methods - either in vivo or post-mortem - to investigate whether components of the ECS are compromised in patients. Overall, the data show changes in cannabinoid receptors in certain brain regions as well as altered levels in endocannabinoid levels in cerebrospinal fluid and/or blood.
CONCLUSIONS: Although a dysfunction of the ECS has been described, results are not entirely consistent across studies. Further data are warrant to better define a role of this system in schizophrenia.

Descriptors: Schizophrenia; Cannabis; Endocannabinoids; Antipsychotics.


6 - Different approaches, one target: understanding cellular mechanisms of Parkinson's and Alzheimer's diseases
Andréa S. Torrão; Cecilia C. Café-Mendes; Caroline C. Real; Marina S. Hernandes; Ana F. B. Ferreira; Taisa O. Santos; Gabriela P. Chaves-Kirsten; Caio H. Y. Mazucanti; Emer S. Ferro; Cristoforo Scavone; Luiz R. G. Britto
Pages: S194 - S218
Abstract

Neurodegenerative disorders are undoubtedly an increasing problem in the health sciences, given the increase of life expectancy and occasional vicious life style. Despite the fact that the mechanisms of such diseases are far from being completely understood, a large number of studies that derive from both the basic science and clinical approaches have contributed substantial data in that direction. In this review, it is discussed several frontiers of basic research on Parkinson's and Alzheimer's diseases, in which research groups from three departments of the Institute of Biomedical Sciences of the University of São Paulo have been involved in a multidisciplinary effort. The main focus of the review involves the animal models that have been developed to study cellular and molecular aspects of those neurodegenerative diseases, including oxidative stress, insulin signaling and proteomic analyses, among others. We anticipate that this review will help the group determine future directions of joint research in the field and, more importantly, set the level of cooperation we plan to develop in collaboration with colleagues of the Nucleus for Applied Neuroscience Research that are mostly involved with clinical research in the same field.

Descriptors: Neurodegeneration; Neuroprotection; Oxidative Stress; Streptozotocin; NADPHoxidase.


7 - BDNF gene polymorphism, cognition and symptom severity in a brazilian population-based sample of first-episode psychosis subjects
Eduardo Martinho Jr; Leandro Michelon; Adriana M Ayres; Marcia Scazufca; Paulo R Menezes; Maristela S Schaufelberger; Robin M Murray; Teresa M. Rushe; Homero Vallada; Geraldo Busatto Filho
Pages: S219 - S232
Abstract

OBJECTIVE: To investigate the influence of brain-derived neurotrophic factor (BDNF) gene variations on cognitive performance and clinical symptomatology in first-episode psychosis (FEP). METHODS: We performed BDNF val66met variant genotyping, cognitive testing (verbal fluency and digit spans) and assessments of symptom severity (as assessed with the PANSS) in a population-based sample of FEP patients (77 with schizophreniform psychosis and 53 with affective psychoses) and 191 neighboring healthy controls. RESULTS: There was no difference in the proportion of Met allele carriers between FEP patients and controls, and no significant influence of BDNF genotype on cognitive test scores in either of the psychosis groups. A decreased severity of negative symptoms was found in FEP subjects that carried a Met allele, and this finding reached significance for the subgroup with affective psychoses (p < 0.01, ANOVA). CONCLUSIONS: These results suggest that, in FEP, the BDNF gene Val66Met polymorphism does not exert a pervasive influence on cognitive functioning but may modulate the severity of negative symptoms.

Descriptors: Positive and Negative Syndrome Scale; Working memory; Attention; Verbal fluency; Schizophrenia; Affective disorder.


8 - Pathophysiology of mood disorders in temporal lobe epilepsy
Ludmyla Kandratavicius; Rafael Naime Ruggiero; Jaime Eduardo Hallak; Norberto Garcia Cairasco; João Pereira Leite
Pages: S233 - S259
Abstract

OBJECTIVE: There is accumulating evidence that the limbic system is pathologically involved in cases of psychiatric comorbidities in temporal lobe epilepsy (TLE) patients. Our objective was to develop a conceptual framework describing how neuropathological, neurochemical and electrophysiological aspects might contribute to the development of psychiatric symptoms in TLE and the putative neurobiological mechanisms that cause mood disorders in this patient subgroup.
METHODS: In this review, clinical, experimental and neuropathological findings, as well as neurochemical features of the limbic system were examined together to enhance our understanding of the association between TLE and psychiatric comorbidities. Finally, the value of animal models in epilepsy and mood disorders was discussed.
CONCLUSIONS: TLE and psychiatric symptoms coexist more frequently than chance would predict. Alterations and neurotransmission disturbance among critical anatomical networks, and impaired or aberrant plastic changes might predispose patients with TLE to mood disorders. Clinical and experimental studies of the effects of seizures on behavior and electrophysiological patterns may offer a model of how limbic seizures increase the vulnerability of TLE patients to precipitants of psychiatric symptoms.

Descriptors: Temporal Lobe Epilepsy; Major Depression; Interictal Dysphoria; Psychiatric Comorbidities; Neuropathology; Synaptic Plasticity; Animal Models.