TIFFANY MOUKBEL CHAIM AVANCINI
Projetos de Pesquisa
Unidades Organizacionais
LIM/21 - Laboratório de Neuroimagem em Psiquiatria, Hospital das Clínicas, Faculdade de Medicina
40 resultados
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bookPart Abuso e dependência de drogas(2014) SCIVOLETTO, Sandra; CHAIM, Tiffany- Country-level gender inequality is associated with structural differences in the brains of women and men(2023) ZUGMAN, Andre; ALLIENDE, Luz Maria; MEDEL, Vicente; BETHLEHEM, Richard A. I.; SEIDLITZ, Jakob; RINGLEIN, Grace; ARANGO, Celso; ARNATKEVICIUTE, Aurina; ASMAL, Laila; BELLGROVE, Mark; BENEGAL, Vivek; BERNARDO, Miquel; BILLEKE, Pablo; BOSCH-BAYARD, Jorge; BRESSAN, Rodrigo; BUSATTO, Geraldo F.; CASTRO, Mariana N.; CHAIM-AVANCINI, Tiffany; COMPTE, Albert; COSTANZI, Monise; CZEPIELEWSKI, Leticia; DAZZAN, Paola; FUENTE-SANDOVAL, Camilo de la; FORTI, Marta Di; DIAZ-CANEJA, Covadonga M.; DIAZ-ZULUAGA, Ana Maria; PLESSIS, Stefan Du; DURAN, Fabio L. S.; FITTIPALDI, Sol; FORNITO, Alex; FREIMER, Nelson B.; GADELHA, Ary; GAMA, Clarissa S.; GARANI, Ranjini; GARCIA-RIZO, Clemente; CAMPO, Cecilia Gonzalez; GONZALEZ-VALDERRAMA, Alfonso; GUINJOAN, Salvador; HOLLA, Bharath; IBANEZ, Agustin; IVANOVIC, Daniza; JACKOWSKI, Andrea; LEON-ORTIZ, Pablo; LOCHNER, Christine; LOPEZ-JARAMILLO, Carlos; LUCKHOFF, Hilmar; MASSUDA, Raffael; MCGUIRE, Philip; MIYATAAAA, Jun; MIZRAHI, Romina; MURRAY, Robin; OZERDEM, Aysegul; PAN, Pedro M.; PARELLADA, Mara; PHAHLADIRA, Lebogan; RAMIREZ-MAHALU, Juan P.; RECKZIEGEL, Ramiro; MARQUES, Tiago Reis; REYES-MADRIGAL, Francisco; ROOS, Annerine; ROSA, Pedro; SALUM, Giovanni; SCHEFFLER, Freda; SCHUMANN, Gunter; SERPA, Mauricio; STEIN, Dan J.; TEPPER, Angeles; TIEGO, Jeggan; UENO, Tsukasa; UNDURRAGA, Juan; UNDURRAG, Eduardo A.; VALDES-SOSAOOO, Pedro; VALLIY, Isabel; VILLARREALU, Mirta; WINTON-BROWNRRR, Toby T.; YALIN, Nefize; ZAMORANO, Francisco; ZANETTI, Marcus V.; WINKLER, Anderson M.; PINE, Daniel S.; EVANS-LACKO, Sara; CROSSLEY, Nicolas A.Gender inequality across the world has been associated with a higher risk to mental health problems and lower academic achievement in women compared to men. We also know that the brain is shaped by nurturing and adverse socio-environmental experiences. Therefore, unequal exposure to harsher conditions for women compared to men in gender-unequal countries might be reflected in differences in their brain structure, and this could be the neural mechanism partly explaining women's worse outcomes in gender-unequal countries. We examined this through a random-effects meta-analysis on cortical thickness and surface area differences between adult healthy men and women, including a meta-regression in which country-level gender inequality acted as an explanatory variable for the observed differences. A total of 139 samples from 29 different countries, totaling 7,876 MRI scans, were included. Thickness of the right hemisphere, and particularly the right caudal anterior cingulate, right medial orbitofrontal, and left lateral occipital cortex, presented no differences or even thicker regional cortices in women compared to men in gender-equal countries, reversing to thinner cortices in countries with greater gender inequality. These results point to the potentially hazardous effect of gender inequality on women's brains and provide initial evidence for neuroscience-informed policies for gender equality.
conferenceObject Increased GDNF but not BDNF Plasma Levels in Type II Compared to Type I Bipolar Disorder(2013) ZANETTI, Marcus V.; TEIXEIRA, Antonio L.; CHAIM, Tiffany M.; SOUSA, Rafael T. de; TALIB, Leda L.; GATTAZ, Wagner F.; BUSATTO, Geraldo F.; MACHADO-VIEIRA, RodrigoBackground: The brain-derived neurotrophic factor (BDNF) is a neurotrophin important for synaptic plasticity and neurogenesis, whereas the glial cell-line derived neurotrophic factor (GDNF) modulates the activity of monoaminergic neurons and glial cells. Previous works have suggested that abnormal peripheral levels of these proteins might relate to different mood states in bipolar disorder (BD), but none study so far have evaluated it with regard to potential differences between the types I (BD-I) and II (BD-II) subtypes of the disorder. Methods: Eighteen BD-I and 19 BD-II patients presenting with an acute mood episode (depressive, manic or mixed), and 23 healthy controls were studied. Plasma levels of BDNF and GDNF were measured using enzyme-linked immunosorbent assay (ELISA). Results: BD-II individuals showed significantly increased levels of GDNF compared to both BD-I patients and controls (ANOVA, df=2, F= 5.74, p=0.005; Tukey for post hoc comparisons). When we focused our analysis on the treatment-naïve patients only (14 BD-I and 13 BD-II), this result became even more significant (ANOVA, df=2, F= 7.33, p=0.002). No significant between-groups differences were observed on BDNF levels. Also, no significant correlation was observed between BDNF or GDNF levels and depressive and manic symptoms. Conclusions: BD-II at an acute phase of the illness is associated with increased plasma levels of GDNF. Previous use of mood stabilizer and antipsychotic agents might produce a chronic effect on GDNF production.- Higher transcription alleles of the MAOA-uVNTR polymorphism are associated with higher seizure frequency in temporal lobe epilepsy(2019) VINCENTIIS, Silvia; ALCANTARA, Juliana; RZEZAK, Patricia; KERR, Daniel; SANTOS, Bernardo dos; ALESSI, Ruda; LINDEN, Helio van der; ARRUDA, Francisco; CHAIM-AVANCINI, Tiffany; SERPA, Mauricio; BUSATTO, Geraldo; GATTAZ, Wagner; DEMARQUE, Renata; VALENTE, Kette D.Background: There is evidence of an imbalance in the neuromodulatory system mediated by serotonin (5-HT) in patients with drug-resistant temporal lobe epilepsy (TLE). This study analyzed the monoamine oxidase A promoter variable number of tandem repeats (MAOA-uVNTR) polymorphism in patients with temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). Therefore, we assessed the association between this genetic variant and seizure predisposition and severity in patients with TLE-HS. Methods: One hundred nineteen patients with TLE-HS and 113 healthy volunteers were assessed. First, we genotyped all individuals for the MAOA-uVNTR genetic polymorphism. Second, we compared patients and controls and evaluated clinical variants of epilepsy. Results: There was no difference between the TLE-HS and control groups regarding genotypic and allelic distributions of MAOA-uVNTR polymorphism (p = 1.000). Higher transcription alleles of the MAOA-uVNTR were associated with higher seizure frequency (p = 0.032) and bilateral tonic-clonic seizures (p = 0.016). Conclusions: In a selected group of patients with TLE-HS, the polymorphism MAOA-uVNTR was associated with some aspects of epilepsy severity, namely seizure frequency and bilateral tonic-clonic seizures.
conferenceObject The Role Of Dopamine Transporter Intron 8 VNTR Polymorphism In The Occurrence Of Depression In Temporal Lobe Epilepsy(2019) VINCENTIIS, S.; ALCANTARA, J.; RZEZAK, P.; KERR, D.; GATTAZ, W.; LINDEN JUNIOR, H. van der; ARRUDA, F.; SANTOS, B. dos; CHAIM-AVANCINI, T.; SERPA, M.; FERNANDES, F.; MORENO, R. A.; BUSATTO, G. F.; DEMARQUE, R.; VALENTE, K. D.; ALESSI, R.conferenceObject Distinct Glycogen Synthase Kinase 3 beta and Phospholipase A2 Expression Profiles in Bipolar I and II Disorders(2016) ZANETTI, Marcus V.; MACHADO-VIEIRA, Rodrigo; JOAQUIM, Helena P. G.; CHAIM, Tiffany M.; SERPA, Mauricio H.; SOUSA, Rafael T. de; GATTAZ, Wagner F.; BUSATTO, Geraldo F.; TALIB, Leda L.- The role of neurocognitive functioning, substance use variables and the DSM-5 severity scale in cocaine relapse: A prospective study(2019) LIM, Danielle Ruiz; GONCALVES, Priscila Dib; OMETTO, Mariella; MALBERGIER, Andre; AMARAL, Ricardo Abrantes; SANTOS, Bernardo dos; CAVALLET, Mikael; CHAIM-AVANCINI, Tiffany; SERPA, Mauricio Henriques; FERREIRA, Luiz Roberto Kobuti; DURAN, Fabio Luis de Souza; ZANETTI, Marcus Vinicius; NICASTR, Sergio; BUSATTO, Geraldo Filho; ANDRAD, Arthur Guerra; CUNH, Paulo JannuzziBackground: The severity of substance use disorder (SUD) is currently defined by the sum of DSM-5 criteria. However, little is known about the validity of this framework or the role of additional severity indicators in relapse prediction. This study aimed to investigate the relationship between DSM-5 criteria, neurocognitive functioning, substance use variables and cocaine relapse among inpatients with cocaine use disorder (CUD). Methods: 128 adults aged between 18 and 45 years were evaluated; 68 (59 males, 9 females) had CUD and 60 (52 males, 8 females) were healthy controls. For the group with CUD, the use of other substances was not an exclusion criterion. Participants were tested using a battery of neurocognitive tests. Cocaine relapse was evaluated 3 months after discharge. Results: Scores for attention span and working memory were worse in patients compared to controls. Earlier onset and duration of cocaine use were related to poorer inhibitory control and global executive functioning, respectively; recent use was related to worse performance in inhibitory control, attention span and working memory. More DSM-5 criteria at baseline were significantly associated with relapse. Conclusions: Recent cocaine use was the most predictive variable for neurocognitive impairments, while DSM-5 criteria predicted cocaine relapse at three months post treatment. The integration of neurocognitive measures, DSM-5 criteria and cocaine use variables in CUD diagnosis could improve severity differentiation. Longitudinal studies using additional biomarkers are needed to disentangle the different roles of severity indicators in relapse prediction and to achieve more individualized and effective treatment strategies for these patients.
- Increased platelet glycogen sysnthase kinase 3beta in first-episode psychosis(2018) JOAQUIM, Helena P. G.; ZANETTI, Marcus V.; SERPA, Mauricio H.; BILT, Martinus T. Van de; SALLET, Paulo C.; CHAIM, Tiffany M.; BUSATTO, Geraldo F.; GATTAZ, Wagner F.; TALIB, Leda L.Past studies have linked intracellular pathways related to psychotic disorders to the GSK3B enzyme. This study aimed to investigate GSK3B protein expression and phosphorylation in drug-naive first-episode psychosis patients (n = 43) at baseline and following symptom remission, and in healthy controls (n = 77). At baseline GSK3B total level was higher in patients (p < 0.001). In schizophrenia spectrum patients (n = 25) GSK3B total and phosphorylated levels were higher than in controls and patients with other non-affective psychotic disorders (n = 18) (p < 0.001; p = 0.027; p = 0.05 respectively). No enzyme changes were found after clinical remission. The implication of this finding for the biology of psychoses warrants further studies to clarify whether increased GSK3B may be useful as a biomarker for psychosis in general, and schizophrenia in particular.
- Association study of functional polymorphisms of dopaminergic pathway in epilepsy-related factors of temporal lobe epilepsy in Brazilian population(2018) ALCANTARA, J. A.; VINCENTIS, S.; KERR, D. S.; SANTOS, B. dos; ALESSI, R.; LINDEN JR., H. van der; CHAIM, T.; SERPA, M. H.; BUSATTO, G. F.; GATTAZ, W. F.; DEMARQUE, R.; VALENTE, K. D.Background and purposeThere are few data about the role of neurotransmission modulated by dopamine in epilepsy, especially temporal lobe epilepsy (TLE). This is the first study that aimed to analyze the dopaminergic polymorphisms in an etiologically homogeneous group of patients with TLE with hippocampal sclerosis. Selected polymorphisms were: (i) the most expressed D2-like receptors in the limbic system (DRD2/ANKK1 TAQ-1A, D4_VNTR and D4_rs1800955); (ii) the dopamine transporter (DAT) 3-untranslated region and intron 8; and (iii) two degrading enzymes regulating the synaptic activity, i.e. the main metabolizer of dopamine, catechol-O-methyltransferase, and monoamine oxidase A. MethodsWe assessed 119 patients with unequivocal TLE with hippocampal sclerosis and 112 healthy volunteers. Individuals were genotyped for the polymorphisms of the gene encoding dopaminergic pathway transporter DAT haplotype, dopaminergic receptors, catechol-O-methyltransferase and monoamine oxidase A. We also evaluated epilepsy-related factors (e.g. seizure frequency, age of onset, duration and status epilepticus). ResultsThere was no difference between the groups for the studied polymorphisms. The polymorphism DRD4_VNTR was associated with family history of epilepsy (P = 0.003), DRD2_rs1800497 was related to status epilepticus (P = 0.022), and intron 8 VNTR DAT was related to higher seizure frequency (P = 0.019) and family history of epilepsy (P = 0.011). ConclusionsOur findings demonstrated that polymorphisms of the dopaminergic pathway are associated with significant clinical features of this form of epilepsy, such as seizure frequency, family history of epilepsy and status epilepticus.
- Lithium increases platelet serine-9 phosphorylated GSK-3 beta levels in drug-free bipolar disorder during depressive episodes(2015) SOUSA, Rafael T. de; ZANETTI, Marcus V.; TALIB, Leda L.; SERPA, Mauricio H.; CHAIM, Tiffany M.; CARVALHO, Andre F.; BRUNONI, Andre R.; BUSATTO, Geraldo F.; GATTAZ, Wagner E.; MACHADO-VIEIRA, RodrigoBackground: Glycogen synthase kinase-3 beta (GSK3 beta) is an intracellular enzyme directly implicated in several neural processes relevant to bipolar disorder (BD) pathophysiology. GSK3 beta is also an important target for lithium and antidepressants. When phosphorylated at serine-9, GSK3 beta becomes inactive. Few studies evaluated serine-9 phosphorylated GSK3 beta(phospho-GSK3 beta) levels in BD subjects in vivo and no study has assessed it specifically in bipolar depression. Also, the effect of lithium monotherapy on GSK3 beta has never been studied in humans. Methods: In 27 patients with bipolar depression, total GSK3 beta and phospho-GSK3 beta were assessed in platelets by enzyme immunometric assay. Subjects were evaluated before and after 6 weeks of lithium treatment at therapeutic levels. Healthy subjects (n = 22) were used as a control group. Results: No differences in phospho-GSK3 beta or total GSK3 beta were observed when comparing drug-free BD subjects in depression and healthy controls. Baseline HAM-D scores were not correlated with phospho GSK3 beta and total GSK3 beta levels. From baseline to endpoint, lithium treatment inactivated GSK3 beta by significantly increasing phospho-GSK3 beta levels (p = 0.010). Clinical improvement (baseline HAM-D endpoint HAM-D) negatively correlated with the increase in phospho-GSK3 beta (p = 0.03). Conclusion: The present results show that lithium inactivates platelet GSK3 beta in BD during mood episodes. No direct association with pathophysiology of BD was observed. Further studies are needed to clarify the role of GSK3 beta as a key biomarker in BD and its association with treatment response as well as the relevance of GSK3 beta in other neuropsychiatric disorders and as a new therapeutic target per se.