Is childhood cat ownership a risk factor for schizophrenia later in life?
Segundo o resumo do trabalho, dois estudos anteriores já sugeriam que a convivência de crianças com gatos seria um possível fator de risco para o desenvolvimento posterior da esquizofrenia ou outro transtorno mental grave. Os três pesquisadores testaram novamente a hipótese e chegaram aos mesmos resultados, sugerindo que a convivência de crianças com gatos é significativamente mais comum em famílias nas quais as crianças desenvolvem doenças mentais graves. Os pesquisadores alertam que a explicação pode ser a presença do parasita Toxoplasma gondii e pedem que mais pesquisas sejam feitas para comprovar os riscos.
Mais informações: http://www.schres-journal.com/article/S0920-9964(15)00176-0/abstract
Por: Cenita Pereira Borges 12 de fevereiro de 2016 às 12:54Oral administration of d-galactose induces cognitive impairments and oxidative damage in rats.
Behav Brain Res. 2015 Dec 31;302:35-43.
Budni J, Pacheco R, da Silva S, Garcez ML, Mina F, Bellettini-Santos T, de Medeiros J, Voss BC, Steckert AV, Valvassori SD, Quevedo J.
Abstract: d-Galactose (d-gal) is a reducing sugar that can be used to mimic the characteristics of aging in rodents; however, the effects of d-gal administration by oral route are not clear. Therefore, the aim of this study was to elucidate if the oral administration of d-gal induces cognitive impairments, neuronal loss, and oxidative damage, mimicking an animal model of aging. Male adult Wistar rats (4 months old) received d-gal (100mg/kg) via the oral route for a period of 1, 2, 4, 6 or 8 weeks. The results showed cognitive impairments in the open-field test in the 4th and 6th weeks after d-gal administration, as well as an impairment in spatial memory in the radial maze test after the 6th week of d-gal administration. The results indicated increase of levels of thiobarbituric acid reactive species-TBARS-and carbonyl group content in the prefrontal cortex from the 4th week, and in all weeks of d-gal administration, respectively. An increase in the levels of TBARS and carbonyl group content was observed in the hippocampus over the entire period of d-gal treatment. In the 8th week of d-gal administration, we also observed reductions in synaptophysin and TAU protein levels in the prefrontal cortex. Thus, d-gal given by oral route caused cognitive impairments which were accompanied by oxidative damage. Therefore, these results indicate that orally administered d-gal can induce the behavioral and neurochemical alterations that are observed in the natural aging process. However, oral d-gal effect in rats deserve further studies to be better described.
Mais informações: http://www.ncbi.nlm.nih.gov/pubmed/26748256
Por: Cenita Pereira Borges 06 de fevereiro de 2016 às 21:30Apresentação pública de mestrado
Na última sexta feira (18/12/2015) realizou-se a apresentação pública do mestrando Ricardo Chiengo Sapalo Cassoma, abordando o tema: "Avaliação do efeito protetor do ácido fólico em um modelo animal de senescência induzido pela d-galactose". A orientação do trabalho foi efetuada pela Prof.ª Dr.ª Josiane Budni, na ocasião a banca relatora composta pela Prof.ª Dr.ª Alexandra Ioppi Zugno. A atuação de Ricardo foi memorável, após a apresentação, relatora e orientadora comentaram não apenas sobre a postura técnica, mais esporam suas admirações pela pessoa de Ricardo, relando sua passagem pelo programa de pós graduação. Ricardo, agora mestre, estará retornando ao seu País de origem (Angola), deixando aqui no Brasil muitos amigos e admiradores. Comovido, abriu seu coração para os presentes falando de suas conquistas e dificuldade que enfrentou pelo caminho, emocionando os presentes. Após, no laboratório de neurodegeneração despediu-se com uma confraternização que ficará na memória de todos. Muito obrigado Ricardo pela sua passagem aqui na Unesc, esperamos seu retorno para o Doutorado ansiosamente!
Direct Conversion of Normal and Alzheimer's Disease Human Fibroblasts into Neuronal Cells by Small Molecules.
_.jpg?1450122553 "Direct Conversion of Normal and Alzheimer's Disease Human Fibroblasts into Neuronal Cells by Small Molecules.")
Cell Stem Cell. 2015 Aug 6;17(2):204-12.
Hu W, Qiu B, Guan W, Wang Q, Wang M2, Li W, Gao L, Shen L, Huang Y, Xie G, Zhao H, Jin Y, Tang B, Yu Y, Zhao J, Pei G.
Abstract
Neuronal conversion from human fibroblasts can be induced by lineage-specific transcription factors; however, the introduction of ectopic genes limits the therapeutic applications of such induced neurons (iNs). Here, we report that human fibroblasts can be directly converted into neuronal cells by a chemical cocktail of seven small molecules, bypassing a neural progenitor stage. These human chemical-induced neuronal cells (hciNs) resembled hiPSC-derived neurons and human iNs (hiNs) with respect to morphology, gene expression profiles, and electrophysiological properties. This approach was further applied to generate hciNs from familial Alzheimer's disease patients. Taken together, our transgene-free and chemical-only approach for direct reprogramming of human fibroblasts into neurons provides an alternative strategy for modeling neurological diseases and for regenerative medicine.
Mais informações: http://www.ncbi.nlm.nih.gov/pubmed/26253202
Por: Cenita Pereira Borges 14 de dezembro de 2015 às 16:26Revisão sistemática e meta-análise: Será que o uso do tabaco causa psicose ?
The Lancet Psychiatry 2015
Gurillo P, Jauhar S, Murray RM, MacCabe JH.
Although the association between psychotic illness and cigarette smoking is well known, the reasons are unclear why people withpsychosis are more likely to smoke than are the general population. We aimed to test several hypotheses. First, that daily tobacco use is associated with an increased risk of psychotic illness in both case-control and prospective studies. Second, that smoking is associated with an earlier age at onset of psychotic illness. Finally, that an earlier age at initiation of smoking is associated with an increased risk of psychosis. We also aimed to derive an estimate of the prevalence of smoking in patients presenting with their first episode of psychosis.We searched Embase, Medline, and PsycINFO and selected observational studies in which rates of smoking were reported in people with psychotic disorders, compared with controls. We calculated the weighted mean difference for age at onset of psychosis and age at initiation of smoking. For categorical outcomes, we calculated odds ratios from cross-sectional studies and risk ratios from prospective studies.Of 3717 citations retrieved, 61 studies comprising 72 samples met inclusion criteria. The overall sample included 14 555 tobacco users and 273 162 non-users. The prevalence of smoking in patients presenting with their first episode of psychosis was 0·57 (95% CI 0·52-0·62; p<0·0001). In case-control studies, the overall odds ratio for the first episode of psychosis in smokers versus non-smokers was 3·22 (95% CI 1·63-6·33), with some evidence of publication bias (Egger's test p=0·018, Begg's test p=0·007). For prospective studies, we calculated an overall relative risk of new psychotic disorders in daily smokers versus non-smokers of 2·18 (95% CI 1·23-3·85). Daily smokers developed psychotic illness at an earlier age than did non-smokers (weighted mean difference -1·04 years, 95% CI -1·82 to -0·26). Those with psychosis started smoking at a non-significantly earlier age than did healthy controls (-0·44 years, 95% CI -1·21 to 0·34).
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