LEDA LEME TALIB

(Fonte: Lattes)
Índice h a partir de 2011
26
Projetos de Pesquisa
Unidades Organizacionais
Instituto de Psiquiatria, Hospital das Clínicas, Faculdade de Medicina
LIM/27 - Laboratório de Neurociências, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 10 de 13
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    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, Rodrigo
    Background: 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.
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    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.
  • article 4 Citação(ões) na Scopus
    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.
  • article 44 Citação(ões) na Scopus
    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, Rodrigo
    Background: 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.
  • conferenceObject
    Anti-psychotic Treatment Decreased iPLA2 Activity in First Episode Drug Naive Patients (DNP)
    (2014) TALIB, Leda Leme; JOAQUIM, Helena P. G.; SERPA, Mauricio H.; BILT, Martinus Th van de; BUSATTO, Geraldo; ZANETTI, Marcus V.; GATTAZ, Wagner F.
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    Increased Glycogen Synthase Kinase-3B (GSK3B) Expression in Platelets of First Onset Psychosis Non-affective Patients
    (2014) JOAQUIM, Helena P. G.; TALIB, Leda L.; BILT, Martinus Th van de; ZANETTI, Marcus V.; BUSATTO, Geraldo; SERPA, Mauricio H.; GATTAZ, Wagner F.
  • article 7 Citação(ões) na Scopus
    Antipsychotic drugs decrease iPLA(2) gene expression in schizophrenia
    (2013) KERR, Daniel Shikanai; TALIB, Leda Leme; YAMAMOTO, Victor Junji; FERREIRA, Aline S.; ZANETTI, Marcus V.; SERPA, Mauricio H.; BUSATTO, Geraldo F.; BILT, Martinus Theodorus Van de; GATTAZ, Wagner Farid
  • conferenceObject
    ANTIPSYCHOTIC TREATMENT DECREASED IPLA2 ACTIVITY IN FIRST EPISODE DRUG NAIVE PATIENTS WITH SCHIZOPHRENIA
    (2014) TALIB, Leda L.; JOAQUIM, Helena; SERPA, Mauricio; BUSATTO, Geraldo; BILT, Martinus van de; ZANETTI, Marcus; GATTAZ, Wagner
  • conferenceObject
    PLA2 GENE EXPRESSION IN FIRST EPISODE DRUG NAIVE PATIENTS
    (2014) KERR, Daniel S.; SERPA, Mauricio; TALIB, Leda L.; BILT, Martinus Theodorus Van De; ALCANTARA, Juliana; CHAIM, Tiffany; BUSATTO, Geraldo; ZANETTI, Marcus; GATTAZ, Wagner
  • conferenceObject
    INCREASED GLYCOGEN SYNTHASE KINASE-3B (GSK-3B) EXPRESSION IN PLATELETS OF FIRST ONSET PSYCHOSIS NON-AFFECTIVE PATIENTS
    (2014) JOAQUIM, Helena P. G.; TALIB, Leda L.; ZANETTI, Marcus; BILT, Martinus van de; BUSATTO, Geraldo; SERPA, Mauricio; GATTAZ, Wagner