DANIEL SHIKANAI KERR
Projetos de Pesquisa
Unidades Organizacionais
LIM/27 - Laboratório de Neurociências, Hospital das Clínicas, Faculdade de Medicina
11 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 11
- Genetic polymorphisms of the 5HT receptors are not related with depression in temporal lobe epilepsy caused by hippocampal sclerosis(2018) VINCENTIIS, Silvia; ALCANTARA, Juliana; RZEZAK, Patricia; KERR, Daniel S.; GATTAZ, Wagner F.; LINDEN JR., Helio van der; SANTOS, Bernardo dos; MELO-SOUZA, Sebastiao E.; ARRUDA, Francisco; RAGAZZO, Paulo; CHAIM-AVANCINI, Tiffany; SERPA, Mauricio H.; FERNANDES, Fernando; MORENO, Ricardo A.; BUSATTO, Geraldo; ALESSI, Ruda; DEMARQUE, Renata; VALENTE, Kette D.Background: Temporal lobe epilepsy caused by hippocampal sclerosis (TLE-HS) is the most frequent form of drug-resistant epilepsy in adults. Mood disorders are the most frequent psychiatric comorbidities observed in these patients. Common pathophysiological mechanisms of epilepsy and psychiatric comorbidities include abnormalities in the serotonin pathway. The primary goal of this study was to determine the possible association between polymorphisms of genes encoding the serotonin receptors 5HT1A (rs6295), 5HT1B (rs6296), and 5HT2C (rs6318) and the presence of mood disorders in patients with TLE-HS. Our secondary goal was to evaluate the possible association between these variants and susceptibility to develop seizures in TLE-HS. Methods: We assessed 119 patients with TLE-HS, with and without psychiatric comorbidities; 146 patients with major depressive disorder; and 113 healthy volunteers. Individuals were genotyped for the rs6295, rs6296, and rs6318 polymorphisms. Results: No difference was observed between the group with TLE-HS, healthy controls, and the group with major depressive disorder without epilepsy regarding the polymorphisms that were evaluated. There was no correlation between rs6318, rs6295, rs6296, and epilepsy-related factors and history of psychiatric comorbidities. Conclusions: Our work suggests that the studied polymorphisms were not related to the presence of TLE, psychiatric comorbidities in TLE, and epilepsy-related factors.
- 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 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, WagnerconferenceObject Global DNA Methylation Status of Patients in the First-episode Psychosis and After Remission(2015) CARDILLO, Giancarlo M.; PAULA, Vanessa J. R. de; CARVALHO, Marlia P. F.; POLHO, Gabriel B.; SERPA, Mauricio H.; TALIB, Leda L.; BILT, Martinus T. van de; ZANETTI, Marcus V.; GATTAZ, Wagner F.; KERR, Daniel S.- COMT Met (158) modulates facial emotion recognition in bipolar I disorder mood episodes(2012) SOEIRO-DE-SOUZA, Marcio Gerhardt; BIO, Danielle Soares; DAVID, Denise Petresco; SANTOS JR., Domingos Rodrigues dos; KERR, Daniel Shikanai; GATTAZ, Wagner Farid; MACHADO-VIEIRA, Rodrigo; MORENO, Ricardo AlbetoBackground: One of the many cognitive deficits reported in bipolar disorder (BD) patients is facial emotion recognition (FER), which has recently been associated with dopaminergic catabolism. Catechol-O-methyltransferase (COMT) is one of the main enzymes involved in the metabolic degradation of dopamine (DA) in the prefrontal cortex (PFC). The COMT gene polymorphism rs4680 (Val(158)Met) Met allele is associated with decreased activity of this enzyme in healthy controls. The objective of this study was to evaluate the influence of Val(158)Met on FER during manic and depressive episodes in BD patients and in healthy controls. Materials and methods: 64 BD type I patients (39 in manic and 25 in depressive episodes) and 75 healthy controls were genotyped for COMT rs4680 and assessed for FER using the Ekman 60 Faces (EK60) and Emotion Hexagon (Hx) tests. Results: Bipolar manic patients carrying the Met allele recognized fewer surprised faces, while depressed patients with the Met allele recognized fewer ""angry"" and ""happy"" faces. Healthy homozygous subjects with the Met allele had higher FER scores on the Hx total score, as well as on ""disgust"" and ""angry"" faces than other genotypes. Conclusion: This is the first study suggesting that COMT rs4680 modulates FER differently during BD episodes and in healthy controls. This provides evidence that PFC DA is part of the neurobiological mechanisms of social cognition. Further studies on other COMT polymorphisms that include euthymic BD patients are warranted. ClinicalTrials.gov Identifier: NCT00969.
- Apolipoprotein E genotype is not associated with cognitive impairment in older adults with bipolar disorder(2016) KERR, Daniel Shikanai; STELLA, Florindo; RADANOVIC, Marcia; APRAHAMIAN, Ivan; BERTOLLUCCI, Paulo Henrique Ferreira; FORLENZA, Orestes VicenteObjectivesCognitive decline is part of the long-term outcome for many individuals with bipolar disorder (BD). The epsilon 4 allele (APOE*4) of apolipoprotein E (APOE) is a well-established risk factor for dementia in Alzheimer's disease (AD). However, its contribution to the risk of cognitive deterioration in BD has not yet been determined. Our aim was to analyze the APOE genotype association with cognitive status in a sample of older adults with BD and compare this to the association in individuals with AD, individuals with mild cognitive impairment (MCI), and healthy controls. MethodsParticipants (n=475) were allocated to four groups: individuals with BD (n=77), those with AD (n=211), those with MCI (n=43), and healthy controls (n=144) according to clinical and neuropsychological assessment. APOE was genotyped by real-time polymerase chain reaction. Tukey's honest significant difference test and Pearson's chi-squared test were used to compare diagnostic groups. ResultsSubjects with BD were similar to controls with respect to the distribution of the APOE genotype (p=0.636) and allele frequencies (p=0.481). Significant differences were found when comparing the AD group to the BD group or to controls (APOE genotype: p<0.0002; allele frequencies: p<0.001). APOE*4 was significantly increased in the AD group when compared to the BD group (p=0.031) and controls (p<0.0001). The cognitively impaired BD subgroup (Mini-Mental State Examination below the cutoff score and/or neuropsychological assessment compatible with MCI) had a statistically significant higher frequency of APOE*2 compared to the AD group (p=0.003). ConclusionsAPOE*4 is not associated with the diagnosis of BD and does not impact the occurrence of dementia in BD. Given the distinct clinical and biological features of cognitive impairment in BD, we hypothesized that dementia in BD is unrelated to AD pathological mechanisms.
- Leukocyte telomere length in patients with schizophrenia: A meta-analysis(2015) POLHO, G. B.; DE-PAULA, V. J.; CARDILLO, G.; SANTOS, B. dos; KERR, D. S.Schizophrenia has been suggested as a syndrome of accelerated aging. Telomere length (TL) decrease is considered one biological marker associated with age and can be accelerated by pathological characteristics present in schizophrenia. Several studies evaluated TL in schizophrenia, but the results are still controversial. The aim of this study was to conduct a meta-analysis of the existing results of TL in leukocytes of individuals with schizophrenia compared to healthy controls. A search was performed in PubMed, using the keywords 'telomere schizophrenia' and 'telomere psychosis'. We included data from original articles that measured TL in leukocytes of human patientswith schizophrenia and healthy control subjects. 45 articles were found, but only 7 met our criteria. Telomere length of controls was not statistically different from that of patients with schizophrenia (p = 0.07). Crossvalidation with the leave-one-out method resulted in a significant model (p = 0.03) in which TL of individuals with schizophrenia is smaller than control (SMD = 0.38; 95% CI = [0.05, 0.72]). We also propose a biological pathway through which schizophrenia could promote telomere erosion and how antipsychotics might compensate this loss. There are few studies made on this subject with diverse methodology and heterogeneous sample. Some articles did not consider other possible influences on TL. Overall our results suggest that TL is decreased in schizophrenia. Although this is consistent with the idea of accelerated aging, schizophrenia is a complex disease and there are several factors that influence TL that should be controlled in future studies.
- Genetic polymorphisms of the serotonin transporter are not related with depression in temporal lobe epilepsy caused by hippocampal sclerosis(2021) VINCENTIIS, Silvia; ALCANTARA, Juliana A.; RZEZAK, Patricia; KERR, Daniel S.; GATTAZ, Wagner F.; JR, Helio van der Linden; SANTOS, Bernardo dos; ARRUDA, Francisco; CHAIM-AVANCINI, Tiffany; SERPA, Mauricio H.; FERNANDES, Fernando; MORENO, Ricardo A.; BUSATTO, Geraldo F.; ALESSI, Ruda; DEMARQUE, Renata; VALENTE, Kette D.Background: Mood disorders are the most frequent psychiatric disorders in patients with temporal lobe epilepsy caused by hippocampal sclerosis (TLE-HS). The pathophysiological mechanisms in common between TLE and mood disorders include abnormalities in the serotonergic pathway. We aimed to evaluate the association between serotonin transporter genetic polymorphisms - 5-HTTLPR and 5-HTTVNTR - and the presence of mood disorders in patients with TLE-HS. Methods: We evaluated 119 patients with TLE-HS, with and without psychiatric disorder; 146 patients diagnosed with major depressive disorder (MDD), and 113 healthy volunteers. Individuals were geno-typed for the 5-HTTLPR and 5-HTTVNTR polymorphisms. Results: No difference was observed between the TLE-HS groups, healthy controls, and MDD without epilepsy. There was a correlation between the 12-allele of the 5-HTTVNTR and the family history of patients with epilepsy with TLE-HS (p = 0.013). Conclusions: In this study conducted in two Brazilian centers, the serotonin transporter polymorphisms evaluated cannot be associated with depressive disorder in patients with TLE-HS. Still, they do have some influence over some clinical characteristics of epilepsy in TLE-HS. These data may not be reproduced in other populations with distinct ethnic characteristics.
- Ghrelin and eating disorders(2015) FABBRI, Alessandra Donzelli; DERAM, Sophie; KERR, Daniel Shikanai; CORDAS, Taki AthanassiosBackground: Ghrelin is a potent hormone with central and peripheral action. This hormone plays an important role in the regulation of appetite, food intake, and energy balance. Studies have suggested that ghrelin is involved with eating disorders (ED), particularly bingeing and purging. Genetic variants have also been studied to explain changes in eating behavior. Methods: We conducted a literature review; we searched PubMed, Scientific Electronic Library Online (SciELO), and LILACS databases using the keywords ""eating disorder"", ""ghrelin"", ""polymorphism"", ""anorexia nervosa"", ""bulimia nervosa"", ""binge eating disorder"", and their combinations. We found 319 articles. Thirty-nine articles met the inclusion criteria. Results: High levels of ghrelin were found in patients with anorexia nervosa (AN), especially in the purging subtype (AN-P). There was also a positive correlation between fasting ghrelin level and frequency of episodes of bingeing/purging in bulimia nervosa (BN) and the frequency of bingeing in periodic binge eating disorder (BED). Some polymorphisms were associated with AN and BN. Conclusion: Changes in ghrelin levels and its polymorphism may be involved in the pathogenesis of EDs; however, further studies should be conducted to clarify the associations.
- Donepezil effects on cholesterol and oxysterol plasma levels of Alzheimer's disease patients(2018) COSTA, Alana C.; JOAQUIM, Helena P. G.; NUNES, Valeria S.; KERR, Daniel S.; FERREIRA, Guilherme S.; FORLENZA, Orestes V.; GATTAZ, Wagner F.; TALIB, Leda LemeCholesterol is an essential component in the structure and function of cell membranes and has been associated with the major pathological signatures of Alzheimer's disease (AD). To maintain brain cholesterol homeostasis, it is converted into 24(S)-hydroxycholesterol (24OHC) which can be driven through the blood-brain barrier. Several studies have already described a decrease in 24OHC and an increase of 27(S)-hydroxycholesterol (27OHC) in AD, as a reflection of disease burden, the loss of metabolically active neurons and the degree of structural atrophy. It is also well known that peripheral cholesterol is altered in AD patients. However, there are no data regarding effects of AD treatment in this cholesterol pathway. Since a study from our group indicated a significant increase in membrane phospholipid metabolism by donepezil, the aim of this study was to evaluate the effect of short- and long-term donepezil treatment on cholesterol and metabolites 24OHC and 27OHC in plasma of AD patients and in healthy volunteers. At baseline, we found a decrease of 24OHC (p = 0.003) in AD patients. Cholesterol levels increased with donepezil treatment (p = 0.04) but no differences were observed regarding 24OHC and 27OHC. However, these results confirm and extend previous studies demonstrating disturbed cholesterol turnover in Alzheimer's disease.