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Objective: To assess the influence of migration on the psychopathological presentation of individuals at ultra-high risk for psychosis (UHR) in São Paulo, Brazil. Methods: This study is part of the Subclinical Symptoms and Prodromal Psychosis (SSAPP) project, a cohort study in São Paulo, Brazil, designed to follow individuals at UHR. After screening with the Prodromal Questionnaire (PQ) and a clinical interview, the Global Assessment of Functioning (GAF) was administered, a neuropsychological assessment was performed, sociodemographic and migration data were obtained. We then analyzed UHR individuals who had migration data to see if migration had any effect on their cognition and psychopathology. Chi-square tests were used for categorical variables, and Student’s t test or analysis of variance (ANOVA) were used for nonparametric and parametric distributions, respectively. Results: The sample was composed of 42 at-risk subjects, of whom 5 had a migration history in the past two generations. Those with migration history showed significantly more formal thought disturbances (p = 0.012) and sleeping problems (p = 0.033) compared to those without. Conclusions: Our data reinforce migration as a risk factor for psychosis in developing countries as well, and highlights the importance of studying the specific effect of this factor in UHR psychopathology.

https://doi.org/10.1590/1516-4446-2019-0685 127 downloads

Precision non-implantable neuromodulation therapies: a perspective for the depressed brain
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Borrione, Lucas

; Bellini, Helena

; Razza, Lais Boralli

; Avila, Ana G.

; Baeken, Chris

; Brem, Anna-Katharine

; Busatto, Geraldo

; Carvalho, Andre F.

; Chekroud, Adam

; Daskalakis, Zafiris J.

; Deng, Zhi-De

; Downar, Jonathan

; Gattaz, Wagner

; Loo, Colleen

; Lotufo, Paulo A.

; Martin, Maria da Graça M.

; McClintock, Shawn M.

; O’Shea, Jacinta

; Padberg, Frank

; Passos, Ives C.

; Salum, Giovanni A.

; Vanderhasselt, Marie-Anne

; Fraguas, Renerio

; Benseñor, Isabela

; Valiengo, Leandro

; Brunoni, Andre R.

Brazilian Journal of Psychiatry

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aug 2020, Volume 42 N. 4 Pages 403 - 419

Abstract: En | Text: En | PDF: En

Current first-line treatments for major depressive disorder (MDD) include pharmacotherapy and cognitive-behavioral therapy. However, one-third of depressed patients do not achieve remission after multiple medication trials, and psychotherapy can be costly and time-consuming. Although non-implantable neuromodulation (NIN) techniques such as transcranial magnetic stimulation, transcranial direct current stimulation, electroconvulsive therapy, and magnetic seizure therapy are gaining momentum for treating MDD, the efficacy of non-convulsive techniques is still modest, whereas use of convulsive modalities is limited by their cognitive side effects. In this context, we propose that NIN techniques could benefit from a precision-oriented approach. In this review, we discuss the challenges and opportunities in implementing such a framework, focusing on enhancing NIN effects via a combination of individualized cognitive interventions, using closed-loop approaches, identifying multimodal biomarkers, using computer electric field modeling to guide targeting and quantify dosage, and using machine learning algorithms to integrate data collected at multiple biological levels and identify clinical responders. Though promising, this framework is currently limited, as previous studies have employed small samples and did not sufficiently explore pathophysiological mechanisms associated with NIN response and side effects. Moreover, cost-effectiveness analyses have not been performed. Nevertheless, further advancements in clinical trials of NIN could shift the field toward a more “precision-oriented” practice.

https://doi.org/10.1590/1516-4446-2019-0741 1546 downloads

Association of BDNF, HTR2A, TPH1, SLC6A4, and COMT polymorphisms with tDCS and escitalopram efficacy: ancillary analysis of a double-blind, placebo-controlled trial
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Brunoni, Andre R.

; Carracedo, Angel

; Amigo, Olalla M.

; Pellicer, Ana L.

; Talib, Leda

; Carvalho, Andre F.

; Lotufo, Paulo A.

; Benseñor, Isabela M.

; Gattaz, Wagner

; Cappi, Carolina

Brazilian Journal of Psychiatry

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apr 2020, Volume 42 N. 2 Pages 128 - 135

Abstract: En | Text: En | PDF: En

Objective: We investigated whether single nucleotide polymorphisms (SNPs) associated with neuroplasticity and activity of monoamine neurotransmitters, such as the brain-derived neurotrophic factor (BDNF, rs6265), the serotonin transporter (SLC6A4, rs25531), the tryptophan hydroxylase 1 (TPH1, rs1800532), the 5-hydroxytryptamine receptor 2A (HTR2A, rs6311, rs6313, rs7997012), and the catechol-O-methyltransferase (COMT, rs4680) genes, are associated with efficacy of transcranial direct current stimulation (tDCS) in major depression. Methods: Data from the Escitalopram vs. Electrical Current Therapy for Treating Depression Clinical Study (ELECT-TDCS) were used. Participants were antidepressant-free at baseline and presented with an acute, moderate-to-severe unipolar depressive episode. They were randomized to receive escitalopram/tDCS-sham (n=75), tDCS/placebo-pill (n=75), or placebo-pill/sham-tDCS (n=45). General linear models assessed the interaction between treatment group and allele-wise carriers. Additional analyses were performed for each group and each genotype separately. Results: Pairwise group comparisons (tDCS vs. placebo, tDCS vs. escitalopram, and escitalopram vs. placebo) did not identify alleles associated with depression improvement. In addition, exploratory analyses also did not identify any SNP unequivocally associated with improvement of depression in any treatment group. Conclusion: Larger, combined datasets are necessary to identify candidate genes for tDCS response.

https://doi.org/10.1590/1516-4446-2019-0620 1172 downloads

Decreased plasmatic spermidine and increased spermine in mild cognitive impairment and Alzheimer’s disease patients
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JOAQUIM, HELENA P. G.

; COSTA, ALANA C.

; FORLENZA, ORESTES V.

; GATTAZ, WAGNER F.

; TALIB, LEDA L.

Archives of Clinical Psychiatry (São Paulo)

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oct 2019, Volume 46 N. 5 Pages 120 - 124

Abstract: En | Text: En | PDF: En

Abstract Background Current evidence suggests that upregulation of polyamines system plays a role both in cognitive deficit and synaptic loss observed in Alzheimer’s disease (AD). Objective The aim of this study was to determine the plasmatic concentration of polyamines in mild cognitive impairment (MCI) and AD patients in comparison with healthy controls (HC). Methods Plasmatic polyamines were quantified using the AbsoluteIDQ® p180 and liquid chromatography coupled to tandem mass spectrometry (LC/MS-MS). Results The study group comprised 34 AD patients, 20 MCI and 25 HC. All individuals were followed for 4 years. During this period 8 amnestic MCI patients (40% of the MCI sample at baseline) converted to AD. Spermidine level was lower in both patient groups (AD; MCI) compared to HC (p = 0.007). Plasma levels of spermine were higher in the MCI group (p < 0.001), but decreased in the sub-sample of MCI patients who converted to AD (p = 0.043). No statistically significant differences were found in ornithine and putrescine levels (p = 0.056 and p = 0.126, respectively). Discussion Our results suggest dynamic changes in the expression of polyamines in the MCI-AD continuum.

https://doi.org/10.1590/0101-60830000000209 768 downloads

A new editorial board for new challenges
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Gattaz, Wagner F.

; Crippa, José A. S.

Archives of Clinical Psychiatry (São Paulo)

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jun 2017, Volume 44 N. 3 Pages 55 - 55

Abstract: En | Text: En | PDF: En

https://doi.org/10.1590/0101-60830000000119 507 downloads

Epistasis between COMT Val158Met and DRD3 Ser9Gly polymorphisms and cognitive function in schizophrenia: genetic influence on dopamine transmission
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Loch, Alexandre A.

; van de Bilt, Martinus T.

; Bio, Danielle S.

; Prado, Carolina M. do

; Sousa, Rafael T. de

; Valiengo, Leandro L.

; Moreno, Ricardo A.

; Zanetti, Marcus V.

; Gattaz, Wagner F.

Brazilian Journal of Psychiatry

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sep 2015, Volume 37 N. 3 Pages 235 - 241

Abstract: En | Text: En | PDF: En

Objective: To assess the relationship between cognitive function, a proposed schizophrenia endophenotype, and two genetic polymorphisms related to dopamine function, catechol-O-methyl transferase (COMT) Val158Met and dopamine receptor 3 (DRD3) Ser9Gly. Methods: Fifty-eight outpatients with schizophrenia/schizoaffective disorder and 88 healthy controls underwent neurocognitive testing and genotyping. Analyses of covariance (ANCOVAs) using age, sex, and years of education as covariates compared cognitive performance for the proposed genotypes in patients and controls. ANCOVAs also tested for the epistatic effect of COMT and DRD3 genotype combinations on cognitive performance. Results: For executive functioning, COMT Val/Val patients performed in a similar range as controls (30.70-33.26 vs. 35.53-35.67), but as COMT Met allele frequency increased, executive functioning worsened. COMT Met/Met patients carrying the DRD3 Ser/Ser genotype performed poorest (16.184 vs. 27.388-31.824). Scores of carriers of this COMT/DRD3 combination significantly differed from all DRD3 Gly/Gly combinations (p < 0.05), from COMT Val/Met DRD3 Ser/Gly (p = 0.02), and from COMT Val/Val DRD3 Ser/Ser (p = 0.01) in patients. It also differed significantly from all control scores (p < 0.001). Conclusion: Combined genetic polymorphisms related to dopamine neurotransmission might influence executive function in schizophrenia. Looking at the effects of multiple genes on a single disease trait (epistasis) provides a comprehensive and more reliable way to determine genetic effects on endophenotypes.

https://doi.org/10.1590/1516-4446-2014-1553 2214 downloads

Mild cognitive impairment (part 1): clinical characteristics and predictors of dementia
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Forlenza, Orestes V.

; Diniz, Breno S.

; Stella, Florindo

; Teixeira, Antonio L.

; Gattaz, Wagner F.

Brazilian Journal of Psychiatry

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jun 2013, Volume 35 N. 2 Pages 178 - 185

Abstract: En | Text: En | PDF: En

Objective: To critically review and evaluate existing knowledge on the conceptual limits and clinical usefulness of the diagnosis of mild cognitive impairment (MCI) and the neuropsychological assessment and short- and long-term prognosis thereof. Methods: We conducted a systematic search of the PubMed and Web of Science electronic databases, limited to articles published in English between 1999 and 2012. Based on the search terms mild cognitive impairment or MCI and epidemiology or diagnosis, we retrieved 1,698 articles, of which 248 were critically eligible (cross-sectional and longitudinal studies); the abstracts of the remaining 1,450 articles were also reviewed. Results: A critical review on the MCI construct is provided, including conceptual and diagnostic aspects; epidemiological relevance; clinical assessment; prognosis; and outcome. The distinct definitions of cognitive impairment, MCI included, yield clinically heterogeneous groups of individuals. Those who will eventually progress to dementia may present with symptoms consistent with the definition of MCI; conversely, individuals with MCI may remain stable or return to normal cognitive function. Conclusion: On clinical grounds, the cross-sectional diagnosis of MCI has limited prognostic relevance. The characterization of persistent and/or progressive cognitive deficits over time is a better approach for identification of cases at the pre-dementia stages, particularly if these cognitive abnormalities are consistent with the natural history of incipient Alzheimer's disease.

https://doi.org/10.1590/1516-4446-2012-3503 13642 downloads

Single-nucleotide polymorphisms of GSK3B, GAB2 and SORL1 in late-onset Alzheimer's disease: interactions with the APOE genotype
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Izzo, Giselle

; Forlenza, Orestes V.

; Santos, Bernardo dos

; Bertolucci, Paulo H. F.

; Ojopi, Elida B.

; Gattaz, Wagner F.

; Kerr, Daniel Shikanai

Clinics

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2013, Volume 68 N. 2 Pages 277 - 280

Abstract: En | Text: En | PDF: En

In this study, we investigated the associations between single-nucleotide polymorphisms in GAB2 (rs2373115), GSK3B (rs6438552) and SORL1 (rs641120) and Alzheimer's disease (AD), both alone and in combination with the APOE*4 allele.

https://doi.org/10.6061/CLINICS/2013(02)RC01 1956 downloads Cited 1 time in SciELO

10.

Revista de Psiquiatria Clínica: 40 years
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Gattaz, Wagner F.

Archives of Clinical Psychiatry (São Paulo)

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2013, Volume 40 N. 3 Pages 01 - 01

Abstract: En | Text: En | PDF: En

12611 downloads

11.

Da arte de fazer ciência e de comer jabuticabas: uma homenagem ao Prof. Dr. Ricardo Renzo Brentani
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Dias-Neto, Emmanuel

; Gattaz, Wagner F.

Archives of Clinical Psychiatry (São Paulo)

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2012, Volume 39 N. 1 Pages 1 - 4

Abstract: Pt | Text: Pt | PDF: Pt

2119 downloads

12.

Insights into Alzheimer disease pathogenesis from studies in transgenic animal models
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Schaeffer, Evelin L.

; Figueiro, Micheli

; Gattaz, Wagner F.

Clinics

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2011, Volume 66 Suppl. 1 Pages 45 - 54

Abstract: En | Text: En | PDF: En

Alzheimer disease is the most common cause of dementia among the elderly, accounting for ~60-70% of all cases of dementia. The neuropathological hallmarks of Alzheimer disease are senile plaques (mainly containing p-amyloid peptide derived from amyloid precursor protein) and neurofibrillary tangles (containing hyperphosphorylated Tau protein), along with neuronal loss. At present there is no effective treatment for Alzheimer disease. Given the prevalence and poor prognosis of the disease, the development of animal models has been a research priority to understand pathogenic mechanisms and to test therapeutic strategies. Most cases of Alzheimer disease occur sporadically in people over 65 years old, and are not genetically inherited. Roughly 5% of patients with Alzheimer disease have familial Alzheimer disease-that is, related to a genetic predisposition, including mutations in the amyloid precursor protein, presenilin 1, and presenilin 2 genes. The discovery of genes for familial Alzheimer disease has allowed transgenic models to be generated through the overexpression of the amyloid precursor protein and/or presenilins harboring one or several mutations found in familial Alzheimer disease. Although none of these models fully replicates the human disease, they have provided valuable insights into disease mechanisms as well as opportunities to test therapeutic approaches. This review describes the main transgenic mouse models of Alzheimer disease which have been adopted in Alzheimer disease research, and discusses the insights into Alzheimer disease pathogenesis from studies in such models. In summary, the Alzheimer disease mouse models have been the key to understanding the roles of soluble b-amyloid oligomers in disease pathogenesis, as well as of the relationship between p-amyloid and Tau pathologies.

7127 downloads

13.

Clinical and biological predictors of Alzheimer's disease in patients with amnestic mild cognitive impairment
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Forlenza, Orestes V.

; Diniz, Breno S.

; Talib, Leda L.

; Radanovic, Marcia

; Yassuda, Monica S.

; Ojopi, Elida B.

; Gattaz, Wagner F.

Brazilian Journal of Psychiatry

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sep 2010, Volume 32 N. 3 Pages 216 - 222

Abstract: Pt En | Text: Pt En | PDF: Pt | PDF: En

OBJETIVO: A identificação de preditores da conversão para a doença de Alzheimer em pacientes com comprometimento cognitivo leve é relevante para o manejo clínico e para decidir sobre a prescrição de drogas antidemência. MÉTODO: Estudo longitudinal em coorte de indivíduos idosos com comprometimento cognitivo leve amnéstico e controles saudáveis; estimativa do risco da progressão para doença de Alzheimer nos dois grupos; determinação das variáveis preditivas desse desfecho. RESULTADOS: Pacientes com comprometimento cognitivo leve amnéstico apresentaram maior risco de desenvolver doença de Alzheimer ao longo do seguimento (odds ratio = 4,5, CI95% [1,3-13,6], p = 0,012). Na avaliação inicial, idade mais avançada, escores mais baixos nos testes cognitivos e do alelo APOE*4 foram preditores da conversão do comprometimento cognitivo leve amnéstico para doença de Alzheimer. Em uma subamostra de pacientes com comprometimento cognitivo leve amnéstico, aqueles que progrediram para doença de Alzheimer tinham concentrações liquóricas mais baixas do peptídeo beta-amilóide (Aβ42, p = 0,020) e mais altas da proteína TAU total (p = 0,030) e TAU fosforilada (p = 0,010) do que os pacientes que não progrediram para doença de Alzheimer. DISCUSSÃO: Este é o primeiro estudo brasileiro com biomarcadores liquóricos a relatar preditores da conversão comprometimento cognitivo leve-doença de Alzheimer. Nossos dados biológicos (aumento de TAU total e fosfo-TAU; redução de Aβ42), e podem auxiliar na identificação dos pacientes com comprometimento cognitivo leve com maior risco de evolução para demência.

OBJECTIVE: To identify predictors of the progression from pre-dementia stages of cognitive impairment in Alzheimer's disease is relevant to clinical management and to substantiate the decision of prescribing antidementia drugs. METHOD: Longitudinal study of a cohort of elderly adults with amnestic mild cognitive impairment and healthy controls, carried out to estimate the risk and characterize predictors of the progression to Alzheimer's disease. RESULTS: Patients with amnestic mild cognitive impairment had a higher risk to develop Alzheimer's disease during follow-up (odds ratio = 4.5, CI95% [1.3-13.6], p = 0.010). At baseline, older age, lower scores on memory tests and presence of the APOE*4 allele predicted the progression from amnestic mild cognitive impairment to Alzheimer's disease. In a sub sample of amnestic mild cognitive impairment patients, those who progressed to Alzheimer's disease had lower cerebrospinal fluid concentrations of amyloid-beta peptide (Aβ42, p = 0.020) and higher concentrations of total TAU (p = 0.030) and phosphorylated TAU (p = 0.010), as compared to non-converters. DISCUSSION: This is the first Brazilian study to report cerebrospinal fluid biomarkers in the prediction of the conversion from MCI to Alzheimer's disease. Our data are in accordance with those reported in other settings. The measurement of cerebrospinal fluid total-TAU, phospho-TAU and Aβ42 may help identify patients with mild cognitive impairment at higher risk for developing Alzheimer's disease.

3946 downloads

14.

Thalamic nuclear abnormalities as a contributory factor in sudden cardiac deaths among patients with schizophrenia
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Scorza, Fulvio A.

; Schmitt, Andrea

; Cysneiros, Roberta M.

; Arida, Ricardo M.

; Cavalheiro, Esper A.

; Gattaz, Wagner F.

Clinics

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2010, Volume 65 N. 5 Pages 539 - 546

Abstract: En | Text: En | PDF: En

Patients with schizophrenia have a two- to three-fold increased risk of premature death as compared to patients without this disease. It has been established that patients with schizophrenia are at a high risk of developing cardiovascular disease. Moreover, an important issue that has not yet been explored is a possible existence of a "cerebral" focus that could trigger sudden cardiac death in patients with schizophrenia. Along these lines, several structural and functional alterations in the thalamic complex are evident in patients with schizophrenia and have been correlated with the symptoms manifested by these patients. With regard to abnormalities on the cellular and molecular level, previous studies have shown that schizophrenic patients have fewer neuronal projections from the thalamus to the prefrontal cortex as well as a reduced number of neurons, a reduced volume of either the entire thalamus or its subnuclei, and abnormal glutamate signaling. According to the glutamate hypothesis of schizophrenia, hypofunctional corticostriatal and striatothalamic projections are directly involved in the pathophysiology of the disease. Animal and post-mortem studies have provided a large amount of evidence that links the sudden unexpected death in epilepsy (SUDEP) that occurs in patients with schizophrenia and epilepsy to thalamic changes. Based on the results of these prior studies, it is clear that further research regarding the relationship between the thalamus and sudden cardiac death is of vital importance.

2463 downloads

15.

Revista de Psiquiatria Clínica indexada no ISI
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Gattaz, Wagner F.

Archives of Clinical Psychiatry (São Paulo)

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2008, Volume 35 N. 4

Abstract: Pt | Text: Pt | PDF: Pt

3368 downloads

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