28 resultados para Memory response


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It has been already shown that delivering tDCS that are spaced by an interval alters its impact on motor plasticity. These effects can be explained, based on metaplasticity in which a previous modification of activity in a neuronal network can change the effects of subsequent interventions in the same network. But to date there is limited data assessing metaplasticity effects in cognitive functioning.

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This study used event-related potentials to examine interactions between mood, sentence context, and semantic memory structure in schizophrenia. Seventeen male chronic schizophrenia and 15 healthy control subjects read sentence pairs after positive, negative, or neutral mood induction. Sentences ended with expected words (EW), within-category violations (WCV), or between-category violations (BCV). Across all moods, patients showed sensitivity to context indexed by reduced N400 to EW relative to both WCV and BCV. However, they did not show sensitivity to the semantic memory structure. N400 abnormalities were particularly enhanced under a negative mood in schizophrenia. These findings suggest abnormal interactions between mood, context processing, and connections within semantic memory in schizophrenia, and a specific role of negative mood in modulating semantic processes in this disease.

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Dissertação de mestrado integrado em Engenharia e Gestão de Sistemas de Informação

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Dissertação de mestrado em Plant Molecular Biology, Biotechnology and Bioentrepreneurship

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Tese de Doutoramento em Engenharia Eletrónica e Computadores.

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An association between obesity and depression has been indicated in studies addressing common physical (metabolic) and psychological (anxiety, low self-esteem) outcomes. Of consideration in both obesity and depression are chronic mild stressors to which individuals are exposed to on a daily basis. However, the response to stress is remarkably variable depending on numerous factors, such as the physical health and the mental state at the time of exposure. Here a chronic mild stress (CMS) protocol was used to assess the effect of high-fat diet (HFD)-induced obesity on response to stress in a rat model. In addition to the development of metabolic complications, such as glucose intolerance, diet-induced obesity caused behavioral alterations. Specifically, animals fed on HFD displayed depressive- and anxious-like behaviors that were only present in the normal diet (ND) group upon exposure to CMS. Of notice, these mood impairments were not further aggravated when the HFD animals were exposed to CMS, which suggest a ceiling effect. Moreover, although there was a sudden drop of food consumption in the first 3 weeks of the CMS protocol in both ND and HFD groups, only the CMS-HFD displayed an overall noticeable decrease in total food intake during the 6 weeks of the CMS protocol. Altogether, the study suggests that HFD impacts on the response to CMS, which should be considered when addressing the consequences of obesity in behavior.

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Spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an untreatable autosomal dominant neurodegenerative disease, and the most common such inherited ataxia worldwide. The mutation in SCA3 is the expansion of a polymorphic CAG tri-nucleotide repeat sequence in the C-terminal coding region of the ATXN3 gene at chromosomal locus 14q32.1. The mutant ATXN3 protein encoding expanded glutamine (polyQ) sequences interacts with multiple proteins in vivo, and is deposited as aggregates in the SCA3 brain. A large body of literature suggests that the loss of function of the native ATNX3-interacting proteins that are deposited in the polyQ aggregates contributes to cellular toxicity, systemic neurodegeneration and the pathogenic mechanism in SCA3. Nonetheless, a significant understanding of the disease etiology of SCA3, the molecular mechanism by which the polyQ expansions in the mutant ATXN3 induce neurodegeneration in SCA3 has remained elusive. In the present study, we show that the essential DNA strand break repair enzyme PNKP (polynucleotide kinase 3'-phosphatase) interacts with, and is inactivated by, the mutant ATXN3, resulting in inefficient DNA repair, persistent accumulation of DNA damage/strand breaks, and subsequent chronic activation of the DNA damage-response ataxia telangiectasia-mutated (ATM) signaling pathway in SCA3. We report that persistent accumulation of DNA damage/strand breaks and chronic activation of the serine/threonine kinase ATM and the downstream p53 and protein kinase C-d pro-apoptotic pathways trigger neuronal dysfunction and eventually neuronal death in SCA3. Either PNKP overexpression or pharmacological inhibition of ATM dramatically blocked mutant ATXN3-mediated cell death. Discovery of the mechanism by which mutant ATXN3 induces DNA damage and amplifies the pro-death signaling pathways provides a molecular basis for neurodegeneration due to PNKP inactivation in SCA3, and for the first time offers a possible approach to treatment.

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Tese de Doutoramento em Ciências da Saúde

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Executive functioning (EF), which is considered to govern complex cognition, and verbal memory (VM) are constructs assumed to be related. However, it is not known the magnitude of the association between EF and VM, and how sociodemographic and psychological factors may affect this relationship, including in normal aging. In this study, we assessed different EF and VM parameters, via a battery of neurocognitive/psychological tests, and performed a Canonical Correlation Analysis (CCA) to explore the connection between these constructs, in a sample of middle- aged and older healthy individuals without cognitive impairment (N = 563, 50+ years of age). The analysis revealed a positive and moderate association between EF and VM independently of gender, age, education, global cognitive performance level, and mood. These results confirm that EF presents a significant association with VM performance.

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Dissertação de mestrado em Educação Especial (área de especialização em Dificuldades de Aprendizagem Específicas)

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Dissertação de mestrado em Genética Molecular

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Dissertação de mestrado integrado em Arquitectura (área de especialização de Cultura Arquitectónica)