No abstract

Ischemic stroke is a major cause of morbidity and mortality all over the world. Among impairments observed in survivors there is a significant cognitive learning and memory deficit. Neuroprotective strategies are being investigated to minimize such deficits after an ischemia event. Here we investigated the neuroprotective potential of physical exercise and green tea in an animal model of ischemia-reperfusion. Eighty male rats were divided in 8 groups and submitted to either transient brain ischemia-reperfusion or a sham surgery after 8 weeks of physical exercise and/or green tea supplementation. Ischemia-reperfusion was performed by bilateral occlusion of the common carotid arteries during 30 min. Later, their memory was evaluated in an aversive and in a non-aversive task, and hippocampus and prefrontal cortex were removed for biochemical analyses of possible oxidative stress effects. Ischemia-reperfusion impaired learning and memory. Reactive oxygen species were increased in the hippocampus and prefrontal cortex. Eight weeks of physical exercise and/or green tea supplementation before the ischemia-reperfusion event showed a neuroprotective effect; both treatments in separate or together reduced the cognitive deficits and were able to maintain the functional levels of antioxidant enzymes and glutathione.

O processo de envelhecimento é acompanhado por uma série de alterações psicossociais e biológicas, dentre as quais está incluído o declínio cognitivo. Dependendo das condições genéticas, estilo de vida, atividades e interações sociais do idoso, o declínio pode ser acelerado ou retardado. O objetivo deste trabalho foi avaliar o perfil cognitivo, o tempo de reação, o risco de quedas e a qualidade do sono de idosos institucionalizados da cidade de Uruguaiana-RS. Foram avaliados 10 idosos de ambos os sexos utilizando como instrumentos o Mini-Exame do Estado Mental (MEEM), a Escala de Depressão Geriátrica (EDG), o Inventário de Ansiedade Traço-Estado, o Teste de Tempo de Reação (TTR), a Escala de Eficácia de Quedas (EEQ) e o Índice de Qualidade de Sono de Pittsburgh (IQSP). Os resultados apontaram a presença de declínio cognitivo em 40% dos idosos, indícios de depressão em 60% deles e tendência ao desenvolvimento de ansiedade. 76% dos idosos classificaram a qualidade de seu sono como boa, mencionando alguns fatores que interferem na mesma, e 64% revelaram haver preocupação ou medo de cair. No TTR os idosos apresentaram escore médio de 2,175 ± 0,32 s. Estes resultados podem estar relacionados ao estilo de vida adotado pela maioria dos idosos institucionalizados, fora do seu convívio familiar, favorecendo seu isolamento e sua inatividade física e mental, gerando declínio da capacidade cognitiva. Nossos resultados demonstram um percentual significativo de risco de demência, depressão e/ou ansiedade nos idosos institucionalizados avaliados.

Early life experiences program lifelong responses to stress. In agreement, resilience and vulnerability to psychopathologies, such as posttraumatic stress disorder (PTSD), have been suggested to depend on the early background. New therapies have targeted memory reconsolidation as a strategy to modify the emotional valence of traumatic memories. Here, we used animal models to study the molecular mechanism through which early experiences may later affect aversive memory reconsolidation. Handling (H)—separation of pups from dams for 10 min—or maternal separation (MS) — 3-h separation—were performed from PDN1–10, using non-handled (NH) litters as controls. Adult males were trained in a contextual fear conditioning (CFC) task; 24 h later, a short reactivation session was conducted in the conditioned or in a novel context, followed by administration of midazolam 3 mg/kg i.p. (mdz), known to disturb reconsolidation, or vehicle; a test session was performed 24 h after. The immunocontent of relevant proteins was studied 15 and 60 min after memory reactivation in the dorsal hippocampus (dHc) and basolateral amygdala complex (BLA). Mdz-treated controls (NH) showed decreased freezing to the conditioned context, consistent with reconsolidation impairment, but H and MS were resistant to labilization. Additionally, MS males showed increased freezing to the novel context, suggesting fear generalization; H rats showed lower freezing than the other groups, in accordance with previous suggestions of reduced emotionality facing adversities. Increased levels of Zif268, GluN2B, β-actin and polyubiquitination found in the BLA of all groups suggest that memory reconsolidation was triggered. In the dHc, only NH showed increased Zif268 levels after memory retrieval; also, a delay in ERK1/2 activation was found in H and MS animals. We showed here that reconsolidation of a contextual fear memory is insensitive to interference by a GABAergic drug in adult male rats exposed to different neonatal experiences; surprisingly, we found no differences in the reconsolidation process in the BLA, but the dHc appears to suffer temporal desynchronization in the engagement of reconsolidation. Our results support a hippocampal-dependent mechanism for reconsolidation resistance in models of early experiences, which aligns with current hypotheses for the etiology of PTSD.